Seleno-amino acid and application thereof
By using seleno amino acids, especially L-selenomethionine, problems such as intestinal flora disorders, intestinal damage and blood function damage caused by carbon tetrachloride poisoning were solved, and significant prevention and treatment effects were achieved.
Patent Information
- Application Number
- CN202411599513.9
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2024-11-08
- Publication Date
- 2025-02-18
AI Technical Summary
The prior art is difficult to effectively prevent and treat symptoms such as intestinal flora disorders, intestinal damage and blood function damage caused by drugs or chemical agents such as carbon tetrachloride.
Selenobio amino acids, especially L-selenomethionine, are used as compositions or formulations for the prevention and treatment of the above symptoms. The seleno amino acid can improve intestinal dysbiosis, increase blood sugar and albumin levels, reduce alanine aminotransferase and cereal aminotransferase activity, increase alkaline phosphatase activity, and improve intestinal damage.
Seleno amino acids significantly improve intestinal flora disorders, intestinal damage and blood function damage caused by carbon tetrachloride poisoning, and have excellent preventive and therapeutic effects.
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Figure CN119454682A_ABST
Abstract
Description
Technical Field
[0001] The present invention relates to the field of medicines, and in particular to a selenoamino acid and a use thereof. Background Art
[0002] Drugs or chemical reagents often have toxic side effects, and their application or poisoning often causes damage to the digestive system and blood system with vigorous metabolism. For example, carbon tetrachloride is a commonly used chemical reagent in the field of pharmaceutical chemical industry, and is often used as a solvent for drug organic synthesis or as an extractant for drug extraction. However, contact, inhalation, application or accidental ingestion of carbon tetrachloride chemical reagents often causes carbon tetrachloride poisoning, which often leads to adverse symptoms in the digestive system and blood system with vigorous metabolism, such as intestinal flora imbalance, intestinal damage and functional damage of the blood system such as decreased blood sugar and albumin levels, abnormal enzyme activity in the blood, etc., which in turn lead to discomfort in the body such as nausea, vomiting, indigestion, fatigue and edema, etc. In severe cases, it can further lead to the occurrence of acute symptoms such as acute enteritis and shock, and even endanger life and health. The effective prevention and treatment of symptoms such as intestinal flora imbalance, intestinal damage and blood function damage caused by carbon tetrachloride chemical reagent poisoning is of great significance to improving carbon tetrachloride chemical reagent poisoning. Therefore, how to prevent and treat the damage caused by the toxic side effects of drugs or chemical reagents, such as intestinal flora imbalance, intestinal damage and blood function damage, has always been a research hotspot today.
[0003] Therefore, there is a need in the art to develop a drug that can effectively treat the damage caused by the toxic side effects of drugs or chemical agents, such as intestinal flora imbalance, intestinal damage, and blood function damage. Summary of the invention
[0004] The object of the present invention is to provide a use of selenoamino acids, which can be used to improve intestinal flora imbalance and have excellent preventive and therapeutic effects on hypoglycemia, hypoalbuminemia, increased alanine aminotransferase and aspartate aminotransferase activities, reduced alkaline phosphatase activity and intestinal damage.
[0005] In a first aspect, the present invention provides a use of a selenoamino acid for preparing a composition or a preparation, wherein the composition or preparation is used for one or more uses selected from the following groups: (i) preventing and / or treating intestinal dysbiosis; (ii) preventing and / or treating hypoglycemia; (iii) increasing blood sugar; (iv) preventing and / or treating hypoalbuminemia; (v) increasing albumin; (vi) preventing and / or treating increased alanine aminotransferase activity; (vii) reducing alanine aminotransferase activity; (viii) preventing and / or treating increased aspartate aminotransferase activity; (ix) reducing aspartate aminotransferase activity; (x) preventing and / or treating decreased alkaline phosphatase activity; (xi) increasing alkaline phosphatase activity; (xii) preventing and / or treating intestinal damage; and / or (xiii) preventing and / or treating carbon tetrachloride poisoning or its complications.
[0006] Preferably, the selenoamino acid comprises selenomethionine.
[0007] Preferably, the selenoamino acid comprises L-selenomethionine.
[0008] Preferably, the selenomethionine is L-selenomethionine:
[0009]
[0010] Preferably, the composition or preparation is administered to a human or non-human mammal.
[0011] Preferably, the composition or preparation is administered to a subject to whom carbon tetrachloride is administered or poisoned by carbon tetrachloride.
[0012] Preferably, the subject of the prevention and / or treatment is a human or non-human mammal.
[0013] Preferably, the subject of the prevention and / or treatment is a subject administered with carbon tetrachloride or poisoned by carbon tetrachloride.
[0014] Preferably, the intestinal microecology is the intestinal microecology of a human or non-human mammal.
[0015] Preferably, the intestinal dysbiosis includes intestinal dysbiosis caused by administration of carbon tetrachloride or carbon tetrachloride poisoning.
[0016] Preferably, the intestinal microecological imbalance includes intestinal flora imbalance.
[0017] Preferably, the intestinal flora imbalance includes intestinal flora quantity imbalance.
[0018] Preferably, the intestinal flora includes one or more of Alistipes, Rikenellaceae_RC9_gut_group, Parabacteroides and Bifidobacterium.
[0019] Preferably, the intestinal dysbiosis includes intestinal hyperbacteriosis.
[0020] Preferably, the intestinal dysbiosis includes intestinal hyperbacteria, and the intestinal flora is selected from the following group: Alistipes, Rikenellaceae_RC9_gut_group, or a combination thereof.
[0021] Preferably, the intestinal dysbiosis includes intestinal flora hyperflora selected from the group consisting of Alistipes, Rikenellaceae_RC9_gut_group, or a combination thereof.
[0022] Preferably, the intestinal flora hyperbiosis includes intestinal flora overabundance disorder.
[0023] Preferably, the intestinal microecological imbalance includes intestinal flora deficiency.
[0024] Preferably, the intestinal dysbiosis includes intestinal flora deficiency, and the intestinal flora is selected from the group consisting of Parabacteroides (genus Parabacteroides), Bifidobacterium (genus Bifidobacterium), or a combination thereof.
[0025] Preferably, the intestinal dysbiosis comprises intestinal flora deficiency selected from the group consisting of Parabacteroides (genus Parabacteroides), Bifidobacterium (genus Bifidobacterium), or a combination thereof.
[0026] Preferably, the intestinal flora deficiency includes intestinal flora quantity deficiency.
[0027] Preferably, the prevention and / or treatment of intestinal dysbiosis comprises preventing and / or treating intestinal dysbiosis by reducing the number of intestinal flora selected from the group consisting of Alistipes, Rikenellaceae_RC9_gut_group, or a combination thereof.
[0028] Preferably, the prevention and / or treatment of intestinal dysbiosis comprises preventing and / or treating intestinal dysbiosis by increasing the number of intestinal flora selected from the group consisting of Parabacteroides, Bifidobacterium, or a combination thereof.
[0029] Preferably, the blood glucose is the blood glucose of a human or non-human mammal.
[0030] Preferably, the hypoglycemia is hypoglycemia in a human or non-human mammal.
[0031] Preferably, the hypoglycemia comprises hypoglycemia caused by administration of carbon tetrachloride or carbon tetrachloride poisoning.
[0032] Preferably, the prevention and / or treatment of hypoglycemia comprises preventing and / or treating hypoglycemia by increasing blood glucose.
[0033] Preferably, said increasing blood sugar comprises increasing the blood sugar content.
[0034] Preferably, the hypoalbuminemia is hypoalbuminemia in humans or non-human mammals.
[0035] Preferably, the hypoalbuminemia includes hypoalbuminemia caused by administration of carbon tetrachloride or carbon tetrachloride poisoning.
[0036] Preferably, the albumin is human or non-human mammal albumin.
[0037] Preferably, the albumin comprises albumin in blood.
[0038] Preferably, the prevention and / or treatment of hypoalbuminemia comprises preventing and / or treating hypoalbuminemia by increasing albumin.
[0039] Preferably, said increasing albumin comprises increasing the albumin content.
[0040] Preferably, the alanine aminotransferase is alanine aminotransferase from a human or non-human mammal.
[0041] Preferably, the increased activity of alanine aminotransferase includes increased activity of alanine aminotransferase caused by administration of carbon tetrachloride or carbon tetrachloride poisoning.
[0042] Preferably, the alanine aminotransferase comprises alanine aminotransferase in blood.
[0043] Preferably, the prevention and / or treatment of elevated alanine aminotransferase activity comprises preventing and / or treating elevated alanine aminotransferase activity by reducing the activity of alanine aminotransferase.
[0044] Preferably, the aspartate aminotransferase is aspartate aminotransferase of a human or non-human mammal.
[0045] Preferably, the increased aspartate aminotransferase activity includes the increased aspartate aminotransferase activity caused by the administration of carbon tetrachloride or carbon tetrachloride poisoning.
[0046] Preferably, the aspartate aminotransferase comprises aspartate aminotransferase in blood.
[0047] Preferably, the prevention and / or treatment of elevated aspartate aminotransferase activity comprises preventing and / or treating elevated aspartate aminotransferase activity by reducing aspartate aminotransferase activity.
[0048] Preferably, the alkaline phosphatase is alkaline phosphatase of human or non-human mammal.
[0049] Preferably, the reduction in alkaline phosphatase activity includes the reduction in alkaline phosphatase activity caused by administration of carbon tetrachloride or carbon tetrachloride poisoning.
[0050] Preferably, the alkaline phosphatase comprises alkaline phosphatase in blood.
[0051] Preferably, the prevention and / or treatment of alkaline phosphatase hypoactivity syndrome comprises preventing and / or treating alkaline phosphatase hypoactivity syndrome by increasing alkaline phosphatase activity.
[0052] Preferably, the subject of the intestinal injury is intestinal injury of a human or non-human mammal.
[0053] Preferably, the intestinal damage includes intestinal damage caused by administration of carbon tetrachloride or carbon tetrachloride poisoning.
[0054] Preferably, the intestinal damage includes one or more characteristics selected from the following group: intestinal mucosal disorder, intestinal mucosal thickening, increased intestinal inflammatory cells, severe intestinal extracellular deposition, or a combination thereof.
[0055] Preferably, the intestine comprises the colon.
[0056] Preferably, the prevention and / or treatment of intestinal injury comprises preventing and / or treating intestinal injury by improving one or more characteristics selected from the following group: intestinal mucosal disorder, intestinal mucosal thickening, increased intestinal inflammatory cells, severe intestinal extracellular deposition, or a combination thereof
[0057] Preferably, the subject of carbon tetrachloride poisoning or its complications is carbon tetrachloride poisoning or its complications in humans or non-human mammals.
[0058] Preferably, the complications of carbon tetrachloride poisoning are selected from the following group: intestinal dysbiosis, hypoglycemia, hypoalbuminemia, increased alanine aminotransferase activity, increased aspartate aminotransferase activity, decreased alkaline phosphatase activity, intestinal damage, or a combination thereof.
[0059] Preferably, the prevention and / or treatment of carbon tetrachloride poisoning or its complications includes (i) prevention and / or treatment of intestinal microecological imbalance; (ii) prevention and / or treatment of hypoglycemia; (iii) increase of blood glucose; (iv) prevention and / or treatment of hypoalbuminemia; (v) increase of albumin; (vi) prevention and / or treatment of increased alanine aminotransferase activity; (vii) reduction of alanine aminotransferase activity; (viii) prevention and / or treatment of increased aspartate aminotransferase activity; (ix) reduction of aspartate aminotransferase activity; (x) prevention and / or treatment of decreased alkaline phosphatase activity; (xi) increase of alkaline phosphatase activity; and / or (xii) prevention and / or treatment of intestinal damage.
[0060] Preferably, the subject comprises a subject to which carbon tetrachloride is administered.
[0061] Preferably, the subject comprises a subject poisoned by carbon tetrachloride.
[0062] Preferably, the subject includes a subject administered with carbon tetrachloride or poisoned by carbon tetrachloride.
[0063] Preferably, the subject comprises a subject suffering from carbon tetrachloride poisoning or its complications.
[0064] Preferably, the subject comprises a subject with intestinal damage.
[0065] Preferably, the intestinal damage includes intestinal damage caused by administration of carbon tetrachloride or carbon tetrachloride poisoning.
[0066] Preferably, the carbon tetrachloride poisoning includes carbon tetrachloride poisoning caused by oral ingestion and / or inhalation of carbon tetrachloride.
[0067] Preferably, the subject includes subjects suffering from intestinal dysbiosis, hypoglycemia, hypoalbuminemia, elevated alanine aminotransferase activity, elevated aspartate aminotransferase activity, reduced alkaline phosphatase activity, intestinal damage, and / or carbon tetrachloride poisoning or its complications.
[0068] Preferably, the non-human mammal is a mouse, rat, rabbit, cow, sheep, dog or horse.
[0069] Preferably, the mice comprise C57BL / 6 mice.
[0070] Preferably, the composition or preparation is a pharmaceutical composition or pharmaceutical preparation.
[0071] Preferably, the composition or preparation further comprises a pharmaceutically acceptable carrier.
[0072] Preferably, the composition or preparation is in the form of a solid preparation, a semisolid preparation or a liquid preparation.
[0073] Preferably, the composition or preparation is in the form of an oral preparation, an external preparation or an injection preparation.
[0074] Preferably, the composition or preparation is in the form of emulsion, tablet, capsule, oral liquid, granule, powder, syrup or injection.
[0075] In a second aspect, the present invention provides a method for (i) preventing and / or treating intestinal dysbiosis; (ii) preventing and / or treating hypoglycemia; (iii) increasing blood sugar; (iv) preventing and / or treating hypoalbuminemia; (v) increasing albumin; (vi) preventing and / or treating elevated alanine aminotransferase activity; (vii) reducing alanine aminotransferase activity; (viii) preventing and / or treating elevated aspartate aminotransferase activity; (ix) reducing aspartate aminotransferase activity; (x) preventing and / or treating reduced alkaline phosphatase activity; (xi) increasing alkaline phosphatase activity; (xii) preventing and / or treating intestinal damage; and / or (xiii) preventing and / or treating carbon tetrachloride poisoning or its complications, the method comprising administering selenoamino acids to the desired subject.
[0076] Preferably, the selenoamino acid comprises selenomethionine.
[0077] Preferably, the selenoamino acid comprises L-selenomethionine.
[0078] Preferably, the selenomethionine is L-selenomethionine:
[0079]
[0080] Preferably, the subject is a human or non-human mammal.
[0081] Preferably, the non-human mammal is a mouse, rat, rabbit, cow, sheep, dog or horse.
[0082] Preferably, the mice comprise C57BL / 6 mice.
[0083] Preferably, the administration is oral administration, external administration or injection administration.
[0084] It should be understood that within the scope of the present invention, the above-mentioned technical features of the present invention and the technical features specifically described below (such as embodiments) can be combined with each other to form a new or preferred technical solution. Due to space limitations, they will not be described one by one here. BRIEF DESCRIPTION OF THE DRAWINGS
[0085] Figure 1 Figure 2 is the hematoxylin-eosin (HE) staining of mouse colon tissues in the normal control group, vehicle group, model group and L-selenomethionine group, where a is the normal control group, b is the vehicle group, c is the model group, and d is the L-selenomethionine group.
[0086] Figure 2 The t-test was used to detect the differences in intestinal microorganisms between the vehicle group and the model group.
[0087] Figure 3 The t-test was used to detect the differences in intestinal microorganisms between the model group and the L-selenomethionine group. DETAILED DESCRIPTION
[0088] The present invention unexpectedly discovered that selenoamino acids such as L-selenomethionine can be used to improve intestinal flora imbalance, and have excellent preventive and therapeutic effects on hypoglycemia, hypoalbuminemia, elevated alanine aminotransferase and aspartate aminotransferase activities, reduced alkaline phosphatase activity and intestinal damage, and can be used to prevent and treat damage caused by the toxic side effects of drugs or chemical reagents such as carbon tetrachloride, such as intestinal flora imbalance, intestinal damage and blood function damage.
[0089] the term
[0090] As used herein, the terms "including", "comprising", and "containing" are used interchangeably and include not only open definitions, but also semi-closed and closed definitions, and the terms include "consisting of", "consisting essentially of".
[0091] In the present invention, the term "PBS" refers to phosphate buffered saline.
[0092] In the present invention, the term "carbon tetrachloride" is Tetrachloromethane, abbreviated as CCl 4 .
[0093] In the present invention, the term "albumin" is referred to as albumin in English.
[0094] In the present invention, the term "alanine aminotransferase" is Alanine aminotransferase in English.
[0095] In the present invention, the term "aspartate aminotransferase" is Aspartate aminotransferase in English.
[0096] In the present invention, the term "alkaline phosphatase" is alkaline phosphatase in English.
[0097] In the present invention, the CAS registration number of the term "L-selenomethionine" is 3211-76-5, and the structural formula is as follows:
[0098]
[0099] In the present invention, the term "prevention" refers to a method of preventing the onset of a disease and / or its attendant symptoms or protecting a subject from acquiring a disease.
[0100] In the present invention, the term "treatment" includes delaying and stopping the progression of the disease, or eliminating the disease, and does not require 100% inhibition, elimination and reversal.
[0101] use
[0102] The present invention provides a use of selenoamino acids for preparing a composition or a preparation, wherein the composition or preparation is used for one or more uses selected from the following groups: (i) preventing and / or treating intestinal microecological imbalance; (ii) preventing and / or treating hypoglycemia; (iii) increasing blood sugar; (iv) preventing and / or treating hypoalbuminemia; (v) increasing albumin; (vi) preventing and / or treating elevated alanine aminotransferase activity; (vii) reducing alanine aminotransferase activity; (viii) preventing and / or treating elevated aspartate aminotransferase activity; (ix) reducing aspartate aminotransferase activity; (x) preventing and / or treating reduced alkaline phosphatase activity; (xi) increasing alkaline phosphatase activity; (xii) preventing and / or treating intestinal damage; and / or (xiii) preventing and / or treating carbon tetrachloride poisoning or its complications.
[0103] Specifically, the use of the selenoamino acid described in the present invention is as described above in the first aspect of the present invention.
[0104] Compositions, formulations and kits
[0105] The present invention also provides a composition or preparation, which is preferably a pharmaceutical composition or preparation. The composition or preparation of the present invention further comprises a pharmaceutically acceptable carrier.
[0106] As used herein, the term "pharmaceutically acceptable carrier" refers to one or more compatible solid, semisolid, liquid or gel fillers that are suitable for human or animal use and have sufficient purity and sufficiently low toxicity.
[0107] It should be understood that in the present invention, the carrier is not particularly limited, and can be selected from materials commonly used in the art, or prepared by conventional methods, or purchased from the market. Examples of pharmaceutically acceptable carriers include cellulose and its derivatives (such as methylcellulose, ethylcellulose, hydroxypropylmethylcellulose, sodium carboxymethylcellulose, etc.), gelatin, talcum powder, solid lubricants (such as stearic acid, magnesium stearate), calcium sulfate, vegetable oils (such as soybean oil, sesame oil, etc.), polyols (such as propylene glycol, glycerol, sorbitol, etc.), emulsifiers (such as Tween), wetting agents (such as sodium lauryl sulfate), buffers, chelating agents, thickeners, pH regulators, transdermal enhancers, colorants, flavoring agents, stabilizers, antioxidants, preservatives, antibacterial agents, pyrogen-free water, etc.
[0108] In the present invention, the dosage form of the composition or preparation includes (but is not limited to) solid preparation, semisolid preparation or liquid preparation.
[0109] In the present invention, the dosage form of the composition or preparation includes (but is not limited to) oral preparations, injection preparations or external preparations.
[0110] Typically, the injection preparation is an intravenous injection preparation, an intramuscular injection preparation, a subcutaneous injection preparation, an intradermal injection preparation or an intraperitoneal injection preparation.
[0111] The pharmaceutical preparation should be matched with the mode of administration. When administering, a therapeutically effective amount of the drug is administered to the desired subject (such as a human or non-human mammal). As used herein, the term "therapeutically effective amount" refers to an amount that produces a function or activity on humans and / or animals and can be accepted by humans and / or animals. It should be understood by those of ordinary skill in the art that the "therapeutically effective amount" may vary depending on the form of the pharmaceutical preparation, the route of administration, the adjuvants of the drug used, the severity of the disease, and the combination of other drugs, etc., which are all within the skill of skilled physicians.
[0112] The main technical effects achieved by the present invention include:
[0113] The present invention finds that selenoamino acids such as L-selenomethionine can be used to improve intestinal flora imbalance, and have excellent preventive and therapeutic effects on hypoglycemia, hypoalbuminemia, elevated alanine aminotransferase and aspartate aminotransferase activities, reduced alkaline phosphatase activity and intestinal damage, and can be used to prevent and treat damage caused by the toxic side effects of drugs or chemical reagents such as carbon tetrachloride, such as intestinal flora imbalance, intestinal damage and blood function damage.
[0114] The present invention is further described below in conjunction with specific examples. It should be understood that the following specific examples are based on the technical solution and provide detailed implementation methods and specific operation processes, but the protection scope of the present invention is not limited to these examples.
[0115] Example 1
[0116] The CAS registration number of "L-selenomethionine" is 3211-76-5, and the structural formula is as follows:
[0117]
[0118] 1. Preparation of liquid medicine:
[0119] 20% carbon tetrachloride oil solution: Mix 1 ml of carbon tetrachloride and 4 ml of olive oil to obtain a 20% carbon tetrachloride oil solution.
[0120] L-selenomethionine solution: dissolve L-selenomethionine in PBS 7.4 buffer to obtain an L-selenomethionine solution.
[0121] 2. Experimental Methods
[0122] Normal healthy male C57BL / 6 mice were divided into normal control group, vehicle group, model group and L-selenomethionine group, with 6 mice in each group. The administration method was as follows:
[0123] Vehicle group: Normal saline was given by gavage once a day for 56 days from the beginning of the experiment. Olive oil was injected intraperitoneally starting from the 15th day (dosage volume was 0.004 ml / g). Olive oil was given 3 times a week for 4 consecutive weeks. The experiment was terminated on the 57th day.
[0124] Model group: Normal saline was gavaged once a day for 56 days from the beginning of the experiment. Starting from the 15th day, 20% carbon tetrachloride oil solution was injected intraperitoneally (the dosage was 0.005 ml / g, calculated as 20% carbon tetrachloride oil solution). The 20% carbon tetrachloride oil solution was administered 3 times / week for 4 consecutive weeks. The experiment was terminated on the 57th day.
[0125] L-selenomethionine group: L-selenomethionine solution (dosage of 0.8 mg / kg, calculated as L-selenomethionine) was administered by gavage once a day within 14 days after the start of the experiment. Starting from the 15th day, 20% carbon tetrachloride oil solution (dosage of 0.005 ml / g, calculated as 20% carbon tetrachloride oil solution) was intraperitoneally injected, and L-selenomethionine solution (dosage of 0.8 mg / kg, calculated as L-selenomethionine) was administered by gavage at the same time. The administration frequency of 20% carbon tetrachloride oil solution and L-selenomethionine solution was 3 times / week respectively and continued for 4 weeks. On the 43rd day, the administration of 20% carbon tetrachloride oil solution was stopped, and L-selenomethionine solution (dosage of 0.8 mg / kg, calculated as L-selenomethionine) was continued by gavage for 2 weeks (3 times / week). The experiment was terminated on the 57th day.
[0126] Normal control group: The normal control group was administered in the same manner as the L-selenomethionine group, except that the L-selenomethionine solution and the 20% carbon tetrachloride oil solution were replaced with the same volume of physiological saline, and the experiment was terminated on the 57th day.
[0127] 3. Experimental results
[0128] 3.1 At the end of the 57th day, the colons of mice in the normal control group, vehicle group, model group and L-selenomethionine group were fixed in a centrifuge tube filled with 4% paraformaldehyde solution. After paraformaldehyde fixation, they were first embedded in paraffin and then dehydrated and sectioned for hematoxylin-eosin (HE) staining. The results are shown in Figure 3. Figure 1 As shown:
[0129] from Figure 1 It can be seen that compared with the vehicle group given olive oil, the mice in the model group given carbon tetrachloride had disordered and thickened colon mucosa, increased inflammatory cells, and severe extracellular deposition, indicating that carbon tetrachloride caused intestinal damage. Compared with the carbon tetrachloride model group, the disorder and thickening of the colon mucosa in the mice in the L-selenomethionine administration group were effectively alleviated, and the inflammatory cells and extracellular deposition were significantly reduced, indicating that L-selenomethionine can effectively improve and treat intestinal damage caused by carbon tetrachloride.
[0130] 3.2 At the end of the 57th day, blood was collected from the eyeballs of mice in the normal control group, solvent group, model group and L-selenomethionine group, placed in labeled and anticoagulant-rinsed 1.5 ml centrifuge tubes, placed in a 4°C refrigerator for 12 hours, and centrifuged in a high-speed desktop refrigerated centrifuge at 4°C and 3500g / min for 10 minutes. After centrifugation, the supernatant was aspirated with a pipette on an ice box and transferred to a pre-cooled clean centrifuge tube. The fasting glucose (Glu-G) and albumin (ALB) levels in serum and the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) were detected using an automatic biochemical analyzer. The results are shown in Table 1 below.
[0131] Table 1 Detection of serum indicators in each group
[0132]
[0133] Note: Compared with the vehicle group, *p<0.05, **p<0.01; compared with the model group, # p<0.05, ## p<0.01.
[0134] As can be seen from Table 1, compared with the vehicle group given olive oil, the fasting glucose (Glu-G) content in the serum of the model group mice given carbon tetrachloride was reduced, the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were increased, and the activity of alkaline phosphatase (ALP) and albumin (ALB) content were reduced. Therefore, carbon tetrachloride can cause a decrease in blood glucose (Glu-G) content, an increase in the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), a decrease in the activity of alkaline phosphatase (ALP) and albumin (ALB), thereby leading to hypoglycemia, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) However, compared with the model group given carbon tetrachloride, the administration of L-selenomethionine could increase the content of glucose (Glu-G) in serum, reduce the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum, and increase the activity of alkaline phosphatase (ALP) and albumin (ALB) in serum, indicating that L-selenomethionine has a therapeutic effect on hypoglycemia, increased activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), decreased activity of alkaline phosphatase (ALP) and hypoalbuminemia.
[0135] 3.3 At the end of the 57th day, the colon contents of the mice in the vehicle group, model group and L-selenomethionine group (10 samples in each group) were collected in sterile cryopreservation tubes, and the frozen contents were subjected to DNA extraction and 16S rDNA sequencing to determine the changes in the intestinal flora of the mice. The results are as follows: Figure 2 and Figure 3 shown.
[0136] from Figure 2 It can be seen that compared with the vehicle group, the abundance of Alistipes and Rikenellaceae_RC9_gut_group in the fecal flora of the model group given carbon tetrachloride was significantly increased. Figure 3It can be seen that compared with the model group given carbon tetrachloride, the abundance of Alistipes and Rikenellaceae_RC9_gut_group in the fecal flora of mice in the L-selenomethionine group treated with selenomethionine was significantly reduced, while the abundance of Parabacteroides and Bifidobacterium was significantly increased, indicating that L-selenomethionine can effectively reduce the abundance of Alistipes and Rikenella in the intestine. ceae_RC9_gut_group (Riken bacteria genus_rc9_gut family) and increase the abundance of Parabacteroides (Parabacteroides distichous) and Bifidobacterium (Bifidobacterium), which is used to prevent and treat Alistipes (Another Mycobacterium) and Rikenellaceae_RC9_gut_group (Riken bacteria genus_rc9_gut family) intestinal overabundance and Parabacteroides (Parabacteroides distichous) and Bifidobacterium (Bifidobacterium) deficiency.
[0137] The above description is only the preferred embodiment of the present application and is not intended to limit the present application. For those skilled in the art, the present application may have various modifications and variations. Any modification, equivalent replacement, improvement, etc. made within the spirit and principle of the present application shall be included in the protection scope of the present application.
Claims
1. A use of selenoamino acid, characterized in that: Used for preparing a composition or preparation, the composition or preparation is used for one or more purposes selected from the following groups: (i) prevention and / or treatment of intestinal microecological imbalance; (ii) prevention and / or treatment of hypoglycemia; (iii) increase of blood sugar; (iv) prevention and / or treatment of hypoalbuminemia; (v) increase of albumin; (vi) prevention and / or treatment of increased alanine aminotransferase activity; (vii) reduction of alanine aminotransferase activity; (viii) prevention and / or treatment of increased aspartate aminotransferase activity; (ix) reduction of aspartate aminotransferase activity; (x) prevention and / or treatment of decreased alkaline phosphatase activity; (xi) increase of alkaline phosphatase activity; (xii) prevention and / or treatment of intestinal damage; and / or (xiii) prevention and / or treatment of carbon tetrachloride poisoning or its complications.
2. The use according to claim 1, characterized in that The selenomethionine is L-selenomethionine:
3. The use according to claim 1, characterized in that The intestinal flora includes one or more of Alistipes, Rikenellaceae_RC9_gut_group, Parabacteroides and Bifidobacterium.
4. The use according to claim 1, characterized in that The intestinal dysbiosis includes intestinal flora hyperbiosis selected from the group consisting of Alistipes, Rikenellaceae_RC9_gut_group, or a combination thereof.
5. The use according to claim 1, characterized in that The intestinal microecological imbalance includes intestinal flora deficiency selected from the group consisting of Parabacteroides (genus Parabacteroides), Bifidobacterium (genus Bifidobacterium), or a combination thereof.
6. The use according to claim 1, characterized in that The intestinal microecological imbalance includes intestinal microecological imbalance caused by administration of carbon tetrachloride or carbon tetrachloride poisoning; The hypoglycemia includes hypoglycemia caused by administration of carbon tetrachloride or carbon tetrachloride poisoning; The hypoalbuminemia includes hypoalbuminemia caused by administration of carbon tetrachloride or carbon tetrachloride poisoning; The increased activity of alanine aminotransferase includes the increased activity of alanine aminotransferase caused by administration of carbon tetrachloride or carbon tetrachloride poisoning; The increased activity of aspartate aminotransferase includes the increased activity of aspartate aminotransferase caused by the administration of carbon tetrachloride or carbon tetrachloride poisoning; The reduced activity of alkaline phosphatase includes reduced activity of alkaline phosphatase caused by administration of carbon tetrachloride or carbon tetrachloride poisoning; and / or The intestinal damage includes intestinal damage caused by administration of carbon tetrachloride or carbon tetrachloride poisoning.
7. The use according to claim 1, characterized in that The complications of carbon tetrachloride poisoning are selected from the following group: intestinal dysbiosis, hypoglycemia, hypoalbuminemia, elevated alanine aminotransferase activity, elevated aspartate aminotransferase activity, reduced alkaline phosphatase activity, intestinal damage, or a combination thereof.
8. The use according to claim 1, characterized in that The composition or preparation is a pharmaceutical composition or pharmaceutical preparation.
9. The use according to claim 1, characterized in that The dosage form of the composition or preparation is an oral preparation, an external preparation or an injection preparation.
10. A method for (i) preventing and / or treating intestinal dysbiosis; (ii) preventing and / or treating hypoglycemia; (iii) increasing blood glucose; (iv) preventing and / or treating hypoalbuminemia; (v) increasing albumin; (vi) preventing and / or treating elevated alanine aminotransferase activity; (vii) reducing alanine aminotransferase activity; (viii) preventing and / or treating elevated aspartate aminotransferase activity; (ix) reducing aspartate aminotransferase activity; (x) preventing and / or treating reduced alkaline phosphatase activity; (xi) increasing alkaline phosphatase activity; (xii) preventing and / or treating intestinal damage; and / or (xiii) preventing and / or treating carbon tetrachloride poisoning or its complications, the method comprising administering selenoamino acids to the subject in need.