The use of erythromycin in the preparation of drugs for treating acute leukemia.

Abstract

This invention discloses the use of epigallocatechin in the preparation of drugs for treating acute leukemia, belonging to the field of biomedical technology. This invention discovers that epigallocatechin can effectively inhibit the proliferation of acute leukemia cells and significantly promote their apoptosis. This provides a new treatment option for leukemia patients, further optimizing treatment plans, improving cure rates, and enhancing long-term quality of life.

Description

Technical Field

[0001] This invention belongs to the field of biomedical technology, specifically relating to the use of phenobarbital in the preparation of drugs for treating acute leukemia. Background Technology

[0002] Acute leukemia (ALL) is a malignant tumor originating from hematopoietic stem cells in the bone marrow. Its main characteristic is the abnormally rapid proliferation of leukemia cells in the bone marrow and peripheral blood, while simultaneously inhibiting the production of normal blood cells, leading to clinical symptoms such as anemia, bleeding, and infection. ALL progresses rapidly, and without timely intervention, patient survival is extremely limited. Current treatments mainly include chemotherapy, radiotherapy, bone marrow transplantation, and molecular targeted therapy. Although these treatments have achieved some clinical efficacy, they still have significant limitations: chemotherapy drugs often bring severe toxic reactions, affecting patients' quality of life; bone marrow transplantation faces difficulties in donor matching and the risk of graft-versus-host disease (GVHD); the efficacy of targeted drugs is limited by specific mutation types and is prone to drug resistance. Therefore, developing safer, more effective anti-ALL drugs with novel mechanisms of action remains a pressing medical challenge.

[0003] Small molecule compounds derived from natural plants have attracted widespread attention in the field of anticancer drug development in recent years due to their wide availability, good biocompatibility, and diverse biological activities. Among them, many natural products have been found to exert antitumor effects through multiple mechanisms, including regulating cell proliferation, inducing apoptosis, inhibiting signaling pathways, and modulating oxidative stress, providing important references for the development of novel antileukemia drugs.

[0004] Epigoitrin is a natural sulfur-containing heterocyclic compound extracted from plants. Its structure belongs to the oxazolidine-2-thione class of compounds, with a five-membered sulfur-containing heterocycle as the core and vinyl side chains. Epigoitrin is mainly found in plants as a metabolic degradation product of glucosinolates and their precursors, possessing a clear natural source and obtainable through plant extraction and chemical separation methods. Previous studies have shown that epigoitrin exhibits significant antioxidant, anti-inflammatory, and antiviral activities, with high safety and low toxicity, demonstrating good medicinal potential. However, to date, there are no systematic reports on the antitumor effects of epigoitrin, particularly its inhibitory effects on the proliferation of acute leukemia cells and its apoptosis-inducing effects, which to some extent limits its application in cancer treatment. Summary of the Invention

[0005] To address the aforementioned shortcomings in the prior art, this invention provides the use of phenobarbital in the preparation of a medicament for treating acute leukemia.

[0006] To achieve the above objectives, the technical solution adopted by the present invention to solve its technical problem is as follows: The purpose of this invention is to provide the use of bacitracin in the preparation of a medicament for treating acute leukemia. Bacitracin has the molecular formula C5H7NOS and a molecular weight of 129.18. It was purchased from MedChemExpress and its chemical structure is as follows: .

[0007] Furthermore, the drug lysine inhibits the proliferation of acute leukemia cells and promotes their apoptosis.

[0008] Furthermore, the effective concentration of epididymine in the drug is ≥30μM.

[0009] Furthermore, the drug also includes pharmaceutically acceptable excipients for acetaminophen.

[0010] Furthermore, the dosage form of the drug is tablets, pills, capsules, drops, granules, ointments, powders, or liquid preparations.

[0011] Another object of the present invention is to provide the use of the above-mentioned derivatives, precursors or analogs of leukemia in the preparation of a medicament for treating acute leukemia.

[0012] Furthermore, the derivative, precursor, or analogue thereof is guanylin, guanylin, guanylin, 3-butenylsinin, thiourea, or oxazolidine-2-thione derivative.

[0013] Another object of the present invention is to provide a medicament for treating acute leukemia, comprising bacitracin and pharmaceutically acceptable excipients thereof.

[0014] Another object of the present invention is to provide a pharmaceutical composition for treating acute leukemia, wherein the active ingredient is bacitracin.

[0015] The beneficial effects of this invention are: This invention reveals that epigallocatechin can effectively inhibit the proliferation of acute leukemia cells and significantly promote their apoptosis. This provides a new treatment option for leukemia patients, further optimizing treatment plans, improving cure rates, and enhancing long-term quality of life. Furthermore, epigallocatechin is derived from a natural plant, has fewer side effects, and possesses broad clinical application prospects. Attached Figure Description

[0016] Figure 1 The graph shows the changes in cell viability of leukemia cells (Thp1) after treatment with different concentrations of erythromycin. Figure 2 Cell status detection of Thrp1 cells after 24 hours of treatment with different concentrations of cytosine. Detailed Implementation

[0017] The specific embodiments of the present invention are described below to enable those skilled in the art to understand the present invention. However, it should be understood that the present invention is not limited to the scope of the specific embodiments. For those skilled in the art, various changes are obvious as long as they are within the spirit and scope of the present invention as defined and determined by the appended claims. All inventions utilizing the concept of the present invention are protected.

[0018] The reagents and culture media used in this invention are as follows: Table 1 Main Reagents

[0019] Culture medium preparation: For every 100 mL of cell culture medium: take 89 mL of RPMI 1640, add 10 mL of fetal bovine serum, then add 1 mL of penicillin-dextrose antibody, mix well, and store at 4°C.

[0020] Example 1: Inhibitory effect of chlorpheniramine on the proliferation of thp1 leukemia cells. Thrp1 cells in logarithmic growth phase were seeded into 96-well plates at a density of 20,000 cells / well. Equal volumes of DMSO (dimethyl sulfoxide, with a final concentration controlled below 1‰ (v / v)) were added to each well at final concentrations of 10, 20, 40, 60, 80, and 100 μM. Cells were then incubated at 37°C, 5% CO2, and 90% humidity for 24, 48, or 72 hours. Afterward, 10 μL of CCK-8 solution was added, and the cells were incubated at 37°C, 5% CO2 for 4 hours. The absorbance (OD) value was measured at 450 nm using a microplate reader, and cell viability curves were fitted. The CCK-8 assay procedure is as follows, and the results are shown in [Figure number missing]. Figure 1 .

[0021] Cell viability assay (CCK-8 assay): Acute leukemia cells in logarithmic growth phase were collected and their density adjusted to (1.5-2) × 10⁻⁶. 5 Cells / mL. 90 μL of cell suspension was added to each well of a 96-well plate. 10 μL of different concentrations of bifidus solution was added to the experimental group, and 10 μL of serum-free RPMI 1640 medium was added to the negative control group. A blank control group was also set up. Each group had 3 replicates, and the experiment was independently repeated 3 times.

[0022] After culturing in a CO2 incubator for 24 hours, 10 μL of CCK-8 solution was added to each well, and incubation continued for another 4 hours. The OD value of each well was measured at 450 nm using a full-wavelength spectrophotometer. The average OD value of each group was calculated, and the cell proliferation inhibition rate was calculated using the following formula: Proliferation inhibition rate (%) = (OD value of control group - OD value of experimental group) / (OD value of control group - OD value of blank group) × 100% like Figure 1 As shown, epididymetra significantly inhibited the proliferation of Thrp1 cells in a concentration-dependent manner. In the control group (0 μM), cell viability remained high, and cell proliferation was normal. In the experimental group, cell viability gradually decreased with increasing epididymetra concentration. Specifically, in the low-concentration group (20 μM), Thrp1 cell viability decreased slightly but remained at a high level; in the medium-concentration group (40 μM), cell viability decreased significantly, showing a significant inhibitory effect on proliferation; in the high-concentration group (≥60 μM), Thrp1 cell viability decreased dramatically, reaching as low as approximately 20%, indicating that most cells were inhibited in proliferation or even died.

[0023] The above experimental results show that the inhibitory effect of epigastrin on Thrp1 leukemia cells is concentration-dependent; the higher the concentration, the more significant the inhibition of cell proliferation. This indicates that epigastrin can effectively interfere with the growth of Thrp1 cells, providing experimental evidence for its potential role as an anti-acute leukemia drug.

[0024] Example 2: Effect of Tablets on Thrp1 Leukemia Cells In a 6-well plate, seed 1 mL at a density of (5-10) × 10⁻⁶. 5 Thrp1 cells / mL were treated with epigolin at final concentrations of 20, 40, and 60 μM. The cells were incubated at 37°C with 5% CO2, with a 0 μM epigolin control group. The culture plates were then placed in an incubator at 37°C, 5% CO2, and 90% humidity for 24 hours. After incubation, the cells were gently washed 1-2 times with PBS buffer to remove unbound epigolin. The cells were gently resuspended in a small amount of culture medium for microscopic observation. Cells were observed under an inverted optical microscope at 400x magnification. Cell count, aggregation state, morphological characteristics, and abnormal changes (such as cell shrinkage, flattening of round cells, and increased cell debris) were recorded between the different concentration treatment groups and the control group. Results are shown in [Figure number missing]. Figure 2 In the figure, the magnification is shown in the lower left corner of each small image, and the scale data is shown in the lower right corner. The magnification is 25.2x and the scale is 20 μm.

[0025] like Figure 2As shown, microscopic observation of the morphology of Thr1 cells in each treatment group revealed that the control group (0 μM episorbent monophosphate) cells maintained good suspension, with uniform cell size, round or oval shape, intact cytoplasm, and no obvious fragmentation or morphological abnormalities. The cells aggregated in a typical suspension growth state. In the experimental groups, Thr1 cells showed significant morphological changes with increasing episorbent monophosphate concentration. In the low concentration group (20 μM), cells slightly decreased in size, some cells became flattened from round shape, the cytoplasmic edges were slightly irregular, and occasional scattered fragments were observed between cells. In the medium concentration group (40 μM), cell volume further decreased, the number of morphologically abnormal cells increased significantly, the degree of cell aggregation decreased, some cells showed obvious cytoplasmic rupture and fragmentation, and the overall suspension state was affected. In the high concentration group (60 μM), the number of cells decreased significantly, most cells were round or irregular in shape, the cytoplasm was obviously fragmented, some cells floated into fragments, and cell aggregation almost disappeared, showing a significant concentration-dependent killing effect. Furthermore, microscopic observation revealed that the spatial distribution of cells in the epigastrin-treated group was sparser than that in the control group, accompanied by a large number of scattered cell fragments, suggesting that epigastrin can directly induce morphological destruction or death of Thrp1 cells. These experimental results indicate that epigastrin has a significant in vitro inhibitory effect on leukemia Thrp1 cells, and this effect is concentration-dependent.

[0026] Finally, it should be noted that the above specific embodiments are only used to illustrate the technical solutions of the present invention and not to limit it. Although the present invention has been described in detail with reference to examples, those skilled in the art should understand that modifications or equivalent substitutions can be made to the technical solutions of the present invention without departing from the spirit and scope of the technical solutions of the present invention, and all such modifications and substitutions should be covered within the scope of the claims of the present invention.

Claims

1. The use of iodine in the preparation of drugs for treating acute leukemia.

2. The use according to claim 1, characterized in that, The drug, called Yichun, inhibits the proliferation of acute leukemia cells and promotes their apoptosis.

3. The use according to claim 1 or 2, characterized in that, The effective concentration of the drug is ≥30μM.

4. The use according to claim 3, characterized in that, The drug also includes pharmaceutically acceptable excipients for phenobarbital.

5. The use according to claim 4, characterized in that, The dosage forms of the drug are tablets, pills, capsules, drops, granules, ointments, powders, or liquid preparations.

6. Use of the derivatives, precursors or analogs of the leukotriene described in claim 1 in the preparation of a medicament for treating acute leukemia.

7. The use according to claim 6, characterized in that, The derivatives, precursors or their analogues are guanylin, guanylin, guanylin, 3-butenylsinin, thiourea or oxazolidine-2-thione derivatives.

8. A drug for treating acute leukemia, characterized in that, This includes acetaminophen and its pharmaceutically acceptable excipients.

9. A pharmaceutical composition for treating acute leukemia, characterized in that, The pharmaceutical composition uses phenobarbital as the active ingredient.

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