Application of indanone sesquiterpenoids or extract containing indanone sesquiterpenoids in preparation of antitumor drugs

Abstract

The invention belongs to the technical field of antitumor drug research, and particularly relates to an application of an indanone sesquiterpenoid compound or an extract containing the indanone sesquiterpenoid compound in preparation of antitumor drugs. The structure of the indanone sesquiterpenoids is as shown in a formula I in the specification. Experiments verify that the indanone sesquiterpenoids can inhibit proliferation of breast cancer cells, human kidney clear cell adenocarcinoma cells, esophageal cancer cells and brain glioma tumor cells, which indicates that the indanone sesquiterpenoids provided by the invention have the potential of being prepared into antitumor drugs; # imgabs0 # R1 is selected from a hydrogen atom or a methyl group, R2 is selected from a hydrogen atom or a hydroxyl group, R3 is selected from any one of hydrogen, a hydroxyl group and glucoside, R4 is selected from hydrogen or an acetyl group, and R5 is selected from any one of hydrogen, a methyl group, a hydroxyl group and glucoside.

Description

Technical Field

[0001] The invention belongs to the technical field of anti-tumor drug research, and specifically relates to an application of an indanone sesquiterpenoid compound or an extract containing the indanone sesquiterpenoid compound in the preparation of an anti-tumor drug. Background Art

[0002] Triple-negative breast cancer (TNBC) is a subtype of breast cancer, accounting for 15% to 20% of primary breast cancer. It has the characteristics of high invasiveness, high metastasis rate, high risk of recurrence and metastasis, high mortality rate, and is more common in young women. Due to the lack of effective targets, TNBC is not ideal for the current clinical endocrine therapy and molecular targeted therapy, and will develop serious drug resistance. Therefore, the discovery of new anti-TNBC small molecule drugs or lead compounds has very important clinical significance and value.

[0003] Pteris wallichiana (scientific name: Pteris wallichiana) is a large terrestrial plant. It is a medium-to-large fern plant of the genus Pteris, the group of Pteris reticulata, and the trident system. The whole plant is used as medicine, slightly bitter, astringent, and cool. It clears away heat and stops bleeding. It is used for dysentery, convulsions, and traumatic bleeding. Pteris wallichiana contains a variety of anti-inflammatory, antibacterial, antiviral, and anti-diabetic ingredients, but whether it contains anti-tumor ingredients has not been reported. Summary of the invention

[0004] In view of the above problems, the present invention provides an indanone sesquiterpenoid compound or an extract containing the indanone sesquiterpenoid compound for use in the preparation of an anti-tumor drug. Experimental verification shows that the indanone sesquiterpenoid compound can inhibit the proliferation of breast cancer cells, human renal clear cell adenocarcinoma cells and brain glioma tumor cells, indicating that the indanone sesquiterpenoid compound provided by the present invention has the potential to be prepared into an anti-tumor drug.

[0005] The specific technical solutions provided by the present invention are as follows:

[0006] In a first aspect, the present invention provides an application of an indanone sesquiterpenoid compound or an extract containing the indanone sesquiterpenoid compound in the preparation of an anti-tumor drug. The structure of the indanone sesquiterpenoid compound is shown in Formula I:

[0007]

[0008] Among them, R1 is selected from hydrogen atom or methyl group, R2 is selected from hydrogen atom or hydroxyl group, R3 is selected from any one of hydrogen, hydroxyl group or glycoside, R4 is selected from hydrogen or acetyl group, and R5 is selected from any one of hydrogen, methyl, hydroxyl group or glycoside.

[0009] As a preferred embodiment of the present invention, the structure of the indanone sesquiterpenoid compound is shown in any one of Formulas II to IV:

[0010]

[0011] As a preferred embodiment of the present invention, the indanone sesquiterpenoid compound or an extract containing the indanone sesquiterpenoid compound is used to prepare a drug for treating breast cancer, kidney cancer, esophageal cancer or brain glioma.

[0012] As a preferred embodiment of the present invention, the indanone sesquiterpenoid compound or an extract containing the indanone sesquiterpenoid compound is used to prepare a drug for inhibiting tumor cell proliferation.

[0013] As a preferred embodiment of the present invention, the tumor cells are breast cancer cells EMT-6 and 4T1, human renal clear cell adenocarcinoma cells 786O, esophageal cancer cells TE10 or glioma cells U87.

[0014] As a preferred embodiment of the present invention, the concentration of the indanone sesquiterpenoid compound shown in formula II that inhibits the proliferation of breast cancer cells EMT-6 and 4T1 is 5 μg / ml to 10 μg / ml, the concentration that inhibits human renal clear cell adenocarcinoma cells 786O and glioma cells U87 is 12 μg / ml to 24 μg / ml, and the concentration that inhibits esophageal cancer cells TE10 is 20 μg / ml to 30 μg / ml;

[0015] The concentration of the indanone sesquiterpenoid compound shown in Formula III to inhibit the proliferation of breast cancer cells EMT-6 and 4T1 is 5 μg / ml to 10 μg / ml, the concentration to inhibit human renal clear cell adenocarcinoma cell 786O and glioma cell U87 is 12 μg / ml to 20 μg / ml, and the concentration to inhibit esophageal cancer cell TE10 is 20 μg / ml to 30 μg / ml;

[0016] The concentration of the indanone sesquiterpenoid compound shown in formula IV that inhibits esophageal cancer cell TE10 and glioma cell U87 is 20 μg / ml to 30 μg / ml, and the concentration that inhibits human renal clear cell adenocarcinoma cell 786O is 30 μg / ml to 40 μg / ml.

[0017] As a preferred embodiment of the present invention, the extract containing the indanone sesquiterpenoid compound is prepared according to the following steps:

[0018] Using methanol as the extraction solvent, the southwestern pteris was extracted, and the extraction extract was obtained after the solvent was recovered from the extraction solution.

[0019] The extract is extracted with petroleum ether, dichloromethane and ethyl acetate in sequence, and the dichloromethane extraction part and the ethyl acetate extraction part are collected. The extract containing the indanone sesquiterpenoid compound is the dichloromethane extraction part or the ethyl acetate extraction part or a mixture of the two in any proportion.

[0020] The second aspect of the present invention provides an anti-tumor drug, which comprises the indanone sesquiterpenoid compound or an extract containing the indanone sesquiterpenoid compound, and a pharmaceutically acceptable excipient or carrier.

[0021] As a preferred embodiment of the present invention, the drug is prepared as an oral preparation or an injection preparation.

[0022] As a preferred embodiment of the present invention, the oral preparation is a capsule, a tablet, a granule or a liquid preparation.

[0023] As a preferred embodiment of the present invention, the injection preparation is an injection solution or an injection powder.

[0024] Compared with the prior art, the beneficial effects of the present invention are:

[0025] The present invention provides an application of an indanone sesquiterpenoid compound or an extract containing the indanone sesquiterpenoid compound in the preparation of an anti-tumor drug. Experimental verification shows that the indanone sesquiterpenoid compound provided by the present invention can inhibit the proliferation of breast cancer cells EMT-6 and 4T1, human renal clear cell adenocarcinoma cell 786O, esophageal cancer TE10 or glioma cell U87. BRIEF DESCRIPTION OF THE DRAWINGS

[0026] Figure 1 This is the flow chart of the separation and purification of Pteris crenata;

[0027] Figures 2-3 The effects of petroleum ether extraction, dichloromethane extraction, ethyl acetate extraction and methanol extraction on the proliferation of EMT-6 and 4T1 cells; **** P < 0.0001;

[0028] Figure 4 Fr.EA-2 and Fr.EA-3 significantly inhibited the proliferation of EMT-6 and 4T1 cells; **** P < 0.0001;

[0029] Figure 5 Fr.DCM-1 and Fr.DCM-8 significantly inhibited the proliferation of EMT-6 and 4T1 cells; **** P < 0.0001;

[0030] Figure 6 is the 24h IC of Fr.EA-2 against EMT-6 cells 50 value;

[0031] Figure 7 is the IC value of Fr.DCM-8 for EMT-6 cells at 24h 50 value;

[0032] Figure 8 It is the IC of Fr.EA-2-4 for EMT-6 and 4T1 50 value;

[0033] Fig. 9 It is the IC of Fr.DCM-8-3 for EMT-6 and 4T1 50 value;

[0034] Fig.10 It is the IC of Pterosin B that inhibits the proliferation of EMT-6 and 4T1 cells 50 value;

[0035] Fig.11 It is the IC of Pterosin B that inhibits the proliferation of renal cancer cell 786O, esophageal cancer TE10 and glioma cell U87 50 value; **** P < 0.0001;

[0036] Fig.12 It is the IC of Pterosin A that inhibits the proliferation of EMT-6 and 4T1 cells 50 value;

[0037] Fig.13 It is the IC of Pterosin A that inhibits the proliferation of renal cancer cell 786O, esophageal cancer TE10 and glioma cell U87 50 value; **** P < 0.0001;

[0038] Fig.14 It is the IC of 14-acetyl-pterosin C 3-O-β-D-glucosidede that inhibits the proliferation of renal cancer cell 786O, esophageal cancer TE10 and glioma cell U87 50 value; **** P < 0.0001;

[0039] Fig.15 The scratch test was used to detect the effect of pterosin B on tumor cell proliferation;

[0040] Fig.16 The scratch assay was used to detect the effect of pterosin A on tumor cell proliferation;

[0041] Fig.17 The radiation sensitivity of pterosin B to EMT-6 and 4T1 cells was observed by increasing radiation;

[0042] Fig.18 The radiation sensitivity of pterosin A to EMT-6 and 4T1 cells was observed by increasing radiation;

[0043] Fig.19 is the effect of pterosin B on the proliferation of paclitaxel-resistant cell lines EMT-6-R and 4T1-R;

[0044] Fig. 20 is the effect of pterosin A on the proliferation of paclitaxel-resistant cell lines EMT-6-R and 4T1-R;

[0045] Fig.21 The DCFH-DA probe method was used to detect the level of cellular reactive oxygen species under the intervention of pteridin B;

[0046] Fig. 22 The DCFH-DA probe method was used to detect the level of cellular reactive oxygen species under the intervention of pteridin A;

[0047] Fig.23 Pterosin B significantly inhibited the growth of tumors in tumor-bearing mice; each horizontal row has 6 parallels;

[0048] Fig.24 It is the change of tumor volume in tumor-bearing mice under the intervention of pterosin B;

[0049] Fig.25 Pterosin A significantly inhibited the growth of tumors in tumor-bearing mice; each horizontal row has 6 parallels;

[0050] Fig.26 It is the change of tumor volume in tumor-bearing mice under the intervention of pterosin A. DETAILED DESCRIPTION

[0051] The present invention will be further described below in conjunction with specific embodiments.

[0052] The present invention provides an indanone sesquiterpenoid compound or an extract containing the indanone sesquiterpenoid compound for use in preparing an anti-tumor drug. The structure of the indanone sesquiterpenoid compound is shown in Formula I:

[0053]

[0054] Among them, R1 is selected from hydrogen atom or methyl group, R2 is selected from hydrogen atom or hydroxyl group, R3 is selected from any one of hydrogen, hydroxyl group or glycoside, R4 is selected from hydrogen or acetyl group, and R5 is selected from any one of hydrogen, methyl, hydroxyl group or glycoside.

[0055] The results of experiments show that the indanone sesquiterpenoid compounds provided by the present invention have anti-tumor effects, especially have better improvement effects on breast cancer, renal cancer, esophageal cancer and glioma. The indanone sesquiterpenoid compounds can inhibit the proliferation of breast cancer cells EMT-6 and 4T1, human renal clear cell adenocarcinoma cells 786O, esophageal cancer TE10 or glioma cells U87.

[0056] The extract containing indanone sesquiterpenoid compounds can be extracted from Pteris fasciata, and the operation process is as follows:

[0057] Using methanol as the extraction solvent, the southwestern pteris was extracted, and the extraction extract was obtained after the solvent was recovered from the extraction solution.

[0058] The extract is extracted with petroleum ether, dichloromethane and ethyl acetate in sequence, and the dichloromethane extraction part and the ethyl acetate extraction part are collected. The extract containing indanone sesquiterpenoid compounds is the dichloromethane extraction part or the ethyl acetate extraction part or a mixture of the two in any proportion.

[0059] Example 1

[0060] Extraction and separation of indanone sesquiterpenoids from Pteris chinensis

[0061] 1. Crude extraction of indanone sesquiterpenoids

[0062] Take 30 kg of dried roots of Pteris crenata, extract them with methanol under reflux for 3 times, recover the solvent and combine the filtrate to obtain 9 kg of methanol extract and pure water dispersed extract.

[0063] The product was extracted with petroleum ether, dichloromethane and ethyl acetate respectively to obtain 340 g of the petroleum ether extraction fraction, 890 g of the dichloromethane extraction fraction and 2 kg of the ethyl acetate extraction fraction.

[0064] 2. Screening of active parts

[0065] Tumor cells EMT-6, 4T1 cells, glioma cells U87 and renal cancer cells 786O in the logarithmic growth phase were counted and prepared into a concentration of 6×10 4 100 μL of the cell suspension of 100 μg / mL was added to a 96-well plate and placed in a 37°C, 5% CO2 cell culture incubator for overnight culture. After the cells adhered to the wall, the petroleum ether extraction fraction, dichloromethane extraction fraction and ethyl acetate extraction fraction were added, and the concentration gradient was: 1000 μg / ml, 750 μg / ml, 500 μg / ml, 250 μg / ml. Three replicates were set for each group, and the drug solvent was used as the control group. After 48 hours of culture, 10 μL of CCK-8 working solution was added, and the cells were incubated in the cell culture incubator for another 3 hours. The OD value was detected at 450 nm and calculated.

[0066] The results are as follows Figures 2-3 As shown. Figures 2-3 It can be seen that the dichloromethane DCM and ethyl acetate EA extracts significantly inhibited the proliferation of EMT-6 and 4T1 cells. In addition, the DCM and EA extracts at a concentration of 250 μg / ml also had a certain inhibitory effect on the proliferation of glioma cells U87 and renal cancer cells 786O.

[0067] 3. Separation and purification

[0068] The dichloromethane and ethyl acetate extraction parts were dissolved in methanol respectively, and 100-200 mesh silica gel was added in a weight ratio of 1:1.5 to mix the sample, and the sample was subjected to normal phase silica gel column chromatography, with the eluent being dichloromethane:methanol=100-0:0-100. The same components were combined by thin layer plate detection to obtain 8 components Fr.DCM-1, Fr.DCM-2, Fr.DCM-3, Fr.DCM-4, Fr.DCM-5, Fr.DCM-6, Fr.DCM-7, Fr.DCM-8 under the dichloromethane extraction part, and 4 components Fr.EA-1, Fr.EA-2, Fr.EA-3, Fr.EA-4 under the ethyl acetate extraction part. Specific separation and purification process detection Figure 1 .

[0069] The 12 components were tested by CCK8 cell proliferation assay. The concentrations of Fr.DCM-1, Fr.DCM-2, Fr.DCM-3, Fr.DCM-4, Fr.DCM-5, Fr.DCM-6, Fr.DCM-7, and Fr.DCM-8 were all 250 μg / ml, and the concentrations of Fr.EA-1, Fr.EA-2, Fr.EA-3, and Fr.EA-4 were all 100 μg / ml. The results are shown in Figures 4-5 shown.

[0070] The results showed that Fr.EA-2, Fr.EA-3, Fr.DCM-1 and Fr.DCM-8 significantly inhibited the proliferation of EMT-6 and 4T1 cells.

[0071] Continue to dilute Fr.EA-2, Fr.EA-3, Fr.DCM-1 and Fr.DCM-8 in a gradient concentration to obtain 200μg / ml, 160μg / ml, 80μg / ml, 40μg / ml, 20μg / ml, 10μg / ml, and 5μg / ml, and act on EMT-6 and 4T1 cells for 24h. CCK8 was used to detect cell proliferation activity, and the IC value of Fr.EA-2 on EMT-6 cells for 24h was obtained. 50 The IC values ​​of Fr.DCM-8 for EMT-6 cells at 24 h were 12.58 μg / ml and 9.26 μg / ml, respectively. 50 14.75 and 16.31 μg / ml respectively, see Figures 6-7 .

[0072] Fr.EA-2 was subjected to silica gel column chromatography, 200-300 mesh silica gel was mixed with the sample, and the eluent was dichloromethane:ethyl acetate = 30:1-5:1, and five components, Fr.EA-2-1, Fr.EA-2-2, Fr.EA-2-3, Fr.EA-2-4, and Fr.EA-2-5, were obtained. Among them, Fr.EA-2-4 had an IC of 0.0447 for EMT-6 and 4T1. 50The values ​​were 9.46μg / ml and 9.87μg / ml, see Figure 8 .

[0073] Fr.DCM-8 was subjected to silica gel column chromatography, 200-300 mesh silica gel was mixed with the sample, and the eluent was dichloromethane: ethyl acetate = 15-1:1, and six components Fr.DCM-8-1, Fr.DCM-8-2, Fr.DCM-8-3, Fr.DCM-8-4, Fr.DCM-8-5 and Fr.DCM-8-6 were obtained. Among them, Fr.DCM-8-3 had an IC of 0.0447 for EMT-6 and 4T1. 50 The values ​​were 8.18 and 8.64 μg / ml, respectively. Fig. 9 .

[0074] Semi-preparative liquid phase separation and purification of Fr.EA-2-4 was performed, the chromatographic column was a YMC liquid chromatography column ODS, 5 μm, detection was performed at 200 mm, and the eluent was methanol and water in a volume ratio of 94:100. The main chemical component pterosin B in Fr.EA-2-4 was obtained, and its structural formula is shown below:

[0075]

[0076] Semi-preparative liquid phase separation and purification of Fr.DCM-8-3, the chromatographic column is a YMC liquid chromatography column ODS, 5μm, detection at 200mm, and the eluent is isocratic elution of methanol and water at a volume ratio of 90:100. The main chemical component of Fr.DCM-8-3, pterosin A, is obtained, and its structural formula is as follows:

[0077]

[0078] Semi-preparative liquid phase separation and purification of Fr.DCM-8-3 was performed, the chromatographic column was a YMC liquid chromatography column ODS, 5 μm, the detection was at 200 mm, and the eluent was isocratic elution of methanol and water at a volume ratio of 85:100. The new chemical component 14-acetyl-pterosin C 3-O-β-D-glucosidede in Fr.DCM-8-3 was obtained, and its structural formula is shown below:

[0079]

[0080] Example 2

[0081] CCK8 method was used to detect the effects of pterosin B, pterosin A and the new chemical component 14-acetyl-pterosin C3-O-β-D-glucosidede on tumor cell proliferation

[0082] The proliferation of tumor cells was detected according to the method in Example 1. The results are as follows Figures 10 to 14 shown.

[0083] The results showed that the IC of pterosin B against EMT-6 and 4T1 50 The values ​​were 7.274μg / ml and 6.175μg / ml respectively; the IC values ​​for the proliferation of renal cancer cell 786O and glioma cell U87 were 50 The value is about 19 μg / ml. IC of Pterosin A for EMT-6 and 4T1 50 The values ​​were 5.24 and 7.87 μg / ml respectively; the IC values ​​for the proliferation of renal cancer cell 786O and glioma cell U87 were 50 The value is about 17μg / ml; the IC 50 The value is about 21μg / ml. IC value of the new chemical component 14-acetyl-pterosin C 3-O-β-D-glucosidede on the proliferation of breast cancer cells EMT-6 and 4T1 50 The value was about 8.45 μg / ml, and the IC value for esophageal cancer cell TE10 and glioma cell U87 was 50 The IC values ​​of the cells were 22.3 μg / ml, and the IC values ​​of the cells inhibiting the activity of human renal clear cell adenocarcinoma cell line 786O were 22.3 μg / ml. 50 The value is 33.6μg / ml.

[0084] Example 3

[0085] Scratch assay to detect the effects of pterosin B and pterosin A on tumor cell proliferation

[0086] 1. Methods

[0087] Take cells in the logarithmic growth phase and inoculate them into 12-well plates and culture them until the cell growth density reaches 100%. Discard the serum, draw a straight line on the cells with a 10μL pipette tip, wash off the fallen cells with PBS, and then replace with serum-free drug-containing medium plus double antibody culture. The concentration of pterosin B or pterosin A in the drug-containing medium is 5μg / ml. Observe and take pictures under a microscope. 24h, discard the medium and wash the cells with PBS, observe and take pictures under a microscope. The results are as follows Figures 15-16 shown.

[0088] The results showed that pterosin B and pterosin A could significantly inhibit the migration ability of EMT-6 and 4T1 cells.

[0089] Example 4

[0090] Effects of pterosin B and pterosin A on the sensitivity of tumor cells

[0091] 1. Increase the sensitivity of EMT-6 and 4T1 cells to radiation

[0092] Through clone formation experiments, we observed that pterosin B and pterosin A increased the sensitivity of paclitaxel-resistant cell lines EMT-6-R and 4T1-R to radiation. The cells were irradiated with a dose of 4Gy and treated with 8μg / ml pterosin B and pterosin A to observe whether pterosin B and pterosin A increased the sensitivity of EMT-6 and 4T1 cell lines to radiation. The results are shown in Figures 17-18 shown.

[0093] The results showed that pterosin B and pterosin A could significantly increase the sensitivity of paclitaxel-resistant cell lines EMT-6-R and 4T1-R to radiation.

[0094] 2. Increase the sensitivity of EMT-6 and 4T1 resistant cells to paclitaxel

[0095] The paclitaxel-resistant cell lines EMT-6-R and 4T1-R in the logarithmic growth phase were counted and prepared into a concentration of 2-6×10 4 100 μL of the cell suspension of cells / mL was aspirated and added to a 96-well plate, and cultured in a 37°C, 5% CO2 cell culture incubator overnight. After the cells adhered to the wall, 8 μg / ml of pterosin B and pterosin A were added respectively. Three replicates were set up for each group, and the drug solvent DMSO was used as the control group, marked as Vehicle. After 48 hours of culture, 10 μL of CCK-8 working solution was added, and the cells were incubated in the cell culture incubator for another 3 hours. The OD value was detected at 450nm and the cell survival rate was calculated. The results are shown in Figures 19-20 shown.

[0096] The results showed that pterosin B and pterosin A significantly increased the sensitivity of drug-resistant cell lines EMT-6-R and 4T1-R to paclitaxel.

[0097] Example 5

[0098] Detection of Cellular Reactive Oxygen Species Levels Using DCFH-DA Probe

[0099] Take EMT-6 and 4T1 cells in the logarithmic growth phase and culture them in 6-well plates. After they grow to 80% and adhere to the wall, intervene the cells with 8μg / ml pterosin B and pterosin A for 12 hours, dilute the DCFH-DA probe with serum-free medium at a ratio of 1:1000, and add no less than 1mL of DCFH-DA working solution to each well except the negative control group. Incubate at 37℃ in the dark for 20min, then wash the cells 3 times with serum-free medium, observe the fluorescence intensity of each group under a fluorescence inverted microscope at an excitation wavelength of 488nm, and take pictures and record. The results are shown in Figures 21-22 shown.

[0100] The results showed that pterosin B and pterosin A could significantly induce the accumulation of reactive oxygen species in EMT-6 and 4T1 cells, thereby inducing cell apoptosis.

[0101] Example 6

[0102] Pterosin B and Pterosin A significantly inhibited tumor growth in tumor-bearing mice

[0103] 1×10 EMT-6 and 4T1 cells in logarithmic growth phase were collected. 6 ~5×10 6 The tumor size was detected every 2 days and the volume of the tumor was 100 mm. 3 The mice were given drugs by intraperitoneal injection every 2 days, 10 mg / mg, 100 uL, and were divided into control group, pterosin B group and pterosin A group. The treatment was terminated after 2 weeks. The tumor volume was detected every 2 days during the period, and the tumor tissues of mice in each group were collected for statistical analysis. Figures 23-26 shown.

[0104] The results showed that pterosin B and pterosin A could significantly inhibit tumor growth.

[0105] The above descriptions and illustrations show the basic principles and main features of the present invention. It should be understood by those skilled in the art that the present invention is not limited by the above embodiments, which are merely illustrative of the basic principles of the present invention. Without departing from the spirit and scope of the present invention, the present invention may be subject to various changes and improvements, which are all within the scope of the present invention to be protected. The scope of protection of the present invention is defined by the appended claims and their equivalents.

Claims

1. Use of indanone sesquiterpenoid compounds or extracts containing them in the preparation of anti-tumor drugs, characterized in that: The structure of the indanone sesquiterpenoid compound is shown in Formula I: Among them, R1 is selected from hydrogen atom or methyl group, R2 is selected from hydrogen atom or hydroxyl group, R3 is selected from any one of hydrogen, hydroxyl group or glycoside, R4 is selected from hydrogen or acetyl group, and R5 is selected from any one of hydrogen, methyl, hydroxyl group or glycoside.

2. The use according to claim 1, characterized in that: The structure of the indanone sesquiterpenoid compound is shown in any one of Formulas II to IV:

3. The use according to claim 2, characterized in that: The indanone sesquiterpenoid compound or the extract containing the indanone sesquiterpenoid compound is used for preparing medicine for treating breast cancer, kidney cancer, esophageal cancer or brain glioma.

4. The use according to claim 3, characterized in that: The indanone sesquiterpenoid compound or the extract containing the indanone sesquiterpenoid compound is used for preparing a medicine for inhibiting the proliferation of tumor cells.

5. The use according to claim 4, characterized in that: The tumor cells are breast cancer cells EMT-6 and 4T1, human renal clear cell adenocarcinoma cells 786O, esophageal cancer cells TE10 or glioma cells U87.

6. The use according to claim 5, characterized in that: The concentration of the indanone sesquiterpenoid compound shown in Formula II that inhibits the proliferation of breast cancer cells EMT-6 and 4T1 is 5 μg / ml to 10 μg / ml, the concentration that inhibits the proliferation of human renal clear cell adenocarcinoma cells 786O and glioma cells U87 is 12 μg / ml to 24 μg / ml, and the concentration that inhibits the proliferation of esophageal cancer cells TE10 is 20 μg / ml to 30 μg / ml; The concentration of the indanone sesquiterpenoid compound shown in Formula III to inhibit the proliferation of breast cancer cells EMT-6 and 4T1 is 5 μg / ml to 10 μg / ml, the concentration to inhibit human renal clear cell adenocarcinoma cell 786O and glioma cell U87 is 12 μg / ml to 20 μg / ml, and the concentration to inhibit esophageal cancer cell TE10 is 20 μg / ml to 30 μg / ml; The concentration of the indanone sesquiterpenoid compound shown in formula IV that inhibits esophageal cancer cell TE10 and glioma cell U87 is 20 μg / ml to 30 μg / ml, and the concentration that inhibits human renal clear cell adenocarcinoma cell 786O is 30 μg / ml to 40 μg / ml.

7. The use according to claim 1, characterized in that: The extract containing the indanone sesquiterpenoid compound is prepared according to the following steps: Using methanol as the extraction solvent, the southwestern pteris was extracted, and the extraction extract was obtained after the solvent was recovered from the extraction solution. The extract is extracted with petroleum ether, dichloromethane and ethyl acetate in sequence, and the dichloromethane extraction part and the ethyl acetate extraction part are collected. The extract containing the indanone sesquiterpenoid compound is the dichloromethane extraction part or the ethyl acetate extraction part or a mixture of the two in any proportion.

8. An anti-tumor drug, characterized in that: The invention comprises the indanone sesquiterpenoid compound or an extract containing the indanone sesquiterpenoid compound according to claim 1, and a pharmaceutically acceptable auxiliary material or carrier.

9. The drug according to claim 8, characterized in that The drug is prepared as an oral preparation or an injection preparation.

10. The drug according to claim 9, characterized in that The oral preparation is a capsule, tablet, granule or liquid preparation.

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