Application of hypericin in preparation of medicine for treating liver cancer

Abstract

The invention relates to the field of biological medicines, in particular to application of hypericin to preparation of a medicine for treating liver cancer. The invention provides application of hypericin in preparation of a medicine for treating liver cancer and a pharmaceutical composition containing the hypericin. The inventor finds that hypericin is used as a traditional Chinese medicine compound, in-vitro experiments prove that hypericin can inhibit liver cancer cell proliferation, inhibit liver cancer cell migration and induce liver cancer cell apoptosis, in-vivo experiments prove that hypericin can significantly inhibit liver tumor cell growth in mice, and it is indicated that hypericin can treat liver cancer. The traditional Chinese medicine composition can be used as a component in medicines for treating liver cancer.

Description

Technical Field

[0001] The invention relates to the field of biomedicine, and in particular to use of hypericin in preparing a medicine for treating liver cancer. Background Art

[0002] Mycoporphyrin is an extract of Hypericum perforatum, which belongs to the dianthrone class of compounds and is the most biologically active substance in Hypericum perforatum. Its chemical formula is C 30 H 16 O8. It is a grayish yellow to brown liquid powder with a slightly bitter taste. It is almost insoluble in water and emits a special fragrance. It has the effect of inhibiting the central nervous system and calming the nerves. It can enhance immunity when added to health products. Hypericin also has a strong antiviral effect and can directly act on viruses such as swine fever and foot-and-mouth disease. It also has a good killing effect on highly pathogenic avian influenza viruses. As a traditional Chinese medicine extract, the medicinal use of hypericin needs to be further developed.

[0003] Existing technologies for treating liver cancer: Surgery, chemotherapy, immunotherapy, interventional therapy, radiotherapy and other treatment methods have been applied to the clinical treatment of hepatocellular carcinoma, but the prognosis of hepatocellular carcinoma patients is still poor. For example, only patients with early hepatocellular carcinoma are eligible for liver resection or liver transplantation. While radiotherapy acts on the tumor, it also damages normal skin tissue, cells and normal tissue around the tumor, causing them to be destroyed by radiation. Therefore, there is an urgent need to find an effective drug to improve the survival rate of liver cancer patients. Summary of the invention

[0004] The present invention aims to solve one of the technical problems in the related art to at least a certain extent. To this end, one object of the present invention is to provide the use of hypericin in the preparation of a drug for treating liver cancer and a pharmaceutical composition containing hypericin. The inventors found that hypericin, as a traditional Chinese medicine compound, can inhibit the proliferation of liver cancer cells, inhibit the migration of liver cancer cells, and induce apoptosis of liver cancer cells in vitro experiments, and can significantly inhibit the growth of liver tumor cells in mice in vivo experiments, indicating that hypericin can treat liver cancer and can be used as a component in a drug for treating liver cancer.

[0005] To this end, the first aspect of the present invention provides the use of hypericin in preparing a medicament for treating liver cancer.

[0006] The inventors have found a traditional Chinese medicine compound that can treat hepatocellular carcinoma, namely hypericin, which can significantly inhibit liver cancer. At the same time, the inventors have explored the mechanism of this traditional Chinese medicine compound in treating liver cancer, bringing new ideas to the treatment of liver cancer.

[0007] According to an embodiment of the present invention, the drug induces hepatocellular carcinoma death by inhibiting the PI3K / Akt signaling pathway.

[0008] The inventors found that drugs containing hypericin can treat liver cancer by inhibiting the PI3K / Akt signaling pathway.

[0009] The second aspect of the present invention provides a drug for treating liver cancer. According to an embodiment of the present invention, the drug includes hypericin.

[0010] Existing treatments for liver cancer have poor prognostic effects. The pharmaceutical composition containing hypericin provided by the present invention has a good therapeutic effect on liver cancer, can effectively reduce tumors, and inhibit the proliferation of liver tumor cells.

[0011] According to an embodiment of the present invention, the hypericin is the active ingredient of the medicine.

[0012] According to an embodiment of the present invention, the mass percentage of the hypericin in the medicine is 0.05-99%.

[0013] According to an embodiment of the present invention, the mass percentage of the hypericin in the medicine is 0.1-70%.

[0014] The third aspect of the present invention provides the use of hypericin in preparing a PI3K / Akt signaling pathway inhibitor.

[0015] Hypericin significantly delays the growth of liver cancer cells by inducing cell apoptosis, and hypericin can also inhibit the PI3K / Akt signaling pathway, so it can be used as a PI3K / Akt signaling pathway inhibitor.

[0016] A fourth aspect of the present invention provides a PI3K / Akt signaling pathway inhibitor. According to an embodiment of the present invention, the PI3K / Akt signaling pathway inhibitor includes hypericin.

[0017] The fifth aspect of the present invention provides the use of hypericin in preparing an agent or a drug for inhibiting the proliferation of liver cancer cells, inhibiting the migration of liver cancer cells, or inducing apoptosis of liver cancer cells.

[0018] The inventors found that hypericin can inhibit the proliferation of liver cancer cells, inhibit the migration of liver cancer cells and induce apoptosis of liver cancer cells, and can significantly reduce the expression level of anti-apoptotic genes, including BCL-XL, XIAP, etc.

[0019] According to an embodiment of the present invention, the concentration of hypericin in the reagent or drug is 0.5-5 μM.

[0020] According to an embodiment of the present invention, the liver cancer cells are selected from at least one of Huh7 cells and HepG2 cells.

[0021] The sixth aspect of the present invention provides an agent or drug for inhibiting the proliferation of liver cancer cells, inhibiting the migration of liver cancer cells, or inducing apoptosis of liver cancer cells. According to an embodiment of the present invention, the agent or drug includes hypericin.

[0022] According to an embodiment of the present invention, the concentration of hypericin in the reagent or drug is 0.5-5 μM.

[0023] According to an embodiment of the present invention, the liver cancer cells are selected from at least one of Huh7 cells and HepG2 cells.

[0024] Additional aspects and advantages of the present invention will be given in part in the following description and in part will be obvious from the following description, or will be learned through practice of the present invention. BRIEF DESCRIPTION OF THE DRAWINGS

[0025] The above and / or additional aspects and advantages of the present invention will become apparent and easily understood from the description of the embodiments in conjunction with the following drawings, in which:

[0026] Figure 1 The effect of hypericin on hepatocellular carcinoma in vitro is shown, wherein A is the result of the effect of different concentrations of hypericin on Huh7 cell toxicity, B is the result of the effect of different concentrations of hypericin on HepG2 cell toxicity, C is the result of the effect of different concentrations of hypericin on HepG2.215 cell toxicity, D is the result of the effect of different concentrations of hypericin on Hepa1-6 cell toxicity, E is the result of the effect of different action time of hypericin on Huh7 cell toxicity, F is the result of different action time of hypericin on HepG2 cell toxicity;

[0027] Figure 2 The effect of different concentrations of hypericin on the proliferation of liver cancer cells is shown, wherein A is the crystal violet staining result of different concentrations of hypericin on Huh7 and HepG2 cells, B is the statistical result of different concentrations of hypericin on crystal violet staining of HepG2 cells, and C is the statistical result of different concentrations of hypericin on crystal violet staining of Huh7 cells;

[0028] Figure 3 The effect of different concentrations of hypericin on the migration of liver cancer cells is shown, wherein A is the effect of different concentrations of hypericin on the migration of Huh7 and HepG2 cells, B is the statistical result of the effect of different concentrations of hypericin on the migration of HepG2 cells, and C is the statistical result of the effect of different concentrations of hypericin on the migration of Huh7 cells;

[0029] Figure 4The results of the effects of different concentrations of hypericin on apoptosis of liver cancer cells are shown, wherein A is the results of the effects of different concentrations of hypericin on apoptosis of HepG2 cells detected by flow cytometry, B is the statistical results of the apoptosis ratio of HepG2 cells detected by different concentrations of hypericin, C is the statistical results of the migration results of Huh7 cells detected by flow cytometry, D is the statistical results of the apoptosis ratio of Huh7 cells detected by different concentrations of hypericin, E is the statistical results of the migration results of Hepa1-6 cells detected by flow cytometry, and F is the statistical results of the apoptosis ratio of Hepa1-6 cells detected by different concentrations of hypericin;

[0030] Figure 5 The results of Western blot detection of the effects of different concentrations of hypericin on the expression of related apoptosis proteins in HepG2 cells are shown;

[0031] Figure 6 The results of the effects of different concentrations of hypericin on the expression of PI3K / Akt signaling pathway proteins in liver cancer cells are shown, wherein A is Western blot detection of different concentrations of hypericin on the expression of PI3K / Akt signaling pathway proteins in Huh7 cells, B is Western blot detection of different concentrations of hypericin on the expression of PI3K / Akt signaling pathway proteins in HepG2 cells; C is Western blot detection of different concentrations of hypericin on the expression of PI3K / Akt signaling pathway proteins in Hepa1-6 cells;

[0032] Figure 7 The results of the effect of hypericin on subcutaneous liver cancer cells in mice in vivo, wherein A is the subcutaneous liver cancer tissue of mice in the treatment group and the control group, B is the weight bar graph of the subcutaneous liver cancer tissue of mice in the treatment group and the control group obtained by weighing the liver cancer tissue of A, C is the tumor growth curve of C57 mice after subcutaneous inoculation of liver cancer cells, and D is the weight change curve of C57 mice after subcutaneous inoculation of liver cancer cells.

[0033] DETAILED DESCRIPTION OF THE EMBODIMENTS The embodiments of the present invention are described in detail below. The embodiments described below are exemplary and are only used to explain the present invention, and should not be construed as limiting the present invention.

[0034] It should be noted that the terms "first" and "second" are used for descriptive purposes only and should not be understood as indicating or implying relative importance or implicitly indicating the number of the indicated technical features. Therefore, the features defined as "first" and "second" may explicitly or implicitly include one or more of the features. Further, in the description of the present invention, unless otherwise specified, the meaning of "plurality" is two or more.

[0035] The endpoints and any values ​​of the ranges disclosed in this article are not limited to the precise ranges or values, and these ranges or values ​​should be understood to include values ​​close to these ranges or values. For numerical ranges, the endpoint values ​​of each range, the endpoint values ​​of each range and the individual point values, and the individual point values ​​can be combined with each other to obtain one or more new numerical ranges, which should be considered as specifically disclosed in this article.

[0036] In order to make the present invention more easily understood, certain technical and scientific terms are specifically defined below. Unless otherwise clearly defined elsewhere in this document, all other technical and scientific terms used herein have the meanings commonly understood by those skilled in the art to which the present invention belongs.

[0037] In this document, the terms “include” or “comprising” are open expressions, that is, including the contents specified in the present invention but not excluding other contents.

[0038] As used herein, the terms "optionally", "optional" or "optionally" generally mean that the subsequently described event or circumstance may but need not occur, and that the description includes instances where the event or circumstance occurs and instances where it does not.

[0039] According to a specific embodiment of the present invention, the present invention provides use of hypericin in preparing a medicament for treating liver cancer.

[0040] Hypericin is a traditional Chinese medicine compound. In vitro experiments have shown that it can inhibit the proliferation of liver cancer cells, inhibit the migration of liver cancer cells, and induce apoptosis of liver cancer cells. In vivo experiments have shown that it can significantly inhibit the growth of liver tumor cells in mice, indicating that hypericin can treat liver cancer and can be used as a component of drugs for the treatment of liver cancer.

[0041] According to a specific embodiment of the present invention, the types of liver cancer include but are not limited to liver cancer associated with abnormal PI3K / Akt signaling pathway, and may also be liver cancer caused by other functional abnormalities. These types of liver cancer are all covered within the protection scope of the present invention.

[0042] It should be noted that, since the inventors have found that hypericin can inhibit the proliferation of liver cancer cells, inhibit the migration of liver cancer cells and induce apoptosis of liver cancer cells, there is no special limitation on the causes of liver cancer. Regardless of the cause, hypericin can act on liver cancer cells.

[0043] According to a specific embodiment of the present invention, the present invention provides a pharmaceutical composition for treating liver cancer, comprising hypericin.

[0044] According to a specific embodiment of the present invention, the hypericin is at least one of the active ingredients in the pharmaceutical composition.

[0045] In the present invention, the pharmaceutical composition may also contain other active ingredients, and such pharmaceutical compositions are all within the scope of protection of the present invention. However, preferably, in the pharmaceutical composition for treating liver cancer provided by the present invention, hypericin is the only active ingredient of the drug.

[0046] It should be noted that, in addition to the active ingredient hypericin, the pharmaceutical composition also includes pharmaceutically acceptable excipients, including one or more of excipients, lubricants, preservatives, diluents, sweeteners, adhesives, colorants, cosolvents and surfactants.

[0047] According to a specific embodiment of the present invention, the mass percentage of the hypericin in the pharmaceutical composition is 0.05-99%.

[0048] According to a preferred embodiment of the present invention, the mass percentage of the hypericin in the pharmaceutical composition is 0.1-70%.

[0049] According to a specific embodiment of the present invention, the present invention provides a PI3K / Akt signaling pathway inhibitor, including hypericin.

[0050] As one of the important intracellular signal transduction pathways, the PI3K-Akt (phosphoinositide 3-kinase / protein kinase B, PI3K / Akt) signaling pathway plays a key role in inhibiting apoptosis and promoting proliferation in cells. The signaling pathway composed of PI3K and its downstream molecule Akt can activate downstream signaling molecules and is closely related to the occurrence and development of breast cancer, gastric cancer, colorectal cancer, ovarian cancer, prostate cancer, etc. With the discovery of PI3K / AKT signaling pathway inhibitors, it can effectively block the apoptosis inhibition effect caused by excessive activation of the pathway, enhance the sensitivity of tumor cells to chemotherapeutic drugs, induce cell apoptosis, and inhibit the growth of tumor cells, which is of great significance for the treatment of cancer.

[0051] The PI3K / Akt signaling pathway inhibitor containing hypericin provided by the present invention can inhibit the proliferation of liver cancer cells, inhibit the migration of liver cancer cells or induce the apoptosis of liver cancer cells, and is of great significance for the treatment of liver cancer.

[0052] According to a specific embodiment of the present invention, the present invention provides an agent or drug for inhibiting the proliferation of liver cancer cells, inhibiting the migration of liver cancer cells, or inducing apoptosis of liver cancer cells, including hypericin.

[0053] According to a specific embodiment of the present invention, the concentration of hypericin in the reagent or drug is 0.5-5 μM. For example, the concentration of hypericin in the reagent or drug is 0.5 μM, 1 μM, 1.5 μM, 2 μM, 2.5 μM, 3 μM, 3.5 μM, 4 μM, 4.5 μM, 5 μM, etc.

[0054] According to a specific embodiment of the present invention, the liver cancer cells are selected from at least one of Huh7 cells and HepG2 cells.

[0055] It should be noted that the present invention only exemplarily demonstrates that hypericin can inhibit the proliferation, migration or induce apoptosis of Huh7 cells or HepG2 cells in the examples. In fact, hypericin also has the ability to inhibit proliferation, migration or induce apoptosis of other types of liver cancer cells. The reagent or drug containing hypericin provided by the present invention can inhibit the proliferation of any type of liver cancer cells, the migration of liver cancer cells or induce apoptosis of liver cancer cells.

[0056] The scheme of the present disclosure will be explained below in conjunction with the examples. Those skilled in the art will appreciate that the following examples are only used to illustrate the present disclosure and should not be considered to limit the scope of the present disclosure. Where specific techniques or conditions are not indicated in the examples, the techniques or conditions described in the literature in this area or the product instructions are used. Where the manufacturers of reagents or instruments are not indicated, they are all conventional products that can be obtained commercially.

[0057] The sources of the reagents and cells used in the following examples are shown in Tables 1-3 below:

[0058] Table 1 Cell information

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[0061] Table 2 Antibody information

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[0063] Table 3 Experimental reagents

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[0066] Example 1 Effect of hypericin on hepatocellular carcinoma in vitro

[0067] 1. CCK-8 method was used to detect the toxicity of hypericin on liver cancer cells (Huh7, HepG2)

[0068] Huh7, HepG2, HepG2.215, and Hepa1-6 cells were seeded into 96-well plates, with 10,000 cells in each well. After culturing overnight, 0, 1, 2.5, 5, 10, 20, 40, 60, 80, and 100 μM hypericin (purchased from Taoshu Biotechnology, catalog number T6S0923) was added to Huh7, HepG2 cells, HepG2.215 cells, and Hepa1-6, respectively. Each concentration was repeated 3 times. After culturing in a 37°C, 5% CO2 incubator for 24 h, 48 h, and 72 h, 100 μL of culture medium containing 10% CCK-8 was added to each well. After incubation in a 37°C, 5% CO2 incubator for 2 h, the cells were tested. Cell inhibition rate = (OD value of the control group - OD value of the drug-treated group) / OD value of the control group × 100%

[0069] Figure 1 The results of A, B, C, and D in Figure 3 show that hypericin significantly inhibited the viability of Huh7, HepG2, HepG2.215, and Hepa1-6 cells after 48 hours of treatment with cells. The IC50 value of Huh7 cells treated with hypericin for 48 hours was 1.923μM, the IC50 value of HepG2 cells treated with hypericin for 48 hours was 1.284μM, the IC50 value of HepG2.215 cells treated with hypericin for 48 hours was 8.122μM, and the IC50 value of Hepa1-6 cells treated with hypericin for 48 hours was 9.106μM.

[0070] Figure 1 The results in E and F show that hypericin significantly inhibited the viability of Huh7 and HepG2 cells after treating the cells for 24h, 48h, and 72h. As the administration time increased, it was found that the cell viability of tumor cells gradually decreased.

[0071] 2. Crystal violet staining was used to detect the antiproliferative effect of different concentrations of hypericin on Huh7 and HepG2 cells

[0072] Huh7 and HepG2 cells were seeded into 6-well plates, with 4000 cells per well. After overnight culture, 0, 1, and 2.5 μM hypericin were added to Huh7 and HepG2 cells, respectively, with 3 replicates for each concentration. The cells were incubated at 37°C and 5% CO. 2 After culturing in an incubator for one week, the cells were stained with crystal violet and photographed under a microscope.

[0073] Figure 2 The AC results in the figure showed that the cloning ability of Huh7 and HepG2 cells was significantly reduced at a concentration of 1 μM and was effectively inhibited at a concentration of 2.5 μM.

[0074] 3. Crystal violet staining was used to detect the anti-migration effect of different concentrations of hypericin on Huh7 and HepG2 cells

[0075] Huh7 and HepG2 cells were digested and centrifuged and then resuspended in serum-free medium. 2 × 10 4 Cells were aspirated into the upper transwell chamber without Matrigel to assess cell migration. 600 μL of DMEM medium containing 10% FBS was added to the lower chamber to stimulate cell migration. After 48 hours of incubation at 37°C in a 5% CO2 incubator, the Transwell chamber was fixed with 4% paraformaldehyde for 30 min and then stained with 1% crystal violet for 15 min. Cells placed on the upper surface of the Transwell membrane were wiped with a cotton swab, and cells moving to the lower surface of the membrane were photographed under a microscope.

[0076] Figure 3 The AC results in the figure showed that the migration ability of Huh7 and HepG2 cells was significantly decreased at a concentration of 1 μM and was effectively inhibited at a concentration of 2.5 μM.

[0077] 4. Flow cytometry detection of the apoptosis-promoting effect of hypericin on liver cancer cells

[0078] Huh7, HepG2 and Hepa1-6 cells were seeded into 12-well plates, with 1.5×10 cells per well. 5 After overnight culture, 0, 1.5, 2.5, and 5 μM hypericin were added to Huh7, HepG2, and Hepa1-6 cells, respectively, with 3 replicates for each concentration. After 48 h of culture in a 37°C, 5% CO2 incubator, the cells were collected and incubated with annexin V and PI for 15 minutes in the dark for each concentration. Annexin V or PI staining alone was used as a control. Flow cytometry was then used to detect the pro-apoptotic effect of hypericin on Huh7, HepG2, and Hepa1-6 cells, and the proportion of apoptotic cells was counted.

[0079] Figure 4 The AF results in the results showed that hypericin induced late apoptosis of Huh7, HepG2 and Hepa1-6 cells, and the apoptosis of Huh7, HepG2 and Hepa1-6 cells induced by hypericin was concentration-dependent.

[0080] Example 2 Hypericin induces apoptosis of liver cancer cells via PI3K / Akt signaling pathway

[0081] 500,000 cells were plated per well. The next day, 0μM, 2μM, and 3μM hypericin were given. After incubation for 48 hours, the cells were centrifuged and washed with PBS. They were lysed on ice for half an hour using RIPA, centrifuged at 12,000 rpm for 15 minutes at four degrees, and the protein concentration was determined using a BCA kit. The samples were placed in a 95° metal bath for 5 minutes and stored at -20°. The samples were loaded onto sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis and then electrotransferred to a PVDF membrane. After blocking with 5% skim milk for 2 hours, the membrane was incubated with the primary antibody at four degrees overnight and washed three times with 1x Tris buffered saline and Tween (TBST), each for 5 minutes. The membrane was then incubated with the corresponding horseradish peroxidase (HRP)-coupled secondary antibody at room temperature for 2 hours. Observed using a chemiluminescent development kit.

[0082] Figure 5 The results showed that compared with the control group, hypericin significantly downregulated the expression of BCL-XL and XIAP, and significantly promoted the expression of c-CASP3. Hypericin induced apoptosis of HepG2 cells in a dose-dependent manner.

[0083] Figure 6 The AC results in the assay showed that compared with the control group, hypericin significantly downregulated the expression of total and phosphorylated proteins of PI3K, AKT and S6 in Huh7, HepG2 and Hepa1-6 cells, and hypericin induced liver cancer cell death by downregulating the PI3K / Akt signaling pathway.

[0084] Example 3 Hypericin inhibits the growth of liver cancer cells in vitro

[0085] Male C57 mice aged 6–8 weeks were maintained under standard conditions and cared for according to institutional animal care guidelines. All animal experiments were approved by the Animal Experimental Ethics Committee of the Hefei Comprehensive National Science Center Institute of Big Health. The study was conducted in accordance with the Declaration of Helsinki. Two million Hepa1-6 cells were injected subcutaneously into the back of mice to establish tumor xenografts. When the tumor xenografts reached 5 mm in diameter, the mice were randomly divided into treatment and control groups. The treatment group was injected intraperitoneally with hypericin (5 mg / kg) every two days, while the control group received only the vehicle (PBS). Body weight and tumor size were measured every two days, and tumor volume was calculated using the following formula: V = (length × width 2 ) / 2.

[0086] Figure 7 The results in A, B, and C show that hypericin can significantly inhibit the growth of subcutaneous tumor cells in mice compared with the PBS group, and Figure D shows that the weight of mice did not decrease during the administration period.

[0087] In the description of this specification, the description with reference to the terms "one embodiment", "some embodiments", "example", "specific example", "some implementation schemes" or "some examples" etc. means that the specific features, structures, materials or characteristics described in conjunction with the embodiment or example are included in at least one embodiment or example of the present invention. In this specification, the schematic representations of the above terms do not necessarily refer to the same embodiment or example. Moreover, the specific features, structures, materials or characteristics described may be combined in any one or more embodiments or examples in a suitable manner. In addition, those skilled in the art may combine and combine the different embodiments or examples described in this specification and the features of the different embodiments or examples, unless they are contradictory.

[0088] Although the embodiments of the present invention have been shown and described above, it is to be understood that the above embodiments are exemplary and are not to be construed as limitations of the present invention. A person skilled in the art may change, modify, replace and vary the above embodiments within the scope of the present invention.

Claims

1. Use of hypericin in the preparation of medicines for treating liver cancer.

2. The use according to claim 1, characterized in that The drug induces hepatocellular carcinoma cell death by inhibiting the PI3K / Akt signaling pathway.

3. A drug for treating liver cancer, characterized in that: Including hypericin.

4. The drug according to claim 3, characterized in that The hypericin is the active ingredient of the medicine; Optionally, the mass percentage of the hypericin in the drug is 0.05-99%, preferably 0.1-70%.

5. Use of hypericin in the preparation of PI3K / Akt signaling pathway inhibitors.

6. A PI3K / Akt signaling pathway inhibitor, characterized in that Including hypericin.

7. Use of hypericin in the preparation of reagents or drugs for inhibiting the proliferation of liver cancer cells, inhibiting the migration of liver cancer cells, or inducing apoptosis of liver cancer cells.

8. The use according to claim 7, characterized in that The concentration of hypericin in the reagent or drug is 0.5-5 μM; Optionally, the liver cancer cells are selected from at least one of Huh7 cells and HepG2 cells.

9. An agent or drug for inhibiting the proliferation of liver cancer cells, inhibiting the migration of liver cancer cells, or inducing apoptosis of liver cancer cells, characterized in that: Including hypericin.

10. The reagent or drug according to claim 9, characterized in that: The concentration of hypericin in the reagent or drug is 0.5-5 μM; Optionally, the liver cancer cells are selected from at least one of Huh7 cells and HepG2 cells.

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