Use of ligustilide H in the preparation of drugs for treating liver cancer.
By developing a drug with ligustrolactone H as the active ingredient, the problem of poor efficacy in existing liver cancer treatments has been solved. This drug effectively inhibits liver cancer cells and reduces side effects, providing a new treatment option for liver cancer.
Patent Information
- Authority / Receiving Office
- CN · China
- Patent Type
- Patents(China)
- Current Assignee / Owner
- Filing Date
- 2024-05-31
- Publication Date
- 2026-03-17
AI Technical Summary
There is a lack of effective drugs for treating hepatocellular carcinoma, especially for patients with advanced liver cancer. Existing treatments such as molecularly targeted drugs and immunotherapy are not very effective and have significant side effects. The application of the traditional Chinese medicine ingredient Ligusticum striatum lactone H in the treatment of liver cancer has not been fully studied.
Using ligustilide H as the active ingredient, drugs in various forms of administration, including tablets, capsules, and injections, were developed. Experiments were conducted to verify its effects on the proliferation, migration, and cell cycle of liver cancer cells. It was found that within a certain concentration range, it can significantly inhibit the proliferation and migration of liver cancer cells and induce cell cycle arrest.
Ligusticum lactone H significantly inhibits the proliferation and migration of liver cancer cells, reduces cell division and proliferation, and provides new possibilities for the treatment of liver cancer. It has low toxicity, is derived from traditional Chinese medicine, is renewable, and reduces side effects.
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Abstract
Description
Technical Field
[0001] This invention relates to the field of pharmaceutical formulation technology, specifically to the use of ligustrazine H in the preparation of drugs for treating liver cancer, especially hepatocellular carcinoma. Background Technology
[0002] According to the latest data released by GLOBOCAN 2020, the number of new cases of primary liver cancer worldwide reached 906,000 annually, of which 72% occurred in Asia, ranking sixth among malignant tumors. Liver cancer caused 830,000 deaths annually, ranking third among malignant tumors. The overall prognosis for liver cancer is particularly poor.
[0003] In primary liver cancer, 85%-90% are diagnosed as hepatocellular carcinoma (HCC), specifically the early stages, namely Barcelona clinic liver cancer (BCLC) stages 0 and A. Surgical resection, local ablation, and liver transplantation can significantly improve patient prognosis, but radical surgery has a relatively narrow scope of application. In actual clinical practice, a considerable number of patients are diagnosed at an intermediate or advanced stage, and patients with advanced HCC have a poor prognosis and high mortality rate.
[0004] However, clinical trials evaluating the efficacy of molecularly targeted drugs sorafenib and lenvatinib in treating advanced liver cancer often yield unsatisfactory results, with poor treatment outcomes or increased side effects. Currently, immunotherapy has brought benefits to patients with advanced liver cancer. According to the IMbrave150 study, the 1-year survival rate was 67.2% in the atezolizumab plus bevacizumab group, compared to 54.6% in the sorafenib group. Although the risk of death for patients with advanced liver cancer has decreased, immunotherapy has not yet changed the predicament of treating advanced liver cancer; apart from clinical data on survival and objective response rates, no breakthrough progress has been achieved. Furthermore, targeted immunotherapy is limited for liver cancer patients with cirrhosis, ascites, liver failure, and systemic symptoms such as weight loss, fatigue, and loss of appetite; therefore, new treatment methods still need to be developed.
[0005] Senkyunolide (SE) is a metabolic component and active substance mainly derived from the traditional Chinese medicinal herbs Angelica sinensis and Ligusticum chuanxiong. Senkyunolide belongs to the phthalide class of compounds, but because its structural core is a bicyclic combination of a γ-lactone ring and a benzene ring, it is also called a lactone compound. Modern pharmacological studies have shown that the pharmacological effects of senkyunolide compounds include anti-inflammatory, antioxidant, anticoagulant, anti-atherosclerotic, and anti-cerebral ischemia-reperfusion injury effects.
[0006] Literature reports that Senkyunolide H (SEH) exerts neuroprotective effects by affecting the expression of apoptosis-related factors Bax and Bcl-2, reducing ROS production, and increasing antioxidant enzyme activity. This neuroprotective effect of SEH has been clinically used to treat Parkinson's syndrome. SEH has a therapeutic effect of inhibiting osteoclast formation in ovariectomized mice by mediating the NF-κB, JNK, and ERK pathways to weaken osteoclast differentiation. SEH's anti-migraine effect is achieved by regulating monoamine neurotransmitters and NO activity in the plasma and brain tissue of migraine rats. Nanoparticles carrying SEH can inhibit autophagy and reduce apoptosis in nerve cells through the PI3K / AKT / mTOR pathway, thereby producing a therapeutic effect on cerebral ischemia. However, there are no published reports on the treatment of hepatocellular carcinoma with SEH in the current technology. The inhibitory effects of SEH on the proliferation and migration of hepatocellular carcinoma cells and its influence on the cell cycle are still unclear. Therefore, further research and expansion are needed to explore the application of SEH in the treatment of hepatocellular carcinoma. Summary of the Invention
[0007] Therefore, the technical problem to be solved by the present invention is to provide the use of ligustilide H in the preparation of drugs for treating liver cancer, especially hepatocellular carcinoma;
[0008] The second technical problem to be solved by the present invention is to provide a drug for treating liver cancer, especially hepatocellular carcinoma, based on ligustrazine lactone H as the active substance.
[0009] To address the aforementioned technical problems, this invention relates to the use of ligustilide H in the preparation of drugs for treating liver cancer.
[0010] Specifically, the liver cancer mentioned includes hepatocellular carcinoma.
[0011] Specifically, the drug includes drugs that target human liver cancer cells HuH-7.
[0012] Specifically, the daily dosage of the ligustrolactone H is 10-15 mg / kg body weight, preferably 13 mg / kg body weight.
[0013] Specifically, the drug includes at least one of oral formulations, injectable formulations, respiratory formulations, or mucosal formulations.
[0014] Specifically, the formulation includes one or more of the following forms: tablets, capsules, granules, aqueous solutions, enteric-coated formulations, injections, emulsions, chewable tablets, gels, syrups, liquid solutions, suspensions, powders, solid crystals, orally disintegrating tablets, or pastes.
[0015] Specifically, the drug also includes pharmaceutically acceptable excipients or carriers.
[0016] The present invention also discloses a pharmaceutical composition, wherein the active ingredient of the composition includes the ligustilide H.
[0017] The present invention also discloses a medicament for treating hepatocellular carcinoma, comprising the ligustilide H or the composition thereof.
[0018] This invention proposes for the first time the role of ligustilide H (SEH) as a potential therapeutic agent for hepatocellular carcinoma, and verifies its potential anti-hepatocellular carcinoma effect based on a series of detailed experimental strategies and procedures, including: using a CCK8 assay to examine the effect of different concentrations of SEH on the proliferation of HuH-7 hepatocellular carcinoma cells; using a Transwell assay to detect the effect of different concentrations of SEH on the migration of HuH-7 hepatocellular carcinoma cells; and using flow cytometry to detect the effect of different concentrations of SEH on the cell cycle of HuH-7 hepatocellular carcinoma cells. The experimental results show that SEH can effectively inhibit the proliferation and migration of hepatocellular carcinoma cells within a certain concentration range and induce cell cycle arrest.
[0019] This invention is the first to propose and verify the potential therapeutic effect of ligustilide H (SEH) on hepatocellular carcinoma. SEH significantly inhibited the proliferation and migration of HuH-7 hepatocellular carcinoma cells, and this inhibitory effect was positively correlated with SEH concentration. Furthermore, SEH could also affect the cell cycle distribution of HuH-7 cells, causing cell arrest in the G2 / M phase, thereby inhibiting cell division and proliferation. This provides a new possibility for hepatocellular carcinoma treatment and plays a significant role in promoting further development and research on the application of SEH in hepatocellular carcinoma therapy.
[0020] The drug for treating liver cancer, especially hepatocellular carcinoma, described in this invention uses SEH as its active ingredient. SEH is a naturally occurring active substance, therefore its toxicity is lower than that of synthetic drugs, which helps reduce the side effects of drug treatment. Furthermore, SEH is a major component derived from traditional Chinese medicine and is renewable; if it can be applied clinically, it may become a new option for liver cancer treatment. Attached Figure Description
[0021] To make the content of this invention easier to understand, the invention will be further described in detail below with reference to specific embodiments and accompanying drawings, wherein...
[0022] Figure 1 The results show the survival rates of HuH-7 cells treated with different concentrations of SEH in Example 1.
[0023] Figure 2 The results of the cell plate cloning experiments in Example 2 are as follows;
[0024] Figure 3 The results of cell migration experiments in each group in Example 3;
[0025] Figure 4 The result is the periodic detection result in Example 4. Detailed Implementation
[0026] Ligustrazine lactone H (SEH) is a naturally occurring active substance, CAS No.: 94596-27-7, molecular formula: C 12 H 16 O4, molecular weight: 224.25, is a slightly yellow oily substance that is soluble in organic solvents such as methanol, ethanol, and DMSO. It is derived from the rhizome of Ligusticum chuanxiong.
[0027]
[0028] Example 1
[0029] This embodiment uses the CCK8 assay to detect the effect of different concentrations of SEH on the proliferation of HuH-7 cells.
[0030] The main reagents and instruments involved in this embodiment are shown in Table 1 below.
[0031] Table 1 Main Reagents and Instruments
[0032]
[0033]
[0034] In this embodiment, the SEH concentration groups include: SEH 0μM, SEH 15μM, SEH 30μM, SEH 45μM, SEH 60μM, SEH 75μM, and SEH 90μM.
[0035] In this embodiment, the specific experimental steps include:
[0036] (1) Huh-7 cells in the logarithmic growth phase were dispersed evenly by pipetting and seeded into 96-well plates at a density of 1×10⁶ cells / well. 4 / well, continue incubation overnight;
[0037] (2) The cells were replaced with complete culture medium containing SEH 0, 15, 30, 45, 60, 75, and 90 μM, and the zero well was set to 100 μL of complete culture medium. The cells were then cultured for 24, 48, and 72 hours.
[0038] (3) Add 10 μl of CCK-8 to each well and incubate at 37°C and 5% CO2 for 1 h;
[0039] (4) OD value is detected by microplate reader at 450nm wavelength.
[0040] In this embodiment, the survival rate of HuH-7 cells treated with different concentrations of SEH is shown in the appendix. Figure 1 (A)-(C).
[0041] Depend on Figure 1 It was found that SEH could inhibit the proliferation of HuH-7 cells, and the inhibitory effect was positively correlated with concentration within a certain range. After 24 hours of treatment with different concentrations of SEH, the inhibitory ability of HuH-7 cells was significantly increased when the SEH concentration was 60 μM or higher compared to the control group (p<0.005). After 48 and 72 hours of treatment with different concentrations of SEH, the inhibitory ability of HuH-7 cells was significantly increased when the SEH concentration was 15 μM or higher compared to the control group. The IC50 of SEH treatment for HuH-7 cells for 48 hours was 140.7 μM. (***P<0.001, **P<0.005).
[0042] Example 2
[0043] This embodiment uses a plate clone experiment to detect the effect of different concentrations of SEH on the clone-forming ability of HuH-7 cells.
[0044] The main reagents and instruments involved in this embodiment are shown in Table 2 below.
[0045] Table 2 Main Reagents and Instruments
[0046] Product Name brand Item number DMEM medium Hyclone SH30022.01 fetal bovine serum Gibco 42F7180K trypsin Genview 89040101100 antibiotic Genview 87020101100 60mm cell culture dish Coring 430166 6-well cell culture plate Coring 3522 Crystal Violet Azure Sky C0121 4% paraformaldehyde Azure Sky P0099-100mL Instrument Name brand model Inverted fluorescence microscope Nikon DS-Fi3 centrifuge ordinary TD6 CO2 incubator Thermo Fisher 3111 Clean bench Huayu BSC-1300-II-A2 Blood cell counter QIUJING XR-K-25
[0047] In this embodiment, the SEH concentration groups include: SEH 0, SEH 30μM, SEH 60μM, and SEH 120μM.
[0048] In this embodiment, the specific experimental steps are as follows.
[0049] (I) Cell resuscitation
[0050] (1) Preheat ddH2O to 37℃;
[0051] (2) Put on gloves, mask and cap, take out the cryovial containing the target cells (containing 1 mL of cell mixture) from the liquid nitrogen tank, and immediately put it into 37℃ ddH2O. Shake the cryovial gently to make it thaw quickly within 1 minute.
[0052] (3) After complete dissolution, wipe the outer wall of the cryovial with 75% alcohol for disinfection and then bring it into the clean bench;
[0053] (4) In a clean bench, add 10 mL of freshly prepared culture medium to a 15 mL sterile centrifuge tube, open the cryopreservation tube, add all the frozen and thawed cell suspensions to the centrifuge tube, centrifuge at 1000 rpm for 3 minutes at room temperature, and remove the upper layer of culture medium.
[0054] (5) Resuspend the cell pellet in 1 mL of culture medium, gently pipette to mix, add to T25 cell culture flask, add culture medium to 5 mL, and incubate at 37°C and 5% CO2.
[0055] (6) Change the medium after 48 hours. When the cells are nearly 80% fused, they can be passaged.
[0056] (II) Cell Culture
[0057] SGC7901 cells were cultured in 1640 medium containing 10% fetal bovine serum and 1% penicillin antibiotics in a 37°C, humidified incubator containing 5% CO2.
[0058] (III) Cell Treatment
[0059] (1) SGC7901 cells in the logarithmic growth phase were digested with 0.25% trypsin and then counted.
[0060] (2) Seed the cells into 6cm culture dishes at a density of 800,000 cells / well and continue culturing;
[0061] (3) Adenovirus infection was performed according to the experimental requirements, and subsequent experiments were conducted 48 hours later.
[0062] (iv) Cloning experiments
[0063] (1) Digest and collect cells from each group, and count the cells;
[0064] (2) Seed cells at a rate of 500 cells / plate into 6-well plates, add 2 mL of culture medium to each plate, and gently rotate to disperse the cells evenly;
[0065] (3) Incubate at 37℃ and 5% CO2 for 12 days;
[0066] (4) After the clones are visible to the naked eye, discard the cell culture medium, carefully wash twice with PBS, and fix with 4% paraformaldehyde at room temperature for 20 min.
[0067] (5) Discard the fixative and rinse once with PBS. After staining with crystal violet at room temperature for 10 min, gently wash away the stain with running water and air dry.
[0068] (6) Place the petri dish upside down on a piece of white paper, put it in a bright place, and take a picture with an ordinary camera;
[0069] (7) Place a transparent film with a grid on a piece of white paper and count the clones directly with the naked eye.
[0070] In this embodiment, the results of the cell plate cloning experiment for each experimental group are shown in the appendix. Figure 2 (A)-(B)
[0071] It was observed that different concentrations of SEH were applied to HuH-7 cells for 14 days. Compared with the control group, the number of HuH-7 liver cancer cell clones in the SEH-treated group decreased, and the colony formation gradually decreased with increasing drug concentration. (***P<0.001, **P<0.005).
[0072] Example 3
[0073] In this embodiment, the effects of different concentrations of SEH on the migration of HuH-7 cells were detected based on the Transwell assay.
[0074] The main reagents and instruments involved in this embodiment are shown in Table 3 below.
[0075] Table 3 Main Reagents and Instruments
[0076] Product Name brand Item number DMEM medium Hyclone SH30022.01 fetal bovine serum Gibco 42F7180K trypsin Genview 89040101100 antibiotic Genview 87020101100 24-well cell culture plate Coring 3524 Migration Room Coring 3422 Crystal Violet Azure Sky C0121 4% paraformaldehyde Azure Sky P0099-100mL Instrument Name brand model Inverted fluorescence microscope Nikon DS-Fi3 centrifuge ordinary TD6 CO2 incubator Thermo Fisher 3111 Clean bench Huayu BSC-1300-II-A2
[0077] In this embodiment, the SEH concentration groups include: SEH 0, SEH 30μM, SEH 60μM, and SEH 120μM.
[0078] In this embodiment, the specific experimental steps are as follows.
[0079] (I) Cell resuscitation
[0080] (1) Preheat ddH2O to 37℃;
[0081] (2) Put on gloves, mask and cap, take out the cryovial containing the target cells (containing 1 mL of cell mixture) from the liquid nitrogen tank, and immediately put it into 37℃ ddH2O. Shake the cryovial gently to make it thaw quickly within 1 minute.
[0082] (3) After complete dissolution, wipe the outer wall of the cryovial with 75% alcohol for disinfection and then bring it into the clean bench;
[0083] (4) In a clean bench, add 10 mL of freshly prepared culture medium to a 15 mL sterile centrifuge tube, open the cryopreservation tube, add all the frozen and thawed cell suspensions to the centrifuge tube, centrifuge at 1000 rpm for 3 minutes at room temperature, and remove the upper layer of culture medium.
[0084] (5) Resuspend the cell pellet in 1 mL of culture medium, gently pipette to mix, add to T25 cell culture flask, add culture medium to 5 mL, and incubate at 37°C and 5% CO2.
[0085] (6) Change the medium after 48 hours. When the cells are nearly 80% fused, they can be passaged.
[0086] (II) Cell Culture
[0087] Huh7 cells were cultured in DMEM medium containing 10% fetal bovine serum and 1% penicillin antibiotics in an incubator at 37°C with saturated humidity and 5% CO2.
[0088] (III) Migration Detection
[0089] (1) Digest and collect cells, and resuspend the cells in serum-free culture medium;
[0090] (2) Add 500 μL of culture medium containing 10% FBS to the lower chamber (outside the transfer chamber, into the well of the 24-well plate);
[0091] (3) Add 300 μL of cell suspension with adjusted cell density (2 × 10⁻⁶ cells / mL). 4 Cells were introduced into the migration chambers and treated according to drug groups: Senkyunolide H (0, 30, 60, 120 μmol / L) was administered to the cells;
[0092] (4) Incubate at 37℃ and 5% CO2 in a cell culture incubator for 24 hours;
[0093] (5) Remove the chamber and fix it with 4% paraformaldehyde for 15-20 minutes;
[0094] (6) Remove the small chamber and place it in a new 24-well plate, add 500 μL of crystal violet and stain for 10 min;
[0095] (7) Gently wipe away cells that have not penetrated the membrane and attached staining solution from the inside of the chamber with a cotton swab;
[0096] (8) Wash twice with PBS to remove excess staining solution;
[0097] (9) Take pictures with a 100x microscope and count the number of cells that pass through each hole.
[0098] In this embodiment, the cell migration experiment results for each experimental group are shown in the appendix. Figure 3 (A)-(B)
[0099] Depend on Figure 3 It was found that different concentrations of SEH treated HuH-7 cells for 24 hours reduced the migration ability of HuH-7 liver cancer cells in the SEH-treated group compared with the control group. At a SEH concentration of 120 μM, the ability of SEH to inhibit cell migration was significantly higher than that in the control group (***P<0.001).
[0100] Example 4
[0101] This embodiment uses flow cytometry to detect the effect of different concentrations of SEH on the cell cycle of HuH-7 cells.
[0102] The main reagents and instruments involved in this embodiment are shown in Table 4 below.
[0103] Table 4 Main Reagents and Instruments
[0104] Product Name brand Item number DMEM medium Hyclone SH30022.01 fetal bovine serum Gibco 42F7180K trypsin Genview 89040101100 antibiotic Genview 87020101100 Cell cycle detection kit KGI Bio KGA511-KGA512 Instrument Name brand model Inverted fluorescence microscope Nikon DS-Fi3 centrifuge ordinary TD6 CO2 incubator Thermo Fisher 3111 Clean bench Huayu BSC-1300-II-A2 Flow cytometer BECKMAN CytoFLEX
[0105] In this embodiment, the SEH concentration groups include: SEH 0, SEH 30μM, SEH 60μM, and SEH 120μM.
[0106] The specific experimental steps in this embodiment are shown below.
[0107] (I) Cell resuscitation
[0108] (1) Preheat ddH2O to 37℃;
[0109] (2) Put on gloves, mask and cap, take out the cryovial containing the target cells (containing 1 mL of cell mixture) from the liquid nitrogen tank, and immediately put it into 37℃ ddH2O. Shake the cryovial gently to make it thaw quickly within 1 minute.
[0110] (3) After complete dissolution, wipe the outer wall of the cryovial with 75% alcohol for disinfection and then bring it into the clean bench;
[0111] (4) In a clean bench, add 10 mL of freshly prepared culture medium to a 15 mL sterile centrifuge tube, open the cryopreservation tube, add all the frozen and thawed cell suspensions to the centrifuge tube, centrifuge at 1000 rpm for 3 minutes at room temperature, and remove the upper layer of culture medium.
[0112] (5) Resuspend the cell pellet in 1 mL of culture medium, gently pipette to mix, add to T25 cell culture flask, add culture medium to 5 mL, and incubate at 37°C and 5% CO2.
[0113] (6) Change the medium after 48 hours. When the cells are nearly 80% fused, they can be passaged.
[0114] (II) Cell Culture
[0115] Huh7 cells were cultured in DMEM medium containing 10% fetal bovine serum and 1% penicillin antibiotics in an incubator at 37°C with saturated humidity and 5% CO2.
[0116] (III) Cell Plating
[0117] (1) After digesting Huh7 cells in the logarithmic growth phase with 0.25% trypsin, the cells were counted;
[0118] (2) Seed the cells into 6-well plates at a density of 3 × 10⁻⁶ cells / well. 5 1 cell / well, continue culturing;
[0119] (3) Perform periodic detection after adding drugs to the cells according to the experimental requirements.
[0120] (iv) Cell cycle detection
[0121] (1) Calculate the required volume of staining working solution based on the number of samples. Incubate each sample with 500 μL of working solution. Before use, prepare the staining working solution by mixing Rnase A:PI working solution at a volume ratio of 1:9.
[0122] (2) Wash the cells once with PBS (centrifuge at 2000 rpm for 5 min), collect and adjust the cell concentration to 1×10⁻⁶. 6 / ml, take 1ml of single-cell suspension;
[0123] (3) After centrifuging the prepared single-cell suspension, remove the supernatant, add 500 μL of 70% cold ethanol to the cells for fixation (2 h to overnight) and store at 4°C. Wash off the fixative with PBS before staining.
[0124] (4) Add 500 μL of pre-prepared PI / Rnase A staining working solution and incubate at room temperature in the dark for 30 to 60 minutes.
[0125] (5) On-machine testing.
[0126] In this embodiment, the periodic detection results of each experimental group are shown in Table 5 below and Appendix. Figure 4 (A)-(B)
[0127] Table 5. Periodic Data Statistics
[0128]
[0129] As can be seen from the above results:
[0130] G1 phase: Compared with the control group, the proportion of cells treated with 60 μM drug was reduced;
[0131] S phase: Compared with the control group, the proportion of cells treated with 30 μM drug increased;
[0132] G2 phase: Compared with the control group, the proportion of cells treated with 60 μM drug increased, while the proportion of cells treated with other drugs decreased.
[0133] It is evident that, compared to the control group, the proportion of cells treated with 30 μM drug in the S phase increased, and the proportion of cells treated with 60 μM drug in the G2 phase increased, indicating cell cycle arrest.
[0134] Example 5
[0135] This invention relates to a drug for treating liver cancer, especially hepatocellular carcinoma, with ligustilide H as the active ingredient.
[0136] This invention relates to a drug for treating liver cancer, especially hepatocellular carcinoma, which can be formulated into conventional dosage forms known in the art, including oral formulations, injectable formulations, respiratory formulations, and mucosal formulations. Specific dosage forms include one or more of the following: tablets, capsules, granules, aqueous solutions, enteric-coated formulations, injections, emulsions, creams, roll-on formulations, capsules, chewable tablets, gels, syrups, liquid solutions, suspensions, powders, solid crystals, orally disintegrating tablets, or pastes.
[0137] In summary, the above embodiments of the present invention verify that the ligustrolactone H (SEH) significantly inhibits the proliferation and migration of HuH-7 hepatocellular carcinoma cells, and this inhibitory effect is positively correlated with the SEH concentration. Furthermore, SEH can also affect the cell cycle distribution of HuH-7 cells, causing cell arrest in the G2 / M phase, thereby inhibiting cell division and proliferation.
[0138] Obviously, the above embodiments are merely illustrative examples for clear explanation and are not intended to limit the implementation. Those skilled in the art will recognize that other variations or modifications can be made based on the above description. It is neither necessary nor possible to exhaustively list all possible implementations here. However, obvious variations or modifications derived therefrom are still within the scope of protection of this invention.
Claims
1. Use of a ligustilide H in the preparation of a medicament for treating liver cancer, characterized in that, the liver cancer comprises hepatocellular carcinoma; the medicament can inhibit the proliferation and migration of liver cancer cells; the medicament can cause cycle arrest of liver cancer cells HuH-7.
2. Use according to claim 1, characterized in that, the medicament comprises an anti-human liver cancer cell HuH-7 drug.
3. Use according to claim 1 or 2, characterized in that, The daily dose of ligustilide H is 10-15 mg / kg body weight.
4. Use according to claim 3, characterized in that, The medicament comprises at least one of oral preparations, injection forms or mucosal administration forms.
5. Use according to claim 4, characterized in that, The preparation comprises one or more of tablets, capsules, injections, emulsions or syrups.
6. Use according to claim 5, characterized in that, The medicament further comprises a pharmaceutically acceptable excipient or carrier.