CN115645416A - Application of Calvasterol A in preparation of medicine for treating hepatic fibrosis - Google Patents
Application of Calvasterol A in preparation of medicine for treating hepatic fibrosis Download PDFInfo
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Abstract
The invention discloses application of Calvasterola in preparation of a medicament for treating hepatic fibrosis, and has great significance for breaking through the bottleneck of hepatic fibrosis treatment. The invention provides the application of Calvasterol A in preparing a medicament for treating hepatic fibrosis for the first time. By using human hepatic stellate cells LX-2 as model cells, calvasterolA is found to be capable of effectively reducing the survival rate of the hepatic stellate cells LX-2, inhibiting the proliferation of the hepatic stellate cells LX-2, reducing the contents of collagen type I (COL 1A 1), smooth muscle actin (alpha-SMA) and Laminin (LN)) which are main markers in the activated hepatic stellate cells LX-2, and remarkably reducing the abnormal rise of aspartate Aminotransferase (AST) and alanine Aminotransferase (ALT) caused by the activation of TGF-beta 1, and has dose dependence.
Description
Technical Field
The invention belongs to the technical field of medicines, and particularly relates to application of Calvasterol A in preparation of a medicine for treating hepatic fibrosis.
Background
Chronic liver disease is one of the major public health concerns worldwide. It is reported that more than 8 million people are affected worldwide each year, and about 200 million people die from liver diseases. China is a big country with liver diseases, and about 1/5 of the population suffers from liver related diseases. Research has shown that liver fibrosis is the common pathological basis for many chronic liver diseases. Therefore, the research on anti-hepatic fibrosis drugs is one of the important ways to treat chronic liver diseases.
Hepatic fibrosis refers to a process in which hepatic cells are changed in inflammation and necrosis due to various factors such as virus, alcohol, obesity, metabolic disorders, autoimmunity, drug toxicity, etc., resulting in an imbalance in the synthesis and degradation of extracellular matrix (ECM) by hepatic tissues. Hepatic Stellate Cells (HSCs) are resident nonparenchymal cells located in the space under the endothelium of the diseases, are main sources of liver ECM, are cytological foundations of hepatic fibrosis formation, are in central positions in the processes of ECM metabolism and production of various cytokines, and play a key role in the process of hepatic fibrosis development. When the liver cells are damaged, hepatic Stellate Cells (HSCs) are activated from resting cells, are differentiated into activated cells, secrete various cytokines, and further act on the HSCs to activate, proliferate and migrate the HSCs; 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 liver fibrosis to liver cirrhosis is caused. Therefore, inhibiting HSC proliferation, activation, migration or promoting HSC apoptosis is an important strategy for slowing and reversing HF, and has become an important target for the research of anti-hepatic fibrosis drugs.
The anti-hepatic fibrosis medicine developed aiming at the occurrence and development mechanism of hepatic fibrosis can obviously improve and even reverse hepatic fibrosis, and brings hope to patients with hepatic diseases. No relevant research literature discloses the application of Calvasterol A in preparing medicaments for treating hepatic fibrosis.
Disclosure of Invention
Aiming at the problems in the existing hepatic fibrosis treatment, the invention provides the application of Calvasterol A as a medicine for treating hepatic fibrosis.
In order to achieve the above purpose, the invention adopts the following technical scheme:
application of Calvasterol A in preparing medicine for treating hepatic fibrosis is provided.
Furthermore, the medicine for treating hepatic fibrosis is prepared by taking Calvasterol A as an active ingredient and other medicine excipients or carriers.
Furthermore, the Calvasterol A has a structural formula of steroid component and a molecular formula of C 28 H 38 O 3 The molecular weight is 422.60, and the chemical name is (22E) -14-hydroxyyergosta-4, 7,9 (11), 22-tetraene-3,6-dione.
Further, the Calvasterol A has the following structural formula:
further, the medicament for treating the hepatic fibrosis is an inhibitor of hepatic stellate cell proliferation.
Further, the medicament for treating the hepatic fibrosis is an inhibitor of hepatic stellate cell activation.
Furthermore, the medicine for treating hepatic fibrosis is an inhibitor of hepatic fibrosis markers in hepatic stellate cells.
Further, the Calvasterol a is directly extracted from a natural product or prepared by chemical synthesis.
Further, the concentration of the Calvasterol A in the medicine for treating hepatic fibrosis is 5-20 mu M.
Further, the concentration of the Calvasterol A in the medicine for treating hepatic fibrosis is 10-20 mu M.
Further, the concentration of Calvasterol a in the drug for treating hepatic fibrosis is 20 μ M.
Furthermore, the dosage forms of the medicine for treating hepatic fibrosis are oral preparations and injection preparations.
Further, the oral preparation is any one or more of tablets, granules, powder, capsules, sustained-release agents and dropping pills.
The principle of the invention is as follows: LX-2 cells are activated to be further activated through TGF-beta 1 intervention, and the LX-2 cells are acted by different concentrations of Calvasterol A, namely high (20 mu M), medium (10 mu M) and low (5 mu M). Finally, calvasterol A is found to be capable of inhibiting the proliferation of hepatic stellate cell LX-2, reducing COL1A1 synthesis, alpha-SMA and LN deposition in hepatic stellate cell LX-2 and remarkably reducing AST and ALT abnormal rise caused by TGF-beta 1 activation. Therefore, the Calvasterol A has good application prospect in the aspect of preparing the medicine for treating hepatic fibrosis.
Due to the adoption of the technical scheme, the invention has the following beneficial effects:
the invention firstly provides the application of Calvasterol A in preparing the medicine for treating hepatic fibrosis. By using human hepatic stellate cells LX-2 as model cells, calvasterol A is found to be capable of effectively reducing the survival rate of the hepatic stellate cells LX-2, inhibiting the proliferation of the hepatic stellate cells LX-2, reducing the contents of collagen type I (COL 1A 1), smooth muscle actin (alpha-SMA) and Laminin (LN)) which are main markers in the activated hepatic stellate cells LX-2, and remarkably reducing the abnormal rise of aspartate Aminotransferase (AST) and alanine Aminotransferase (ALT) caused by the activation of TGF-beta 1, and has dose dependence. The new application of Calvasterol A in preparing medicine for treating hepatic fibrosis provided by the invention has great significance in breaking 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 bar graph showing the effect of Calvasterol A in different concentrations on LX-2 cell proliferation activity measured by MTT method in example 1 of the present application;
FIG. 2 is a bar graph showing the effect of the kit of example 2 of the present application in detecting the AST content in LX-2 cells by different concentrations of Calvasterol A;
FIG. 3 is a bar graph of the effect of the kit of example 2 of the present application on ALT content in LX-2 cells measured by different concentrations of Calvasterol A;
FIG. 4 is a bar graph of the effect of the ELISA kit in example 3 of the present application for detecting the content of Calvasterol A on the content of LX-2 cell alpha-SMA;
FIG. 5 is a bar graph showing the effect of ELISA kit to detect the content of COL1A1 in LX-2 cells of Calvasterol A with different concentrations in example 4 of the present application;
FIG. 6 is a bar graph showing the effect of ELISA kit to detect the influence of different concentrations of Calvasterol A on LN content of LX-2 cells in example 5 of the present application.
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 invention claimed in the claims.
Example 1
Preparation of Calvasterol A
Talaromyces amestolkiae is inoculated into a rice solid culture medium and is statically fermented for 28 days in a constant temperature incubator at 28 ℃. The fermentate was leached with ethyl acetate at room temperature for 2 days, filtered and the filtrate was concentrated under reduced pressure to give the total metabolite of t.amestolkiae, which was eluted by silica gel column chromatography with a gradient of the petroleum ether-acetone (10 → 1 → 0, v) system to give 4 fractions (fr.a, fr.b, fr.c, fr.d), wherein fr.a was further eluted by silica gel column chromatography with a dichloromethane-ethyl acetate (10, v) system to give calvasterol a.
MTT method for detecting influence of Calvasterol A on proliferation of hepatic stellate cells
Using high-sugar medium DMEM containing 10% fetal bovine serum and 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 the cell density was adjusted to 5X 10 using medium 4 And (4) inoculating into a 96-well plate, and dividing the cells into a normal group, a TGF-beta 1 (10 ng/mL) group, a low-dose Calvasterol A (5 mu M) group, a medium-dose Calvasterol A (10 mu M) group and a high-dose Calvasterol A (20 mu M) group. 6 duplicate wells per set, 100. Mu.L of cell suspension per well, blank zeroing wells, 200. Mu.L sterile PBS added around the cell wells, 5% CO at 37 ℃% 2 Culturing for 24h under saturated humidity, adding 20 μ LMTT into each well, culturing for 3h under the same culture condition, sucking out the culture medium, adding 100 μ LDMSO, shaking for 10min, measuring absorbance (A) at 490nm of each well with enzyme-labeling instrument, and calculating cell proliferation rate.
Cell proliferation rate = (experimental group-a zeroing group)/(control group a-a zeroing group) × 100%. The results of the experiment are shown in FIG. 1. As can be seen from FIG. 1, calvasterol A significantly reduced the survival rate of LX-2 cells and was concentration-dependent.
Example 2
Kit for detecting influence of Calvasterol A on AST and ALT contents in LX-2 cells
Using a high sugar medium DMEM containing 10% fetal bovine serum and 100kU/L penicillin and 100mg/L streptomycin at 37 ℃ 5% 2 Culturing LX-2 cells in an incubator, counting by an LX-2 cell counting plate, and then counting according to 5X 10 5 The individual cells/well were seeded in 6-well plates, incubated at 37 ℃ and 5% CO 2 Constant temperature of (2)Carrying out adherent culture for 24h in an incubator, and then respectively carrying out corresponding intervention treatment on each group of cells according to experimental grouping:
normal group: media (blank);
TGF-. Beta.1 group: TGF-. Beta.1 (10 ng/mL);
calvasterol a high dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (20. Mu.M);
calvasterol a medium dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (10. Mu.M);
calvasterol a low dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (5. Mu.M);
intervening and culturing all groups for 24h at the same time, collecting culture medium supernatant of each group, centrifuging at room temperature at 1000rpm for 10min, carefully sucking the centrifuged culture medium supernatant, subpackaging, and storing at-80 ℃. During detection, each experimental sample is processed strictly according to AST and ALT kit instructions. The experimental results are shown in fig. 2 and table 1.
TABLE 1 influence of Calvasterol A on AST and ALT contents in LX-2 cells: (
n＝3)
| Group of | AST(U/T) | ALT(U/T) |
| Normal group | 2.553±0.506 | 3.978±0.533 |
| TGF- |
6.224±0.414*** | 9.450±1.903** |
| Calvasterola high dose group | 0.178±0.575 ### | 1.770±0.480 ### |
| Calvasterola medium dose group | 0.879±0.969 ### | 2.151±0.238 ### |
| Calvasterola low dose group | 3.715±0.919 ## | 6.147±1.026 ## |
Note: p <0.001, P <0.01, compared to normal group; compared with the TGF-beta 1 group, # # # P <0.001, # # P <0.01.
As shown in FIG. 2 and the experimental results in Table 1, compared with the normal group, the ALT and AST content in the supernatant of the TGF-beta 1 activated LX-2 cell culture medium is remarkably increased (P < 0.001), while the abnormal elevation of ALT and AST caused by TGF-beta 1 stimulation is remarkably relieved and is concentration-dependent after the drug containing Calvasterol A is dried (P <0.001, P < 0.05).
Example 3
ELISA kit for detecting influence of Calvasterol A on alpha-SMA content in LX-2 cell
Using high-sugar medium DMEM containing 10% fetal bovine serum and 100kU/L penicillin and 100mg/L streptomycin at 37 ℃ with 5% CO 2 Culturing LX-2 cells in an incubator, counting by an LX-2 cell counting plate, and then counting according to 5X 10 5 The individual cells/well were seeded in 6-well plates, incubated at 37 ℃ and 5% CO 2 After the cells are cultured for 24 hours in an adherence manner in the constant temperature incubator, the cells of each group are respectively treated correspondingly according to experimental groups:
normal group: media (blank);
TGF-. Beta.1 group: TGF-. Beta.1 (10 ng/mL);
calvasterol a high dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (20. Mu.M);
calvasterol a medium dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (10. Mu.M);
calvasterol a low dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (5. Mu.M);
and then intervening and culturing, wherein after intervening and culturing for 24h, each group of culture medium supernatant is collected, centrifuging is carried out for 10min at the room temperature at 1000rpm, the centrifuged culture medium supernatant is carefully absorbed, and split charging and storing at-80 ℃. During detection, each experimental sample is processed strictly according to the ELISA kit instruction. The results are shown in fig. 4 and table 2.
As can be seen from the detection results of FIG. 4 and Table 2, the stimulation of TGF-beta 1 obviously increases the content of alpha-SMA (P < 0.001); after Calvasterol A intervention, the abnormal increase of cellular alpha-SMA content caused by TGF-beta 1 stimulation (P <0.001; P < -0.05) is obviously reduced by high dose and medium dose, and is in concentration dependence.
TABLE 2 Effect of Calvasterol A on the content of alpha-SMA in LX-2 cells: (
n＝3)
| Group of | α-SMA(pg/mg) |
| Normal group | 3.166±0.019 |
| TGF- |
12.820±0.354*** |
| Calvasterol A high dose group | 6.379±0.187 ### |
| Calvasterol A Medium dose group | 10.068±0.211 ## |
| Calvasterol a low dose group | 12.609±0.368 |
Note: p <0.001 compared to normal group; compared with TGF-beta 1 group, # # # P <0.001, # # P <0.01.
Example 4
ELISA kit for detecting influence of Calvasterol A on COL1A1 content in LX-2 cells
Using a high sugar medium DMEM containing 10% fetal bovine serum and 100kU/L penicillin and 100mg/L streptomycin at 37 ℃ 5% 2 Culturing LX-2 cells in an incubator, counting by an LX-2 cell counting plate, and then counting according to 5X 10 5 The individual cells/well were seeded in 6-well plates, incubated at 37 ℃ and 5% CO 2 After the cells are cultured for 24 hours in an adherence manner in the constant temperature incubator, the cells of each group are respectively treated correspondingly according to experimental groups:
normal group: media (blank);
TGF-. Beta.1 group: TGF-. Beta.1 (10 ng/mL);
calvasterol a high dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (20. Mu.M);
calvasterol a medium dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (10. Mu.M);
calvasterol a low dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (5. Mu.M);
and then intervening and culturing, wherein after intervening and culturing for 24h, the culture medium supernatant of each group is collected, the culture medium supernatant is centrifuged at 1000rpm for 10min at room temperature, the centrifuged culture medium supernatant is carefully sucked, and the culture medium supernatant is stored at minus 80 ℃ after being subpackaged. During detection, each experimental sample is processed strictly according to the ELISA kit instruction. The results are shown in fig. 5 and table 3.
TABLE 3 Effect of Calvasterol A on COL1A1 content in LX-2 cells: (
n＝3)
| Group of | Cola1(pg/mg) |
| Normal group | 13.462±0.207 |
| TGF- |
17.982±0.681*** |
| Calvasterol A high dose group | 7.409±2.237 ### |
| Calvasterol A Medium dose group | 9.486±2.109 ### |
| Calvasterol a low dose group | 11.132±4.460 ## |
Note: p <0.001 compared to normal group; compared with the TGF-beta 1 group, # # # P <0.001, # # P <0.01.
As can be seen from the detection results of FIG. 5 and Table 3, the content of Cola1 is remarkably increased by TGF-beta 1 stimulation (P < 0.001); after Calvasterol A drying, the abnormal increase of cellular Cola1-1 content (P <0.001; P < -0.01) caused by TGF-beta 1 stimulation is remarkably reduced in high dose, medium dose and concentration dependence (P < 0.001).
Example 5
ELISA kit for detecting influence of Calvasterol A on LN content in LX-2 cell
Using high-sugar medium DMEM containing 10% fetal bovine serum and 100kU/L penicillin and 100mg/L streptomycin at 37 ℃ with 5% CO 2 Culturing LX-2 cells in an incubator, counting by an LX-2 cell counting plate, and then counting according to 5X 10 5 The individual cells/well were seeded in 6-well plates, incubated at 37 ℃ and 5% CO 2 After the cells are cultured for 24 hours in an adherence manner in the constant temperature incubator, the cells of each group are respectively treated correspondingly according to experimental groups:
normal group: media (blank);
TGF-. Beta.1 group: TGF-. Beta.1 (10 ng/mL);
calvasterol a high dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (20. Mu.M);
calvasterol a medium dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (10. Mu.M);
calvasterol a low dose group: TGF-. Beta.1 (10 ng/mL) + Calvasterol A (5. Mu.M);
and then intervening and culturing, wherein after intervening and culturing for 24h, the culture medium supernatant of each group is collected, the culture medium supernatant is centrifuged at 1000rpm for 10min at room temperature, the centrifuged culture medium supernatant is carefully sucked, and the culture medium supernatant is stored at minus 80 ℃ after being subpackaged. During detection, each experimental sample is processed strictly according to the ELISA kit instruction. The results are shown in fig. 6 and table 4.
TABLE 4 Effect of Calvasterol A on LN content in LX-2 cells: (
n＝3)
| Group of | LN(pg/mg) |
| Normal group | 12.498±0.439 |
| TGF- |
19.224±0.436** |
| Calvasterol a high dose group | 10.658±0.881 ### |
| Calvasterol A medium dose group | 12.040±1.127 ## |
| Calvasterol a low dose group | 16.190±3.674 # |
Note: p <0.01 compared to normal group; compared with TGF-beta 1 group, # # # P <0.001, # # P <0.01, # P <0.05.
As can be seen from the results of the tests in FIG. 6 and Table 4, the stimulation of TGF-beta 1 significantly increases the LN content (P < 0.01); after Calvasterol A drying, the abnormal increase in cellular LN content (P <0.001, P-bundle-0.01, P-bundle-0.05) both at high dose, at medium dose and at significantly reduced TGF-. Beta.1 stimulation was concentration-dependent.
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 Calvasterol A in preparing the medicine for treating hepatic fibrosis is characterized in that: the medicine for treating hepatic fibrosis is prepared by using CalvasterolA as an active ingredient and other medicine excipients or carriers.
- 2. The use of CalvasterolA according to claim 1 for the preparation of a medicament for the treatment of liver fibrosis, wherein: the structural formula of the Calvasterol A is steroid component, and the molecular formula is C 28 H 38 O 3 Molecular weight 422.60, chemical name (22E) -14-hydroxyyergosa-4, 7,9 (11), 22-tetraene-3,6-dione; the structural formula of the Calvasterol A is as follows:
- 3. the use of CalvasterolA according to claim 1 in the preparation of a medicament for treating liver fibrosis, wherein: the medicine for treating hepatic fibrosis is an inhibitor of hepatic stellate cell proliferation.
- 4. The use of CalvasterolA according to claim 1 in the preparation of a medicament for treating liver fibrosis, wherein: the medicine for treating hepatic fibrosis is an inhibitor for activating hepatic stellate cells.
- 5. The use of CalvasterolA according to claim 1 in the preparation of a medicament for treating liver fibrosis, wherein: the medicine for treating hepatic fibrosis is an inhibitor of hepatic fibrosis markers in hepatic stellate cells.
- 6. The use of CalvasterolA according to claim 1 for the preparation of a medicament for the treatment of liver fibrosis, wherein: the Calvasterola is directly extracted from natural products or prepared by chemical synthesis.
- 7. The use of CalvasterolA according to claim 1 for the preparation of a medicament for the treatment of liver fibrosis, wherein: the concentration of the Calvasterola in the medicine for treating hepatic fibrosis is 5-20 mu M.
- 8. The use of CalvasterolA according to claim 1 in the preparation of a medicament for treating liver fibrosis, wherein: the concentration of the Calvasterola in the medicine for treating hepatic fibrosis is 10-20 mu M.
- 9. The use of CalvasterolA according to claim 1 for the preparation of a medicament for the treatment of liver fibrosis, wherein: the concentration of the Calvasterola in the medicine for treating hepatic fibrosis is 20 mu M.
- 10. The use of CalvasterolA according to claim 1 for the preparation of a medicament for the treatment of liver fibrosis, wherein: the dosage forms of the medicine for treating hepatic fibrosis are oral preparations and injection preparations; the oral preparation is one or more of tablet, granule, powder, capsule, sustained release agent and dripping pill.
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Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US20050191385A1 (en) * | 2004-10-25 | 2005-09-01 | Amato Daniel K. | Natural product derivatives as food supplements and pharmaceuticals |
| US20140128357A1 (en) * | 2010-12-13 | 2014-05-08 | Rutgers University | Methods of producing and using brassinosteroids to promote growth, repair and maintenance of skeletal muscle and skin |
| CN107343890A (en) * | 2016-05-06 | 2017-11-14 | 北京大学 | The application of Antrodia camphorata and monomer lanostane 32 in NASH is prevented and treated |
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Patent Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US20050191385A1 (en) * | 2004-10-25 | 2005-09-01 | Amato Daniel K. | Natural product derivatives as food supplements and pharmaceuticals |
| US20140128357A1 (en) * | 2010-12-13 | 2014-05-08 | Rutgers University | Methods of producing and using brassinosteroids to promote growth, repair and maintenance of skeletal muscle and skin |
| CN107343890A (en) * | 2016-05-06 | 2017-11-14 | 北京大学 | The application of Antrodia camphorata and monomer lanostane 32 in NASH is prevented and treated |
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| Title |
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| NOBUO KAWAHARA ET AL.，: "TWO STEROIDS FROM CALVATIA C YATHIFORMIS", 《PHYTOCHEMISTRY》, vol. 38, no. 4, pages 947 - 950 * |
| SHAO-HUA WU ET AL.，: "Two New Steroids from an Endophytic Fungus Phomopsis sp", 《CHEMISTRY & BIODIVERSITY》, vol. 10, pages 1276 - 1283, XP072352336, DOI: 10.1002/cbdv.201200415 * |
| 韩雪花等: "白及内生菌Penicillium oxalicum的化学成分", 《应用与环境生物学报》, vol. 25, no. 2, pages 438 - 444 * |
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