CN115105488A - Application of Dankasterone A in preparation of medicine for treating hepatic fibrosis - Google Patents
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Abstract
The invention discloses an application of Dankasterone A in preparing a medicament for treating hepatic fibrosis, wherein the medicament for treating hepatic fibrosis is prepared by using Dankasterone A as an active ingredient and other medicament excipients or carriers; the concentration of Dankasterone A in the medicine for treating hepatic fibrosis is 5-20 mu M. The application discovers for the first time that Dankasterone A can obviously inhibit the proliferation of hepatic stellate cells LX-2, reduce the protein expression of main hepatic fibrosis markers in the hepatic stellate cells LX-2, inhibit the migration capacity of the hepatic stellate cells LX-2 and induce the apoptosis of the hepatic stellate cells LX-2, has the function of inhibiting or reversing hepatic fibrosis, and has good application prospect in the aspect of preparing medicines for treating the hepatic fibrosis.
Description
Technical Field
The invention belongs to the technical field of medicines, and particularly relates to application of Dankasterone A in preparation of a medicine for treating hepatic fibrosis.
Background
Hepatic Fibrosis (HF) is a process in which various factors (such as HBV, HCV, alcohol, etc.) act on the liver to cause an imbalance of extracellular matrix (ECM), and further development thereof may cause cirrhosis and liver cancer, seriously affecting the life health of patients. Hepatic Stellate Cells (HSCs) are the major source of liver ECM, are the cytological basis for liver fibrosis, and are central in ECM metabolism and the production of various cytokines. When the liver is injured, the HSC is activated and secretes various cytokines, and further acts on the HSC to activate, proliferate and migrate the HSC; myofibroblast-like phenotype transformation occurs, so that a large amount of ECM components such as type I collagen, type III collagen, fibronectin and the like are synthesized and secreted and accumulated in the liver in a large amount, scar tissues gradually replace liver parenchyma, and finally hepatic fibrosis is formed. Therefore, inhibiting HSC proliferation, activation, migration, or promoting HSC apoptosis is an important strategy to slow down and reverse HF, and has become an important target for the research of anti-liver fibrosis drugs.
Dankasterone a belongs to the group of structurally specific ergosta-type steroid compounds, which are characterized in that they contain a fused cis-a/B ring structure. Ergosterol compounds are widely present in natural compounds, and many have specific physiological activities and pharmacological actions. Dankasterone A was originally isolated from Amagata and Numata et al in Halichondria japonica. Patent application CN201210044441.2 discloses the application of Dankasterone A in preparing antiviral drugs, which has the effect of resisting HIV virus activity.
However, no relevant research literature discloses the application of Dankasterone A in preparing medicaments for treating hepatic fibrosis.
Disclosure of Invention
The invention provides an application of Dankasterone A in preparing a medicament for treating hepatic fibrosis to solve the technical problems.
In order to achieve the above purpose, the invention adopts the following technical scheme:
an application of Dankasterone A in preparing the medicine for treating hepatic fibrosis is disclosed, which is prepared from Dankasterone A as active component and other excipient or carrier.
Further, the concentration of the Dankasterone A in the medicine for treating hepatic fibrosis is 5-20 mu M.
Further, the concentration of the Dankasterone A in the medicine for treating hepatic fibrosis is 10-20 mu M.
Further, the concentration of Dankasterone A in the medicament for treating hepatic fibrosis is 20 μ M.
Further, the Dankasterone A is directly extracted from natural products or is prepared by combination synthesis, and has the chemical name of (4aR,4bR,6aR,7R,10aR) -3,4,4a,4b,5,6,6a,7,8,9-Decahydro-4a,6a-dimethyl-7- [ (1R,2E,4R) -1,4,5-trimethyl-2-hexenyl]indeno[1,7a-a]naphthalene-2,10,12(11H) -trione; molecular formula C 28 H 40 O 3 (ii) a The molecular weight is 424.62.
Further, the structural formula of the Dankasterone A is a steroid component, and the structural formula is as follows:
further, the medicament for treating the hepatic fibrosis is an inhibitor of proliferation or survival of hepatic stellate cells.
Furthermore, the medicament for treating hepatic fibrosis is an inhibitor of hepatic fibrosis marker protein expression in hepatic stellate cells, and achieves the effect of resisting hepatic fibrosis by inhibiting survival, proliferation and apoptosis of the hepatic stellate cells and hepatic fibrosis marker protein expression.
Furthermore, the medicine for treating hepatic fibrosis can promote the apoptosis of hepatic stellate cells.
Furthermore, the dosage form of the medicine for treating hepatic fibrosis is oral preparation or injection.
Further, the oral preparation is any one of granules, capsules, tablets, powder, dripping pills and sustained release preparations.
Further, the medicament for treating liver fibrosis is a medicament for inhibiting or reversing liver fibrosis.
Due to the adoption of the technical scheme, the invention has the following beneficial effects:
the invention provides the application of Dankasterone A in preparing a medicament for treating hepatic fibrosis for the first time. By using human hepatic stellate cell LX2 as a model cell, experiments show that Dankasterone A can reduce the expression level of collagen which is a main hepatic fibrosis marker in hepatic stellate cell LX-2, can obviously inhibit the proliferation and migration capacity of the hepatic stellate cell LX-2, can induce the apoptosis of the hepatic stellate cell LX-2, has the function of inhibiting or reversing hepatic fibrosis, has dose dependence and has good application prospect in the aspect of preparing medicaments for treating the hepatic fibrosis. The novel application of Dankasterone A in preparing the medicament for treating hepatic fibrosis has great significance for breaking through the bottleneck of hepatic fibrosis treatment.
Drawings
In order to illustrate the embodiments of the present invention or the technical solutions in the prior art more clearly, the drawings needed in the description of the embodiments or the prior art will be briefly introduced below, it is obvious that the drawings in the following description are only some examples of the present invention, and for a person skilled in the art, without inventive step, other drawings can be obtained according to these drawings:
FIG. 1 is a graph showing the effect of Dankasterone A at various concentrations in the present application on LX-2 cell proliferation activity;
FIG. 2 is an inverted microscope image of different concentrations of Dankasterone A on LX-2 cell migration observed in the cell-scratching experiment of the present application;
FIG. 3 is a graph showing the effect of different concentrations of Dankasterone A on LX-2 cell migration ability observed in the cell scratch test of the present application;
FIG. 4 is an inverted microscope image of the Transwell experiment of the present application observing the effect on LX-2 cell migration under intervention of Dankasterone A at different concentrations;
FIG. 5 is a graph showing the effect of Dankasterone A on LX-2 cell migration ability observed in a Transwell experiment of the present application at various concentrations;
FIG. 6 is an inverted fluorescence microscope image of LX-2 cells with early and late apoptosis observed by Hoechst/PI dual fluorescence staining under treatment with Dankasterone A of various concentrations according to the present application;
FIG. 7 is a graph showing the effect of LX-2 apoptosis observed under flow cytometry using Annexin V-FITC and PI dyes under the treatment of Dankasterone A at various concentrations in the present application;
FIG. 8 is a graph of the effect on LX-2 apoptosis of Dankasterone A treatment at various concentrations herein;
FIG. 9 is a histogram of a protein of interest in a chemiluminescent imaging system using Dankasterone A at various concentrations according to the present application;
FIG. 10 is a graph showing the effect of Dankasterone A at various concentrations in the present application on the protein expression level of Collagen I.
In the drawings: hoechst stained bright blue cells indicate early apoptosis, and PI stained cells late apoptosis.
Detailed Description
The following is a detailed description of the embodiments of the present invention, but the present invention is not limited to these embodiments, and any modifications or substitutions in the basic spirit of the embodiments are included in the scope of the present invention as claimed in the claims.
Example 1
An application of Dankasterone A in preparing the medicine for treating hepatic fibrosis is disclosed, which is prepared from Dankasterone A as active component and other excipient or carrier.
Further, the concentration of Dankasterone A in the medicine for treating hepatic fibrosis is 5 mu M; the Dankasterone A is directly extracted from natural products or prepared by combination synthesis, and has the chemical name of (4aR,4bR,6aR,7R,10aR) -3,4,4a,4b,5,6,6a,7,8,9-Decahydro-4a,6a-dimethyl-7- [(1R,2E,4R)-1,4,5-trimethyl-2-hexenyl]indeno[1,7a-a]naphthalene-2,10,12(11H) -trione; molecular formula C 28 H 40 O 3 (ii) a The molecular weight is 424.62; the structural formula of the Dankasterone A is a steroid component, and the structural formula is as follows:
further, the medicament for treating hepatic fibrosis is an inhibitor of proliferation or survival of hepatic stellate cells; the medicament for treating hepatic fibrosis is an inhibitor of hepatic fibrosis marker protein expression in hepatic stellate cells, and achieves the effect of resisting hepatic fibrosis by inhibiting survival, proliferation and apoptosis of the hepatic stellate cells and hepatic fibrosis marker protein expression; the medicine for treating hepatic fibrosis can promote the apoptosis of hepatic stellate cells; the dosage form of the medicine for treating hepatic fibrosis is oral preparation or injection; the oral preparation is any one of granules, capsules, tablets, powder, dripping pills and sustained release preparations; the medicament for treating hepatic fibrosis is a medicament for inhibiting or reversing hepatic fibrosis.
Example 2
An application of Dankasterone A in preparing the medicine for treating hepatic fibrosis is disclosed, which is prepared from Dankasterone A as active component and other excipient or carrier.
Further, the concentration of Dankasterone A in the medicine for treating hepatic fibrosis is 15 mu M; the Dankasterone A is directly extracted from natural products or is prepared by chemical combination synthesis, and has the chemical name of (4aR,4bR,6aR,7R,10aR) -3,4,4a,4b,5,6,6a,7,8,9-Decahydro-4a,6a-dimethyl-7- [ (1R,2E,4R) -1,4,5-trimethyl-2-hexenyl]indeno[1,7a-a]naphthalene-2,10,12(11H) -trione; molecular formula C 28 H 40 O 3 (ii) a The molecular weight is 424.62; the structural formula of the Dankasterone A is a steroid component, and the structural formula is as follows:
further, the medicament for treating hepatic fibrosis is an inhibitor of proliferation or survival of hepatic stellate cells; the medicine for treating hepatic fibrosis is an inhibitor for expressing hepatic fibrosis marker protein in hepatic stellate cells, and achieves the effect of resisting hepatic fibrosis by inhibiting survival, proliferation and apoptosis of the hepatic stellate cells and expression of the hepatic fibrosis marker protein; the medicine for treating hepatic fibrosis can promote the apoptosis of hepatic stellate cells; the dosage form of the medicine for treating hepatic fibrosis is oral preparation or injection; the oral preparation is any one of granules, capsules, tablets, powder, dripping pills and sustained release preparations; the medicament for treating hepatic fibrosis is a medicament for inhibiting or reversing hepatic fibrosis.
Example 3
An application of Dankasterone A in preparing the medicine for treating hepatic fibrosis is disclosed, which is prepared from Dankasterone A as active component and other excipient or carrier.
Further, the concentration of Dankasterone A in the medicine for treating hepatic fibrosis is 10 mu M; the Dankasterone A is directly extracted from natural products or is prepared by chemical combination synthesis, and has the chemical name of (4aR,4bR,6aR,7R,10aR) -3,4,4a,4b,5,6,6a,7,8,9-Decahydro-4a,6a-dimethyl-7- [ (1R,2E,4R) -1,4,5-trimethyl-2-hexenyl]indeno[1,7a-a]naphthalene-2,10,12(11H) -trione; molecular formula of C 28 H 40 O 3 (ii) a The molecular weight is 424.62; the structural formula of the Dankasterone A is a steroid component, and the structural formula is as follows:
further, the medicament for treating hepatic fibrosis is an inhibitor of proliferation or survival of hepatic stellate cells; the medicament for treating hepatic fibrosis is an inhibitor of hepatic fibrosis marker protein expression in hepatic stellate cells, and achieves the effect of resisting hepatic fibrosis by inhibiting survival, proliferation and apoptosis of the hepatic stellate cells and hepatic fibrosis marker protein expression; the medicine for treating hepatic fibrosis can promote the apoptosis of hepatic stellate cells; the dosage form of the medicine for treating hepatic fibrosis is oral preparation or injection; the oral preparation is any one of granules, capsules, tablets, powder, dripping pills and sustained release preparations; the medicament for treating hepatic fibrosis is a medicament for inhibiting or reversing hepatic fibrosis.
Example 4
An application of Dankasterone A in preparing the medicine for treating hepatic fibrosis is disclosed, which is prepared from Dankasterone A as active component and other excipient or carrier.
Further, the concentration of Dankasterone A in the medicine for treating hepatic fibrosis is 13 mu M; the Dankasterone A is directly extracted from natural products or is prepared by chemical combination synthesis, and has the chemical name of (4aR,4bR,6aR,7R,10aR) -3,4,4a,4b,5,6,6a,7,8,9-Decahydro-4a,6a-dimethyl-7- [ (1R,2E,4R) -1,4,5-trimethyl-2-hexenyl]indeno[1,7a-a]naphthalene-2,10,12(11H) -trione; molecular formula C 28 H 40 O 3 (ii) a The molecular weight is 424.62; the structural formula of the Dankasterone A is a steroid component, and the structural formula is as follows:
further, the medicament for treating hepatic fibrosis is an inhibitor of proliferation or survival of hepatic stellate cells; the medicament for treating hepatic fibrosis is an inhibitor of hepatic fibrosis marker protein expression in hepatic stellate cells, and achieves the effect of resisting hepatic fibrosis by inhibiting survival, proliferation and apoptosis of the hepatic stellate cells and hepatic fibrosis marker protein expression; the medicine for treating hepatic fibrosis can promote the apoptosis of hepatic stellate cells; the dosage form of the medicine for treating hepatic fibrosis is oral preparation or injection; the oral preparation is any one of granules, capsules, tablets, powder, dripping pills and sustained release preparations; the medicament for treating hepatic fibrosis is a medicament for inhibiting or reversing hepatic fibrosis.
Example 5
An application of Dankasterone A in preparing the medicine for treating hepatic fibrosis is disclosed, which is prepared from Dankasterone A as active component and other excipient or carrier.
Further, the concentration of Dankasterone A in the medicine for treating hepatic fibrosis is 18 mu M; the Dankasterone A is directly extracted from natural products or is prepared by chemical combination synthesis, and has the chemical name of (4aR,4bR,6aR,7R,10aR) -3,4,4a,4b,5,6,6a,7,8,9-Decahydro-4a,6a-dimethyl-7- [ (1R,2E,4R) -1,4,5-trimethyl-2-hexenyl]indeno[1,7a-a]naphthalene-2,10,12(11H) -trione; molecular formula C 28 H 40 O 3 (ii) a The molecular weight is 424.62; the structural formula of the Dankasterone A is a carrier component, and the structural formula is as follows:
further, the medicament for treating hepatic fibrosis is an inhibitor of proliferation or survival of hepatic stellate cells; the medicament for treating hepatic fibrosis is an inhibitor of hepatic fibrosis marker protein expression in hepatic stellate cells, and achieves the effect of resisting hepatic fibrosis by inhibiting survival, proliferation and apoptosis of the hepatic stellate cells and hepatic fibrosis marker protein expression; the medicine for treating hepatic fibrosis can promote the apoptosis of hepatic stellate cells; the dosage form of the medicine for treating hepatic fibrosis is oral preparation or injection; the oral preparation is any one of granules, capsules, tablets, powder, dripping pills and sustained release preparations; the medicament for treating hepatic fibrosis is a medicament for inhibiting or reversing hepatic fibrosis.
To further illustrate that the present invention can achieve the technical effects, the following experiments were performed:
MTT method for detecting cell proliferation activity.
Using high-sugar Medium DMEM containing 10% fetal bovine serum, 100kU/L penicillin and 100mg/L streptomycin at 37 ℃ with 5% CO 2 LX-2 cells were cultured in an incubator. LX-2 cells were harvested in logarithmic growth phase, digested with 0.25% trypsin, and cell density adjusted with medium (10% FBS + 1% double antibody)Degree to 5 x 10 4 one/mL, the cells were inoculated into a 96-well plate, and divided into a control group, a TGF-. beta.1 (10ng/mL) group, a Dankasterone A (5. mu.M) group, a Dankasterone A (10. mu.M) group, and a Dankasterone A (20. mu.M) group. Each group of 6 duplicate wells, 100. mu.L of cell suspension per well, blank zeroing wells were set, 200. mu.L of sterile PBS was added around the wells at 37 ℃, 5% CO 2 After culturing for 24h under the saturated humidity condition, adding 20 mu L MTT into each hole, culturing for 3h under the same culture condition, sucking out the culture medium, adding 100 mu L MSO, oscillating for 10min, measuring the absorbance (A) at 490nm of each hole by using an enzyme-labeling instrument, and calculating the cell proliferation rate. The cell proliferation rate was (experiment group-a zero-adjusted group)/(control group a-a zero-adjusted group) × 100%, and the results are shown in fig. 1.
It can be understood from FIG. 1 that Dankasterone A significantly decreased the survival rate of LX-2 cells and was concentration-dependent.
Cell scratch and Transwell experiments the effect of Dankasterone A on LX-2 cell migration was observed.
After counting on an LX-2 cell counting plate, the number is 5X 10 5 The cells/well were seeded in 6-well plates at 37 ℃ with 5% CO 2 The culture is performed for 24 hours in an adherence way in a constant temperature incubator. A scratch band without cells was scribed in the adherent cells with a 200 pipette and a ruler, and washed 3 times with PBS to remove the scribed adherent cells. And (3) medicine intervention: and (3) carrying out corresponding treatment on each group of cells according to the experimental grouping, wherein the model group comprises: changing into complete medium containing TGF-beta 1(10 ng/mL); dankasterone a intervention group: TGF-. beta.1 (10ng/mL) intervenes simultaneously with drugs at concentrations of 20, 10, 5. mu.M. Adding 5% CO at 37 deg.C 2 The constant temperature incubator continuously cultures for 2d, cell scratches are photographed at two time points of 0h and 24h by using an inverted microscope, and the area of the scratches is measured by using ImageJ software. Scratch mobility 24h ═ scratch area 0 h-scratch area 24 h/scratch area 0 h. Transwell experiment: transwell chamber was placed in 24-well plate at a cell concentration of 5X 10 5 Perml cell suspension in the upper chamber by adding 200. mu.L of cell and 500. mu.L of culture medium containing 10% fetal bovine serum in DMEM Medium in the lower chamber, placing at 37 ℃ with 5% CO 2 The incubator is incubated for 24 hours. The upper chamber was removed, 600. mu.L of 4% paraformaldehyde was added, and the mixture was fixed at room temperature for 20 minutesmin, then transfer the upper chamber into 1% crystal violet dye solution, stain at room temperature for 25min in the dark, wash 2 times with PBS. The chamber was placed under an inverted microscope and 3 fields were randomly selected for photography and ImageJ software was used to count the number of membrane-penetrating cells and all experiments were repeated 3 times. The results are shown in fig. 2, 3,4 and 5.
As is clear from FIGS. 2, 3,4 and 5, Dankasterone A significantly inhibited the migratory ability of LX-2 cells.
Apoptosis detection experiments.
And respectively adopting a Hochest/PI double staining method and a flow cytometry method for detection. Adjusting cell density to 1X 10 5 one/mL, which was inoculated in 6-well plates at 1X 10 5 Individual cells/well were seeded in 6-well plates at 37 ℃ in 5% CO 2 After culturing for 24h in an incubator, fixing for 30min by 4% paraformaldehyde, adding Hoechst33342 dye, incubating for 5min in a dark place, washing for 3 times by PBS, adding PI dye, incubating for 10min in a dark place, and observing under an inverted fluorescence microscope. Cell flow experiments: adjusting the cell density to 1 × 10 6 one/mL, which was inoculated into a 6-well plate, annexin V-FITC and PI dye were added according to the kit instructions, cell death was detected by flow cytometry, and analyzed by FlowJo7.6. Uniformly mixing, and reacting for 5-15 min at room temperature in a dark place; and (4) performing detection on a flow cytometer. The results are shown in fig. 6, 7 and 8.
As can be seen from fig. 6, 7 and 8, the apoptosis rate was decreased in the TGF- β 1 group compared with the control group, but the difference was not statistically significant, as determined by flow cytometry; compared with TGF-beta 1 group, the Dankasterone A5, 10 and 20 mu M group has obviously increased apoptosis rate (P < 0.01).
Western Blot experiment.
After LX-2 cells were treated with the drug, 100. mu.L of lysate was added to each well of 6-well plate cells, and after the cells were sufficiently lysed, the cells were centrifuged at 12000rpm at 4 ℃ for 10min, and the supernatant was collected. Protein concentration was determined using BCA assay kit. Adjusting protein concentration, mixing with 4 × Sample buffer, heating at 100 deg.C for 10min to completely denature protein, and storing the extracted protein Sample in a refrigerator at-80 deg.C. The target band was transferred to PVDF membrane using SDS-PAGE gel electrophoresis at 10% or 8% by mass, and blocked in 5% by mass of skim milk for 2h at room temperature. Incubate primary antibody overnight at 4 ℃. After incubation, TBST was washed 3 times for 10min each. After incubation of the secondary antibody at room temperature for 2h, the secondary antibody was washed 3 times with TBST for 10min each. And soaking the PVDF membrane in a developing solution, and observing a target protein band through a chemiluminescence imaging system. The results are shown in FIGS. 9 and 10.
As is clear from FIGS. 9 and 10, the expression of the Collagen I protein was significantly reduced in the TGF-. beta.1 group cells as compared with the control group (P <0.05), and in the Dankasterone A5, 10, and 20. mu.M group cells as compared with the TGF-. beta.1 group (P < 0.01).
Therefore, the Dankasterone A can obviously inhibit the proliferation of the hepatic stellate cell LX-2, reduce the protein expression of a main hepatic fibrosis marker in the hepatic stellate cell LX-2, inhibit the migration capacity of the hepatic stellate cell LX-2 and induce the apoptosis of the hepatic stellate cell LX-2, has the function of inhibiting or reversing the hepatic fibrosis, and has good application prospect in the aspect of preparing medicaments for treating the hepatic fibrosis.
In conclusion, the invention provides the application of Dankasterone A in preparing the medicament for treating hepatic fibrosis for the first time. The novel application of Dankasterone A in preparing the medicament for treating hepatic fibrosis has great significance for breaking through the bottleneck of hepatic fibrosis treatment.
It will be evident to those skilled in the art that the invention is not limited to the details of the foregoing illustrative embodiments, and that the present invention may be embodied in other specific forms without departing from the spirit or essential attributes thereof. The present embodiments are therefore to be considered in all respects as illustrative and not restrictive, the scope of the invention being indicated by the appended claims rather than by the foregoing description, and all changes which come within the meaning and range of equivalency of the claims are therefore intended to be embraced therein.
Claims (10)
- The application of Dankasterone A in preparing a medicament for treating hepatic fibrosis is characterized in that: the medicine for treating hepatic fibrosis is prepared by taking Dankasterone A as an active ingredient and other medicine excipients or carriers.
- 2. The use of Dankasterone a in the preparation of a medicament for treating liver fibrosis according to claim 1, wherein: the concentration of Dankasterone A in the medicine for treating hepatic fibrosis is 5-20 mu M.
- 3. The use of Dankasterone a in the preparation of a medicament for treating liver fibrosis according to claim 1, wherein: the Dankasterone A is directly extracted from natural products or is prepared by chemical combination synthesis, and has the chemical name of (4aR,4bR,6aR,7R,10aR) -3,4,4a,4b,5,6,6a,7,8,9-Decahydro-4a,6a-dimethyl-7- [ (1R,2E,4R) -1,4,5-trimethyl-2-hexenyl]indeno[1,7a-a]naphthalene-2,10,12(11H) -trione; molecular formula C 28 H 40 O 3 (ii) a The molecular weight is 424.62.
- 4. The use of Dankasterone a in the preparation of a medicament for treating liver fibrosis according to claim 1, wherein: the structural formula of the Dankasterone A is a steroid component, and the structural formula is as follows:
- 5. the use of Dankasterone a in the preparation of a medicament for treating liver fibrosis according to claim 1, wherein: the medicament for treating hepatic fibrosis is an inhibitor of proliferation or survival of hepatic stellate cells.
- 6. The use of Dankasterone a in the preparation of a medicament for treating liver fibrosis according to claim 1, wherein: the medicine for treating hepatic fibrosis is an inhibitor of hepatic fibrosis marker protein expression in hepatic stellate cells, and achieves the effect of resisting hepatic fibrosis by inhibiting survival, proliferation and apoptosis of the hepatic stellate cells and hepatic fibrosis marker protein expression.
- 7. The use of Dankasterone a in the preparation of a medicament for treating liver fibrosis according to claim 1, wherein: the medicine for treating hepatic fibrosis can promote the apoptosis of hepatic stellate cells.
- 8. The use of Dankasterone a in the preparation of a medicament for treating liver fibrosis according to claim 1, wherein: the dosage form of the medicine for treating hepatic fibrosis is oral preparation or injection.
- 9. The use of Dankasterone a in the preparation of a medicament for treating liver fibrosis according to claim 8, wherein: the oral preparation is any one of granules, capsules, tablets, powder, dripping pills and sustained release preparations.
- 10. The use of Dankasterone a in the preparation of a medicament for treating liver fibrosis according to claim 1, wherein: the medicament for treating hepatic fibrosis is a medicament for inhibiting or reversing hepatic fibrosis.
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