CN114053285A - Application of ganoderic acid X in treating tumor - Google Patents
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- CN114053285A CN114053285A CN202111045875.XA CN202111045875A CN114053285A CN 114053285 A CN114053285 A CN 114053285A CN 202111045875 A CN202111045875 A CN 202111045875A CN 114053285 A CN114053285 A CN 114053285A
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Abstract
The application provides an application of ganoderic acid X in preparing a medicine for treating tumors and a corresponding medicine composition. Research shows that ganoderic acid X has good inhibition effect on tumors, particularly liver cancer; ganoderic acid X can inhibit cancer cell activity, inhibit cancer cell proliferation by inhibiting cell cycle, and induce cancer cell apoptosis.
Description
Technical Field
The application belongs to the field of tumor treatment and the field of natural pharmaceutical compounds, and particularly provides application of ganoderic acid X in treating tumors.
Background
Liver cancer is one of malignant tumors with high incidence in China, and research on treatment of liver cancer has become a research hotspot. Currently, the surgical treatment of liver cancer is the most effective method, but most liver cancer patients have no symptoms in the early stage, the diagnosis is already in the middle and late stage, and the curative treatment such as hepatectomy or liver transplantation is not suitable at the moment, so that the hepatectomy only benefits a few patients. Clinically, radiation therapy is obviously damaged to the liver, and liver transplantation operation is expensive and accompanied by complications, so that systemic treatment is the first choice for patients with liver cancer. In the existing anticancer chemotherapeutic drugs used in clinic, sorafenib is a first-line molecular targeted therapeutic drug. Sorafenib is an oral multi-kinase inhibitor and is directed primarily against RAF kinase and Vascular Endothelial Growth Factor (VEGF). Although sorafenib is the only clinical treatment for patients with advanced liver cancer, some patients are intolerant to sorafenib with median survival rates of less than one year. Therefore, the search for novel, high-efficiency and low-toxicity antitumor drugs becomes a research hotspot for tumor treatment. The Chinese herbal medicine has many advantages including multiple targets, multiple effects, low toxic and side effects and the like, and plays an important role in treating tumors.
Ganoderma (Ganoderma lucidum), also known as Ganoderma and Thymus vulgaris, is a fungus of the genus Ganoderma of the family Ganodermataceae of the order Polyporales of the class Agaricales of the phylum Basidiomycota. The fruit body is a rare Chinese medicament which is a traditional tonifying Chinese medicament in China, is listed as the top grade in Shen nong's herbal Jing, and is always regarded as a treasure for nourishing and strengthening body, strengthening body resistance and consolidating constitution and prolonging life. Modern researches have shown that ganoderma contains about 400 different bioactive substances, including polysaccharides, triterpenes, sterols, alkaloids, fatty acids, proteins/polypeptides, etc., and has various activities of regulating immunity, resisting tumor, protecting liver, resisting aging, etc. Ganoderic acid compounds are a large class of antitumor compounds in ganoderma, and the cancer inhibition and anticancer mechanisms of the ganoderic acid compounds become hot spots of research in recent years.
Disclosure of Invention
In one aspect, the application provides the use of ganoderic acid X in the preparation of a medicament for treating a tumor.
Further, the tumor is liver cancer.
Further, the tumor is hepatoblastoma.
On the other hand, the application provides the application of the ganoderic acid X in preparing the medicine for inducing the apoptosis of the liver cancer cells.
On the other hand, the application provides the application of the ganoderic acid X in preparing the medicine for inhibiting the cell viability of the liver cancer cells.
On the other hand, the application provides the application of the ganoderic acid X in preparing the medicine for inhibiting the proliferation of the hepatoma cells.
On the other hand, the application provides the application of ganoderic acid X in preparing the medicine for inhibiting the cell cycle of the liver cancer.
In another aspect, the present application provides the use of ganoderic acid X in the preparation of a reagent that inhibits the cyclin gene and the cyclin kinase gene.
In another aspect, the present application provides a pharmaceutical composition for treating tumors, which comprises ganoderic acid X as an active ingredient.
Further, the tumor is hepatoblastoma.
The pharmaceutical composition of the application can take ganoderic acid X as the only active ingredient, and can also comprise other active ingredients with known anti-tumor effect or auxiliary anti-tumor effect.
The pharmaceutical composition of the present application can be used alone or in combination with other drugs known to have an anti-tumor effect or an auxiliary anti-tumor effect.
The cyclin genes and cycle kinase genes described herein include, but are not limited to, those known and studied in the art, including, but not limited to, CDK1, CDK2, CDK4, Ccnb2, Ccnd1, Ccne 1.
The medicine/medicine composition of the application is preferably an injection preparation or an oral preparation, and specifically includes but is not limited to tablets, capsules, oral liquid preparations, pills, granules, powder, water injection, oil injection, emulsion injection, powder injection and the like.
In addition to oral or injectable dosage forms, other known or under-developed dosage forms such as transdermal administration, inhalation administration, targeted carrier administration, may be routinely selected and designed by those skilled in the pharmaceutical arts as appropriate.
Drawings
Figure 1 is the effect of GAX on HepG2 cell viability (. P <0.001, compared to control);
figure 2 is the effect of GAX on H22 cell viability (. P <0.001, compared to control);
FIG. 3 shows GAX treatment time versus HepG2 cell IC50A change in (c);
FIG. 4 shows GAX treatment time versus H22 cell IC50A change in (c);
FIG. 5 is a graph of the effect of GAX on the proliferative capacity of HepG2 cells;
FIG. 6 shows the effect of GAX on the apoptotic proteins of HepG2 (. P <0.05, compared to control;. P <0.001, compared to control);
FIG. 7 shows the effect of GAX on the apoptotic proteins of H22 cells (P <0.05, compared to control;. P <0.01, compared to control;. P <0.001, compared to control);
FIG. 8 shows the effect of GAX on the cell cycle of HepG2 (. P <0.05, compared to control;. P <0.01, compared to control);
FIG. 9 shows the effect of GAX on the H22 cell cycle (. SP <0.05, compared to control;. SP <0.01, compared to control);
figure 10 shows the effect of GAX on the H22 cell cycle (P <0.05, compared to control;. P <0.01, compared to control;. P <0.001, compared to control).
FIG. 11 is a graph showing the inhibitory effect of ganoderic acid X on leukemia, tongue squamous carcinoma, breast cancer and cervical cancer cells; IC50 for HL-60 acute promyelocytic leukemia cells was: 27 mu M; IC50 for K562 chronic myelogenous leukemia cells is: 31 mu M; IC50 for Hela cervical carcinoma cells was: 12 mu M; IC50 for Cal27 human tongue squamous carcinoma cells is: 12 mu M; IC50 for 231 human breast cancer cells is: 10 mu M; IC50 for MCF-7 human breast cancer cells is: 12 μ M.
Detailed Description
Example 1 Experimental procedure
Cell culture
H22 cells were purchased from Beijing Zhuang Union International BioGene technology Ltd (cat # 2KC2010-2), and HepG2 cells were recovered from the cryopreserved cells in the group. HepG2 cells were cultured in high-sugar DMEM medium containing 10% fetal calf serum, and H22 cells were cultured in 1640 medium containing 10% fetal calf serum at 37 ℃ in 5% CO2Culturing in a constant temperature incubator. When HepG2 cells grow to 90% confluence, the original culture solution is discarded, cells are digested and blown into single cell suspension by adding pancreatin for 1: 4 passages, and the single cell suspension is inoculated into a new T75 culture bottle. H22 cells were grown to 1X 106At/ml, the cell suspension was transferred to a centrifuge tube, centrifuged at 1000rpm for 5 minutes, discardedFresh 1640 medium containing 10% fetal bovine serum was added to the serum for 1 to 4 passages.
Ganoderic acid X was purchased from a source leaf organism (cat # B27127) and frozen in 50mM stock solution with DMSO added. After being digested and diluted, HepG2 cells in a logarithmic growth phase are inoculated in a 96-well plate at 12000/well; after centrifugation and resuspension of H22 cells, 10000 cells/well were plated in 96-well plates. At 37 ℃ with 5% CO2And (5) performing adherent culture for 24 hours in a constant-temperature incubator. Discarding the culture medium supernatant, diluting the ganoderic acid X mother liquor to a target concentration by using a serum-free culture medium, adding the diluted ganoderic acid X mother liquor into a 96-well plate, culturing in a constant-temperature incubator, and measuring the cell activity by using CCK 8.
Western blot
Cells were lysed with cell lysates containing 1% protease inhibitor and phosphatase inhibitor and sonicated for 3 min. Insoluble material was removed by centrifugation at 12000rpm for 30 minutes at 4 ℃. Protein concentration was determined by BCA quantification. Adding 5 Xloading buffer with proper amount, mixing uniformly, heating in boiling water for 10 min to denature protein completely. The gel concentration is selected according to the molecular weight of the protein of interest. Proteins in the sample were separated by dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred to nitrocellulose membrane. Blocked with 5% skim milk for 2 hours at room temperature and incubated overnight at 4 ℃ with primary antibody as follows: Anti-Caspase-3 antibody (ab184787), Anti-Bax antibody (ab32503), Anti-Bcl-2 antibody (ab194583) and Anti-beta Actin antibody (ab 8226). Then, washed three times with TBST, incubated with secondary antibody at 1:2000 dilution for 2 hours, followed by three TBST washes. The blot was visualized by enhanced chemiluminescence using a BioRad imaging system (Bio-Rad, Hercules, Calif., USA).
Cell clonal formation
After trypsinizing HepG2 cells in log phase, the cells were diluted in full culture medium and seeded at 1000/well in 6-well plates. At 37 ℃ with 5% CO2And (5) performing adherent culture for 24 hours in a constant-temperature incubator. Discarding culture medium supernatant, diluting with complete culture medium to prepare ganoderic acid X, and adding into 6-well plate. When it is observed that a single cell proliferated a colony of more than 50 cells, the medium is discarded, the cells are washed with PBS, and4% paraformaldehyde fixing solution is added, and the mixture is fixed at 4 ℃ overnight. 0.1g of crystal violet was dissolved in 20ml of methanol to prepare a 0.5% crystal violet mother liquor. When in use, the mother solution: PBS 1: 4, preparing working liquid. The cell fixative was discarded, washed three times with PBS, and 1ml of crystal violet staining solution was added to each well for 10 minutes. After discarding the staining solution, the sample was washed five times with PBS and then observed by photography.
Flow cytometer
After trypsinizing HepG2 cells in log phase, the cells were diluted in serum-free DMEM medium and seeded in 6-well plates at 80 ten thousand per well. After centrifugation of H22 cells, the cells were diluted in 1640 medium without serum and seeded in 6-well plates at 100 ten thousand per well. At 37 ℃ with 5% CO2And (5) carrying out starvation culture for 24 hours in a constant-temperature incubator. Diluting with serum-free culture medium to obtain ganoderic acid X, adding into 6-well plate, treating with the medicine for 6 hr, and collecting cells. After centrifugation to remove the medium supernatant, the cells were homogenized with 50. mu.l of pre-cooled PBS, added to 1ml of pre-cooled 75% ethanol fixative and fixed overnight at low temperature. Centrifuge at 1000g for 5 minutes, pellet cells, and aspirate supernatant. 1ml PBS was added to resuspend the cells and centrifuge. PBS was discarded, 500. mu.l of propidium iodide staining solution was added to each sample, and the mixture was incubated at 37 ℃ in the dark for 30 minutes, and the cell cycle was measured by flow cytometry.
RT-PCR
Collecting cells treated by ganoderic acid X administration, adding 1ml Trizol, and grinding. Then, 0.2ml of chloroform was added thereto, the mixture was vigorously shaken for 15 seconds, allowed to stand at room temperature for 5 minutes, and centrifuged at 12000rpm at 4 ℃ for 15 minutes. And (3) taking an upper water sample, adding equivalent isopropanol, inverting, uniformly mixing, standing at room temperature for 10 minutes, centrifuging at 12000rpm at 4 ℃ for 10 minutes. The supernatant was discarded, and the pellet was washed with 75% ethanol and centrifuged. Discarding the ethanol solution, adding a proper amount of enzyme-removed water to dissolve the precipitate, and measuring the nucleic acid concentration. Reverse transcription was performed using the Takara reverse transcription kit (RR 036A). Fluorescence quantification was performed using the Takara fluorescence quantification kit (RR820A), and the primer sequences for fluorescence quantification were as follows:
data processing
Statistical analysis was performed using SPSS statistical software. Statistical analysis of the metrology data was performed using unpaired t-test and One-way ANOVA, with statistical differences at P < 0.05.
Example 2 results of the experiment
Ganoderic acid X treatment can reduce liver cancer cell activity
As shown in FIG. 1, after 48 hours of treatment of human liver cancer HepG2 cells with Ganoderic Acid X (GAX), cell viability was measured by CCK 8. Compared with the control group, GAX can inhibit the activity of human hepatoma cells. IC of GAX on HepG2 cells5016 μ M.
As shown in FIG. 2, GAX can inhibit the activity of murine hepatoma carcinoma cells compared to the control group 48 hours after the treatment of murine hepatoma carcinoma H22 cells with GAX. IC of GAX on H22 cells50At 15. mu.M.
The inhibitory effect of ganoderic acid X on hepatocarcinoma cell is time-dependent
As shown in FIG. 3, the IC of GAX versus HepG2 increased with the GAX treatment time50And gradually decreases. Indicating that GAX treatment significantly inhibited cell viability of HepG2 cells in a time-dependent manner.
As shown in FIG. 4, the IC of GAX versus H22 increases with the time of GAX treatment50And gradually decreases. Indicating that GAX treatment significantly inhibited the cell viability of H22 cells in a time-dependent manner.
Ganoderic acid X inhibits HepG2 cell proliferation
The cell clone formation rate is the cell inoculation survival rate. As shown in fig. 5, GAX treatment significantly reduced the number of HepG2 cell colonies compared to the blank control, indicating that GAX inhibited HepG2 cell proliferation.
Ganoderic acid X treatment induced liver cancer cell apoptosis
As shown in FIG. 6, GAX treatment induced the expression of the apoptosis-related protein caspase-3, Bax, of HepG2 cells and reduced the expression of the inhibitor apoptosis protein Bcl2, as compared to the control group. Indicating that the treatment of ganoderic acid X induces HepG2 cell apoptosis.
As shown in FIG. 7, GAX treatment induced the expression of caspase-3, Bax, an apoptosis-related protein of H22, and decreased the expression of Bcl2, which is an apoptosis-inhibiting protein, compared to the control group. Indicating that the treatment of ganoderic acid X induces H22 apoptosis. Ganoderic acid X treatment for inhibiting liver cancer cell cycle
As shown in fig. 8, a significant increase in S phase was observed after treatment of serum-starved HepG2 cells at GAX administration concentrations of 2, 6, 10 μ M compared to the control group. Indicating that GAX can inhibit HepG2 cell cycle.
As shown in fig. 9, the H22 cell cycle is more sensitive to GAX. A significant increase in S phase was observed after treatment of serum-starved H22 cells at GAX dosing concentrations of 1, 2, 3 μ M compared to the control group. It is suggested that the inhibition of proliferation of hepatoma cells by GAX may be achieved by inhibiting the cell cycle.
Effect of Ganoderic acid X on cycle-related genes
As shown in fig. 10, significant reduction in the expression of the cycle-associated cyclin gene and cycle kinase gene was observed after 12 hours of treatment of H22 cells at GAX administration concentrations of 5, 10, 20 μ M compared to the control group, indicating that GAX had a significant inhibitory effect on the H22 cell cycle.
Effect of Ganoderic acid X on other cancer cells
IC50 for HL-60 acute promyelocytic leukemia cells was: 27 mu M; IC50 for K562 chronic myelogenous leukemia cells is: 31 mu M; IC50 for Hela cervical carcinoma cells was: 12 mu M; IC50 for Cal27 human tongue squamous carcinoma cells is: 12 mu M; IC50 for 231 human breast cancer cells is: 10 mu M; IC50 for MCF-7 human breast cancer cells is: 12 μ M.
SEQUENCE LISTING
<110> institute of medicinal plants of academy of Chinese medical science
<120> application of ganoderic acid X in treating tumor
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<170> PatentIn version 3.5
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Claims (10)
1. Application of ganoderic acid X in preparing medicine for treating tumor is provided.
2. The use of claim 1, wherein the tumor is liver cancer, leukemia, breast cancer, tongue squamous carcinoma or cervical cancer.
3. The use according to claim 2, wherein the tumor is hepatoblastoma, acute promyelocytic leukemia, chronic myelogenous leukemia, breast cancer, tongue squamous carcinoma or cervical cancer.
4. Application of ganoderic acid X in preparing medicine for inducing cancer cell apoptosis is provided.
5. Application of ganoderic acid X in preparing medicine for inhibiting cancer cell activity is provided.
6. Application of ganoderic acid X in preparing medicine for inhibiting cancer cell proliferation is provided.
7. Application of ganoderic acid X in preparing medicine for inhibiting cancer cell cycle is provided.
8. Application of ganoderic acid X in preparing reagent for inhibiting cyclin gene and periodic kinase gene is provided.
9. A pharmaceutical composition for treating tumors, comprising ganoderic acid X as an active ingredient.
10. The pharmaceutical composition of claim 9, wherein the tumor is hepatoblastoma, acute promyelocytic leukemia, chronic myelogenous leukemia, breast cancer, tongue squamous carcinoma, or cervical cancer.
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Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN1823787A (en) * | 2005-12-29 | 2006-08-30 | 华东理工大学 | Application of lucid ganoderma acid in preparation of cancer transfer inhibitor |
| CN104000829A (en) * | 2014-05-15 | 2014-08-27 | 上海应用技术学院 | Application of ganoderic acid as p53-MDM2 interaction inhibitor |
| TW201444561A (en) * | 2013-05-28 | 2014-12-01 | Double Crane Biotechnology Co Ltd | Therapeutic composition for treating cancers |
-
2021
- 2021-09-07 CN CN202111045875.XA patent/CN114053285A/en active Pending
Patent Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN1823787A (en) * | 2005-12-29 | 2006-08-30 | 华东理工大学 | Application of lucid ganoderma acid in preparation of cancer transfer inhibitor |
| TW201444561A (en) * | 2013-05-28 | 2014-12-01 | Double Crane Biotechnology Co Ltd | Therapeutic composition for treating cancers |
| CN104000829A (en) * | 2014-05-15 | 2014-08-27 | 上海应用技术学院 | Application of ganoderic acid as p53-MDM2 interaction inhibitor |
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