Application of antarctic red pigment in preparation of drugs for treatment and prevention of hyperuricemia
The Antarctic red dye derived from Geomyces sp. wnf-18C or Geomyces sp. wnf-15A effectively treats hyperuricemia by reducing uric acid levels without adverse side effects, addressing the limitations of current drugs.
Patent Information
- Application Number
- JP2023186027
- Authority / Receiving Office
- JP · JP
- Patent Type
- Applications
- Current Assignee / Owner
- Priority Date
- 2023-06-09
- Filing Date
- 2023-10-30
- Publication Date
- 2024-12-19
- Estimated Expiration
- 2043-10-30
AI Technical Summary
Existing drugs for treating hyperuricemia often have significant side effects and do not effectively manage high uric acid levels without causing harm to the patient.
Utilizing Antarctic red dye derived from the fermentation product of the fungus Geomyces sp. wnf-18C or Geomyces sp. wnf-15A to develop a drug for treating and preventing hyperuricemia, which is induced by high purine and yeast fructose.
The Antarctic red dye demonstrates a therapeutic effect on hyperuricemia without causing toxicity or teratogenic effects, significantly reducing uric acid levels in animal models.
Smart Images

Figure 2024177024000001_ABST
Abstract
Description
[Technical field]
[0001] The present invention belongs to the field of biotechnology, specifically relates to the use of Antarctic Red pigment in the manufacture of medicine for the treatment and prevention of hyperuricemia. [Background technology]
[0002] Hyperuricemia is a condition in which the concentration of uric acid in the blood is too high (men > 7.0 mg / dL, women > 6.0 mg / dL), and is mainly caused by excessive production of uric acid in the body or failure to timely excrete it from the body. Hyperuricemia can be divided into primary and secondary. Primary hyperuricemia is often caused by genetic defects. A defect in the HGPRT gene increases uric acid production in the body. Decreased uric acid excretion is the main cause of primary hyperuricemia. Hyperuricemia occurs when there is a decrease in uric acid filtration by the glomerulus, a decrease in uric acid excretion by the renal tubules, or an increase in heavy absorption. Secondary hyperuricemia is closely related to drug use and diet, and the intake of high-purine foods and drinking alcohol are likely to induce hyperuricemia. In addition to causing gout, hyperuricemia often occurs together with non-alcoholic fatty liver disease, diabetes, and cardiovascular disease. If there are no symptoms of hyperuricemia or the uric acid level is within the controllable range, intervention is mainly through exercise, dietary control, and alcohol abstinence. If the uric acid level is high or there are gout symptoms, drug treatment is required. The mode of action of drugs is to inhibit the production of uric acid or promote the excretion of uric acid. For example, allopurinol and febuxostat mainly inhibit the production of uric acid by inhibiting the activity of xanthine oxidase, which is an important enzyme in the production of uric acid, while benzbromarone and probenecid promote the excretion of uric acid by inhibiting the heavy absorption of uric acid by renal tubules. When these drugs are used clinically, there are often obvious side effects such as allergies and liver and kidney dysfunction.
[0003] The patent invention, with the invention patent number 2015101171967 and the patent title Antarctic fungus color-producing compound, discloses a fungus Geomyces sp.wnf-15A(phy) isolated from Antarctic soil, which can be fermented to produce Antarctic red pigment; the patent invention, with the invention patent number 2019101866038 and the patent title Geomyces sp.wnf-15A(phy) mutant, discloses a mutant of the fungus Geomyces sp.wnf-15A(phy), which has improved red pigment pigmentation ability produced by the mutant, and the Antarctic red pigment has high color value, good coloring ability, high safety, and even antioxidant health care function, and can be used as a food additive in the food industry. However, the medicinal value of the compound has not been discovered. Summary of the Invention [Problem to be solved by the invention]
[0004] The technical problem that the present invention aims to solve is to provide the use of Antarctic Red dye in the manufacture of a medicament for the treatment and prevention of hyperuricemia. [Means for solving the problem]
[0005] The present invention is realized by the following technical means.
[0006] Use of Antarctic Red pigment in the manufacture of a medicament for the treatment and prevention of hyperuricemia, said Antarctic Red pigment being derived from the fermentation product of the fungus Geomyces sp. wnf-18C or Geomyces sp. wnf-15A.
[0007] Moreover, said hyperuricemia is induced by high purine and / or yeast fructose.
[0008] The present invention further provides a medicament comprising said Antarctic Red pigment for treating or preventing hyperpurine and yeast fructose-induced hyperuricemia, said Antarctic Red pigment being derived from the fermentation product of the fungus Geomyces sp. wnf-18C or Geomyces sp. wnf-15A. Effect of the Invention
[0009] Compared with the prior art, the present invention has the following advantageous effects:
[0010] The Antarctic Red pigment of the present invention has good therapeutic effect on hyperpurine-induced hyperuricemia, so that the pigment is useful for preparing drugs for hyperpurine-induced hyperuricemia. [Brief description of the drawings]
[0011] [Figure 1] 1 is a bar graph of the effect of Antarctic Red dye on survival rate of hyperuricemic mice. [Diagram 2] FIG. 1 is a line diagram of the effect of Antarctic Red dye on survival rate in hyperuricemia mice. [Diagram 3] FIG. 1 shows the effect of Antarctic Red dye on uric acid levels in fructose+yeast powder-induced hyperuricemia mice for 14 days. [Figure 4] FIG. 1 shows the effect of Antarctic Red dye on uric acid levels in fructose+yeast powder-induced hyperuricemia mice over a 21-day period. [Diagram 5] FIG. 1 shows the effect of Antarctic Red dye on uric acid levels in fructose+yeast powder-induced hyperuricemia mice over a 28-day period. [Figure 6] FIG. 13 shows the effect of Antarctic Red dye on uric acid levels in fructose+yeast powder-induced hyperuricemia mice for 35 days. DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS
[0012] Hereinafter, the technical solutions of the present invention will be further explained through the embodiments with reference to the drawings, but the protection scope of the present invention is not limited to any form of the embodiments.
[0013] The Antarctic Red pigment used in the following examples is prepared by the method disclosed in the patent invention having patent number 2019101866038 and titled Geotrichum commune mutant strain and its use, in which the mutant strain is mutated based on a primitive strain, and the patent invention having patent number 2015101171967 and titled Antarctic Fungus chromogenic compound discloses a primitive strain and an Antarctic Red pigment.
[0014] Example 1: Toxicity experiment of Antarctic Red dye
[0015] 1. About the characteristics and processing of the sample, This is an Antarctic Red pigment sample; it is a red powder and should be stored at 4-8°C, away from light.
[0016] 2. Experimental animals and reagents 2.1 The experimental ICR mice were provided by Zhejiang Provincial Experimental Animal Center and were SPF level. The experimental animal production permit number was SCXK(Zhejiang)2019-0002, and the experimental animal use permit number was SYXK(Zhejiang)2019-0011. The experimental animal feed was provided by Zhejiang Provincial Experimental Animal Center. The detection environmental conditions were: temperature range 20-25℃, relative humidity range 40-70%. 2.2 The experimental SD rats were provided by Zhejiang Provincial Experimental Animal Center and were SPF level. The experimental animal production permit number was SCXK(Zhejiang)2019-0002, and the experimental animal use permit number was SYXK(Zhejiang)2016-0022. The experimental animal feed was provided by Zhejiang Provincial Experimental Animal Center. The detection environmental conditions were: temperature range 20-25℃, relative humidity range 40-70%. 2.3 Experimental reagents: 2-Acetaminofluorene: Sigma-Aldrich, Lot No.: STBF2332V; 1,8-Dihydroxyanthraquinone: Sigma-Aldrich, Lot No.: WXBC4791V; Sodium azide: Beijing Dingguo Biological Technology Co., Ltd., Lot No.: 81G10150; Fenaminosulf: Chemservice, Lot No.: 285-75B; Mitomycin C: Roche, Lot No.: M0308A; Cyclophosphamide: Sigma-Aldrich, Lot No.: WXBC5093V.
[0017] 3. Animal testing 3.1 Mouse toxicity experiment: Select 20 healthy, mature ICR mice weighing 18-22g, half male and half female. Dosage and administration method: Set up a dose group of 10.0g / kgBW according to the limited method. Weigh 100g of sample and prepare 200mL of sample liquid using distilled water as a solvent. The mice are fasted for 6 hours (no water prohibition) before intragastric administration, and a single intragastric administration volume of 20mL / kgBW is administered, and the animals are allowed to eat freely after 2 hours. After intragastric administration, the general condition, toxic symptoms and death status of the mice are observed. The observation period is 14 days, and the weights at the beginning and end of the mouse experiment are recorded. At the end of the experiment, the mice are killed, and macroscopic anatomical examination is performed to record the changes in the macroscopic pathology of the mice. 3.2 Rat test: Select 20 healthy, mature SD rats weighing 180-220g, half male and half female. Set up a dose group of 10.0g / kgBW according to the limiting method. Weigh 100g of sample and prepare 200mL of sample solution using distilled water as a solvent. The rats are fasted for 16 hours (no water prohibition) before intragastric administration, and a single intragastric administration volume of 20mL / kgBW is administered, and the animals are allowed to eat freely after 3 hours. After intragastric administration, the rats' general condition, toxic symptoms and death status are observed. The observation period is 14 days, and the rats' body weights are recorded at the beginning and end of the experiment. At the end of the experiment, the rats are killed, and gross anatomical examination is performed to record the changes in the rats' gross pathology. 3.3 Mammalian Erythrocyte Micronucleus Test: Select 50 healthy, mature mice weighing 25-30g, half male and half female. Randomly divide the mice into 5 groups, 10 mice in each group, half male and half female. Set three dosage groups of 1.25, 2.5, and 5.0g / kgBW in the experiment, weigh 2.5, 5.0, and 10.0g of sample, respectively, and prepare 40mL of sample solution using distilled water as solvent. Set one negative control group (distilled water) and one positive control group (cyclophosphamide 40mg / kgBW, weigh 80mg of cyclophosphamide, add sterile saline, and dissolve in 40mL for later use) separately. Mice are orally administered the test object intragastrically at an intragastric administration volume of 20mL / kgBW, and intragastric administration twice at an interval of 24 hours. Six hours after the second intragastric administration, the animals are sacrificed by cervical dislocation and the sternal bone marrow is harvested to prepare bone marrow tablets, which are fixed in methanol and stained with Giemsa. Observation index: At least 200 red blood cells are observed in the bone marrow of each animal, and the proportion of polychromatic red blood cells (PCE) in total red blood cells (RBC) is counted. 2,000 polychromatic red blood cells are observed in each animal, and the frequency of micronucleated polychromatic red blood cells, i.e., the rate of cells containing micronuclei, is counted and expressed as a percentage per thousand. The average number and standard deviation of the rate of cells containing micronuclei in each group by animal sex are statistically calculated, and the rate of cells containing micronuclei in each dose group of the test sample and the negative control group are compared using Poisson distribution.
[0018] 4. Experimental results Acute oral toxicity test: During the experiment, there were no obvious symptoms of poisoning in any of the rats or mice, no deaths, and no pathological changes were found in any of the organs of the rats or mice upon macroscopic dissection. The oral LD50 of the Antarctic Red dye sample (dried powder) for both male and female rats and mice exceeded 10.0g / kgBW, which is a practically non-toxic level. Mammalian erythrocyte micronucleus test: The PCE / RBC ratios of each dosage group in both sexes were more than 20% of the negative control group, and Antarctic Red dye had no cytotoxicity. Compared with the negative control group, the micronucleus cell rate of each dosage group in both sexes was not significantly different (P>0.05), and the micronucleus rate of the positive control group was significantly higher than that of the negative control group, and the difference was of great significance (P<0.01). Under the test conditions, Antarctic Red dye was not found to have a significant effect on the micronucleus cell rate of mouse bone marrow erythrocytes, and the detection result was negative.
[0019] Example 2 Teratogenicity experiment of Antarctic Red dye 1.1 Test object: Antarctic Red pigment sample, red powder. 1.2 Experimental animals: Select 100 female SD rats and 30 male rats, weighing 180-220g, which are healthy and SPF level, provided by Zhejiang Provincial Experimental Animal Center. The experimental animal production permit number is SCXK(Zhejiang)2019-0002, and the experimental animal use permit number is SYXK(Zhejiang)2016-0022. Adapt for 3 days before testing. 1.3 The animal rearing environment should be at room temperature 20-25°C and relative humidity 40-70%. Animals should be reared in stainless steel cages. 1.4 Animal feed: Provided by Zhejiang Provincial Experimental Animal Center. 1.5 Test method: oral intragastric administration. The samples were prepared in different concentrations with distilled water according to different dosage demands, and pregnant rats were administered with an intragastric administration volume of 10mL / kgBW once a day in the morning from the 6th to 15th days of pregnancy, and the control group was administered with the corresponding volume of distilled water. Three dosage groups of Antarctic Red pigment were set up: 0.125g / kgBW, 0.25g / kgBW, and 0.5g / kgBW, and a separate control group was set up. Control group: distilled water. Low-dose group: Weigh out 3.75 g of Antarctic Red pigment, add 300 mL of distilled water, mix well and store in a 4°C refrigerator. Prepare weekly. Medium dose group: Weigh out 7.5 g of Antarctic Red pigment, add 300 mL of distilled water, mix well and store in a 4°C refrigerator. Prepare weekly. High-dose group: Weigh out 15 g of Antarctic Red pigment, add 300 mL of distilled water, mix well and store in a 4°C refrigerator. Prepare weekly.
[0020] 2. Animal grouping and test index: Female rats and male rats were placed in the same cage overnight in a ratio of 2:1, and rats with sperm in the vaginal smear were determined to be fertilized rats every morning. The day was determined to be day 0 of conception, and their weights were recorded and randomly divided into 4 groups, each group containing at least 19 rats. In order to obtain enough fetuses to evaluate its teratogenic effect, the number of pregnant rats per dose group was at least 16. The experimental rats were allowed to eat and drink freely, and the general symptoms, behavior, signs of poisoning and death of the animals were observed and recorded. From the 6th to 15th day of conception, the test object was orally administered intragastrically every day. The weights were recorded on the 0th, 6th, 9th, 12th, 15th and 20th days of rat pregnancy. On the 20th day of pregnancy, the mother rats were killed, the abdomen was opened, the uterus was removed and weighed, and the number of corpora lutea, live fetuses, resorbed fetuses and dead fetuses were examined and recorded. The body length, tail length, weight and sex of the live fetuses are recorded one by one, and the external appearance of the fetuses is checked for malformations. Half of the rat fetuses from each nest are taken and fixed in 95% ethanol for 3 weeks, then showered and cleared in 2% potassium hydroxide for 3 days, and after clearing, they are taken out and stained in Alizarin Red dyeing solution, and the staining effect is regularly observed, and finally, skeletal malformations are observed, and the remaining half are fixed in Bouins' solution (formaldehyde-acetic acid-picric acid solution) for 2 weeks, and internal organs are observed for malformations.
[0021] 3. Data processing: Calculate the average number, standard deviation, incidence rate, etc. of each observation index, and use the PSS13.0 statistical software package to perform variance analysis and chi-square test.
[0022] 4. Experimental results: During the test, no abnormalities were observed in the feeding and drinking habits of the pregnant rats in each group, their weight gain was good, and no toxic symptoms or signs were observed, nor were there any deaths. The effect of Antarctic Red on the weight gain of pregnant rats: The results are shown in Table 1.
[0023] At least 19 fertilized rats were allocated to each group, and more than 16 non-pregnant fertilized rats were removed, and all the indicators of pregnant rats were within the test statistical range. The weight gain of pregnant rats in each dosage group was good, and the weight, weight gain and net weight gain of pregnant rats on days 0, 6, 9, 12, 15 and 20 were not statistically significant compared with the control group (P>0.05).
[0024] [Table 1]
[0025] The effects of Antarctic Red on the reproductive function of pregnant rats: The results are shown in Table 2. The indexes of implantation, resorption, live fetuses, dead fetuses, pre-implantation mortality and other indicators of pregnant rats in each dosage group were close to those of the control group, and all the differences were not statistically significant (P>0.05). Under the conditions of this test, no effects of Antarctic Red on the reproductive function of pregnant rats were observed.
[0026] [Table 2]
[0027] 4.1 Effect of Antarctic Red dye on the growth and development of rat fetuses: The results are shown in Table 3. The body length (length + tail length), weight and sex ratio of the rat fetuses in each dosage group were statistically insignificantly different from the control group (P>0.05).Administering Antarctic Red dye to pregnant rats under the conditions of this test had no effect on the growth and development of the rat fetuses.
[0028] [Table 3]
[0029] 4.2 Effect of Antarctic Red dye on malformations in rat fetuses: The results are shown in Tables 4, 5, and 6. No external malformations were observed in rat fetuses in any of the dose groups or the control group, indicating that under the test conditions, there is no effect of Antarctic Red dye on the occurrence of external malformations in rat fetuses.
[0030] [Table 4]
[0031] In both the control group and each dose group, some rat fetuses were observed to have sternal defects and enlarged fontanelles. The sternal defects and enlarged fontanelles in each dose group were not statistically significant compared to the control group (P>0.05). Under the conditions of this test, no effect of Antarctic Red on the occurrence of skeletal malformations in rat fetuses was observed.
[0032] [Table 5]
[0033] No rat fetuses were observed to have visceral malformations in the control group or in any of the dose groups, indicating that under the test conditions, Antarctic Red dye has no effect on the occurrence of visceral malformations in rat fetuses.
[0034] [Table 6]
[0035] 5. Conclusion: In the rat teratogenicity test of Antarctic Red pigment, three dosage groups of Antarctic Red pigment were set: 0.125g / kgBW, 0.25g / kgBW, and 0.5g / kgBW. No toxic signs were observed in pregnant rats, and Antarctic Red pigment had no obvious harmful effects on weight gain, conception rate, live birth rate, resorption and death rates, preimplantation mortality, and average live birth rate. The weight, body length, and sex ratio of rat fetuses in each dosage group were not statistically significant compared with the control group (P>0.05). In this test, no external or internal malformations were observed in rat fetuses, and the sternum defects and fontanelle enlargement of rat fetuses in each dosage group were not statistically significant compared with the control group (P>0.05). The Antarctic Red pigment sample has no teratogenic effect on SD rats under the test conditions.
[0036] Example 3: Effect of Antarctic Red Pigment on Hyperpurine-Induced Hyperuricemia Model
[0037] 1. Experimental animals: Balb / c male mice, 6-8 weeks old, weighing 16-18g, purchased from Beifong (Beijing) Biotechnology Co., Ltd. They were kept in the Experimental Animal Center of Qingdao University. All mice were kept in a pathogen-free facility, maintained at appropriate temperature and relative humidity, with a 12-hour light and dark cycle, allowed to eat and drink freely, and had clean mats replaced daily.
[0038] 2. Experimental drugs: yeast impregnated powder (Y820625), allopurinol (A800424), potassium oxonate (P831461), and Antarctic red dye purchased from Macklin Biochemical Technology Co., Ltd.
[0039] 3. Establishment of hyperuricemia model and grouping: 25 healthy Balb / c male mice were randomly divided into an untreated control group, a hyperuricemia model group, a high-dose Antarctic Red dye treatment group, a low-dose Antarctic Red dye treatment group, and an allopurinol treatment group, with 5 mice in each group. Antarctic Red dye, purine fermentation, and yeast impregnated powder were mixed uniformly in 0.5% sodium carboxymethylcellulose (0.5% CMC-Na) solution, respectively. The mice in the high-dose Antarctic red dye treatment group were intragastrically administered Antarctic red dye at 100mg / kg body weight, and the mice in the low-dose Antarctic red dye treatment group were intragastrically administered Antarctic red dye at 25mg / kg body weight for 3 consecutive days. The other groups were not treated, and the remaining 4 groups, except for the untreated group, were each administered 20g / kg body weight of yeast-impregnated powder suspension (0.4g / mouse). At the same time, the mice in the high-dose Antarctic red dye treatment group were intragastrically administered Antarctic red dye at 100mg / kg body weight, the mice in the low-dose Antarctic red dye treatment group were intragastrically administered Antarctic red dye at 25mg / kg body weight, the allopurinol treatment group was intragastrically administered allopurinol at 20mg / kg body weight, and the untreated group was intragastrically administered an equal volume of 0.5% CMC-Na, which was Day 1 and continued for 7 consecutive days. From day 5 to day 7, except for the untreated control group, the remaining four groups were each intraperitoneally injected with 0.1 ml (6 mg / animal) of potassium oxonate.
[0040] 4. As can be seen from the results, no mice died in the untreated control group and the allopurinol treatment group, 4 mice died in the hyperuricemia model group, 2 mice died in the low-dose Antarctic Red dye treatment group, and 3 mice died in the high-dose Antarctic Red dye treatment group (Figure 1). As can be seen, the survival rate of hyperuricemia mice can be significantly improved after Antarctic Red dye treatment, and there is a certain improvement effect on hyperuricemia (Figure 2).
[0041] Example 4: Effect of Antarctic Red Pigment on a Hyperuricemia Model Induced by Fructose + Yeast Diet
[0042] 1. Experimental animals: Male Balb / c mice, aged 6-8 weeks and weighing 16-18g, were purchased from Beifong (Beijing) Biotechnology Co., Ltd. They were kept in the Experimental Animal Center of Qingdao University. All mice were kept in a pathogen-free facility, maintained at appropriate temperature and relative humidity, with a 12-hour light and dark cycle, allowed to eat and drink freely, and had clean mats replaced daily.
[0043] 2. Experimental reagents and consumables: Reagents: allopurinol (A800424, MACKLIN), fructose (D809612, MACKLIN), blood glucose meter (950B, yuwell), blood glucose test strips (591146, yuwell), uric acid reagent kit (C012-2-1, Nanjing Jiancheng Institute of Biological Engineering).
[0044] 3. Modeling method: 36 male Balb / c mice were divided into 6 groups, with 6 mice in each group, consisting of the untreated group (normal food and water), the high uric acid model group (yeast food and water + 10% fructose food), the high uric acid model + allopurinol group (yeast food and water + 10% fructose food and water + 20 mg / kg allopurinol), the high uric acid model + low concentration pigment group (yeast food and water + 10% fructose food and water + 10 mg / kg Antarctic Red pigment), the high uric acid model + medium concentration pigment group (yeast food and water + 10% fructose food and water + 20 mg / kg Antarctic Red pigment), and the high uric acid model + high concentration pigment group (yeast food and water + 10% fructose food and water + 40 mg / kg Antarctic Red pigment).
[0045] Allopurinol and Antarctic Red pigment were dissolved in double distilled water and mixed uniformly. From day 0, the Antarctic Red pigment treatment group was intragastrically administered with 10 mg / kg, 20 mg / kg, and 40 mg / kg, the allopurinol treatment group was intragastrically administered with 20 mg / kg, and the hyperuric acid model group was intragastrically administered with an equal amount of double distilled water, once a day for 35 consecutive days. From day 0, the body weight of the mice in each group was recorded.
[0046] 4. Blood glucose recording: On days 0, 7, 14, 21, 28, and 35, blood samples of the mice were collected from the retro-orbital venous plexus at 8 pm after the mice were fasted for 12 h to perform blood glucose detection, and the blood glucose levels of the mice in each group were recorded.
[0047] 5. Uric acid detection: On the 14th, 21st, 28th, and 35th days, at 8 a.m., the mice were fasted for 12 h, and then blood samples were collected from the retroorbital venous plexus of the mice for uric acid detection. After the collection of mouse blood was completed, it was left to stand at room temperature for 1 hour, and then centrifuged at a rotation speed of 3000 rpm for 5 minutes to obtain the pale yellow upper serum, which was detected by a uric acid reagent kit (C012-2-1, Nanjing Jiancheng Bioengineering Institute). The data was then collected. Analyze using the formula: Uric acid concentration (μmol / L) = {(A measurement - A untreated) / (A standard - A untreated)}*C standard.
[0048] 6. Results: As can be seen from the analysis of serum uric acid level changes in mice in each group (see Figure 3-6), after 14 days of the experiment, the uric acid levels of mice in the high uric acid model group, high uric acid model + allopurinol group, and high uric acid model + high / medium / low concentration pigment groups reached 275.1±16.18 μmol / L, 191.5±21.95 μmol / L, 192.9±17.05 / 209.6±29.68 / 236.4±12.59 μmol / L, respectively, all of which were significantly increased compared with the control group (P<0.05), increasing by 79.10%, 24.67%, 25.59%, 36.46%, and 53.91%, respectively, indicating that the modeling was successful. The uric acid levels in the high uric acid model + allopurinol group and the high uric acid model + high / medium / low concentration dye groups were lowered by 30.39%, 29.88%, 23.81%, and 14.07%, respectively, than those in the high uric acid model group, indicating the therapeutic effect of Antarctic red dye.
[0049] On the 21st day, the uric acid levels in the high uric acid model + allopurinol group and the high uric acid model + medium / low concentration pigment group were significantly lower than those in the high uric acid model group (P<0.05), dropping to 247.2±48.98 μmol / L, 249.6±27.02 μmol / L, and 215.9±13.12 μmol / L, respectively, while the high concentration pigment group increased to 293.6±45.2 μmol / L.
[0050] On the 28th day, the uric acid levels in the high uric acid model + allopurinol group and the high uric acid model + high / medium / low concentration dye group were significantly lower than those in the high uric acid model group (P<0.05), dropping to 264.9±54.87μmol / L, 324.8±26.57μmol / L, 258.2±15.54μmol / L, and 239.2±16.63μmol / L, respectively. On the 35th day, the uric acid level of the high uric acid model + allopurinol group (215.8±37.132μmol / L), high uric acid model + high (236.6±37.1μmol / L) / medium (241.5±23.98μmol / L) / low (215.7±38.43μmol / L) concentration dye group was significantly lower than that of the high uric acid model group (P<0.05), and there was no significant difference in the uric acid level between the two groups of high and medium concentration dye groups. Low concentration dye can significantly lower the hyperuric acid caused by yeast fructose.
Claims
1. Use of Antarctic Red pigment in the manufacture of a medicament for the treatment and prevention of hyperuricemia, characterized in that the Antarctic Red pigment is derived from a fermentation product of the fungus Geomyces sp. wnf-18C or Geomyces sp. wnf-15A.
2. The use of Antarctic Red Pigment in the manufacture of a medicament for the treatment and prevention of hyperuricemia according to claim 1, characterized in that the hyperuricemia is induced by hyperpurine and / or yeast fructose.
Citation Information
Patent Citations
Geomyces sp.wnf-15A(phy) coloring compound
CN104804007A
Red yeast rice and natto tablet candy and preparation method thereof
CN110169485A
Curative agent
JP2009249341A
Monascus-fermented black bean vinegar, method for manufacturing thereof and application thereof
KR1020180031480A
