CN117159560A - Application of cyclovirobuxine D in preparing medicament for treating breast cancer - Google Patents
Application of cyclovirobuxine D in preparing medicament for treating breast cancer Download PDFInfo
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- CN117159560A CN117159560A CN202311335209.9A CN202311335209A CN117159560A CN 117159560 A CN117159560 A CN 117159560A CN 202311335209 A CN202311335209 A CN 202311335209A CN 117159560 A CN117159560 A CN 117159560A
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- cyclovirobuxine
- breast cancer
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- GMNAPBAUIVITMI-ABNIRSKTSA-N cyclovirobuxine d Chemical compound CC(C)([C@@H](NC)CC1)[C@H]2[C@@]31C[C@@]13CC[C@]3(C)[C@@H]([C@H](C)NC)[C@H](O)C[C@@]3(C)[C@@H]1CC2 GMNAPBAUIVITMI-ABNIRSKTSA-N 0.000 title claims abstract description 51
- AXGWYABSYNCIMX-UHFFFAOYSA-N Cycloprotobuxin D Natural products C1CC(NC)C(C)(C)C2C31CC13CCC3(C)C(C(C)NC)CCC3(C)C1CC2 AXGWYABSYNCIMX-UHFFFAOYSA-N 0.000 title claims abstract description 50
- GMNAPBAUIVITMI-UHFFFAOYSA-N Cyclovirobuxin D Natural products C1CC(NC)C(C)(C)C2C31CC13CCC3(C)C(C(C)NC)C(O)CC3(C)C1CC2 GMNAPBAUIVITMI-UHFFFAOYSA-N 0.000 title claims abstract description 50
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Landscapes
- Pharmaceuticals Containing Other Organic And Inorganic Compounds (AREA)
Abstract
The invention discloses an application of cyclovirobuxine D in preparing a medicament for treating breast cancer, and belongs to the technical field of medicines. The MTT experiment, the cell cycle experiment, the scratch experiment, the hoechst33342 staining experiment and the mitochondrial membrane potential detection experiment show that the cyclobuxine D can obviously inhibit proliferation and migration of breast cancer cells and induce apoptosis. Therefore, cyclovirobuxine D can be applied to the preparation of medicaments for treating breast cancer.
Description
Technical Field
The invention belongs to the technical field of medicines, and particularly relates to application of cyclovirobuxine D in preparation of a medicine for treating breast cancer.
Background
Breast cancer is a malignant tumor that occurs in human mammary gland epithelial tissue, severely compromising female health. As a common malignant tumor in female suffering, the incidence rate is first, the proportion is about 10%, the incidence rate is about forty-three parts per million, and the data shows a gradually rising situation under the influence of various factors such as life style and the like.
In recent years, with innovations of diagnosis and treatment modes of early breast cancer and perfection of treatment schemes of late breast cancer, the death rate of the breast cancer is obviously reduced. However, current surgical and adjuvant treatment modalities, although somewhat advanced, still plagues patients suffering from breast cancer with disease progression and recurrence.
Therefore, the development of new drugs for inhibiting proliferation and migration of breast cancer cells and inducing apoptosis has great clinical demands, has important practical significance for treating breast cancer, and is also a hotspot of current international research.
Cyclobuxine D (Cyclobuxine D), CAS no: 2241-90-9 is a steroid alkaloid refined from Buxus microphylla and other congeneric plants, and is white crystalline powder, soluble in chloroform and insoluble in water. At present, no report on the application of cyclovirobuxine D as an active ingredient in breast cancer treatment is found.
Disclosure of Invention
The invention aims to: the invention aims to provide an application of cyclovirobuxine D in preparing a medicament for treating breast cancer. Proved by researches, the cyclovirobuxine D can obviously inhibit proliferation, migration and apoptosis of human breast cancer cells MCF-7. The cyclovirobuxine D is applied to preparing the medicine for treating breast cancer, so that not only is the new medicinal value of the cyclovirobuxine D dug, but also a certain medical prospect and economic value are achieved.
The technical scheme is as follows: the aim of the invention is achieved by the following technical scheme:
the invention provides an application of cyclovirobuxine D in preparing a medicament for treating breast cancer.
The cyclovirobuxine D inhibits proliferation and migration of human breast cancer cells MCF-7.
Cyclovirobuxine D induces apoptosis of breast cancer cells.
The cyclovirobuxine D acts on IC of breast cancer cells MCF-7 for 24h, 48h and 72h 50 The values were 159.4. Mu. Mol/L, 48.9. Mu. Mol/L and 13.1. Mu. Mol/L, respectively.
The medicament comprises cyclovirobuxine D or a derivative or pharmaceutically acceptable salt thereof.
The invention relates to the above pharmaceutically acceptable salts which are converted into cyclobuxine D in vivo. For example, within the scope of the present invention, cyclovirobuxine D according to the invention is converted into a pharmaceutically acceptable salt form and used in salt form according to processes known in the art.
The pharmaceutically acceptable salt comprises a hydrochloride, phosphate, oxalate, sulfate or citrate salt.
The medicine also comprises pharmaceutically acceptable auxiliary materials.
The auxiliary materials comprise one or more of an emulsifying agent, a binding agent, a preservative, a diluting agent, a solubilizing agent, a disintegrating agent, an antioxidant, a wetting agent and a lubricating agent.
The emulsifier is at least one selected from tween, span, glycerol fatty acid esters, pectin, agar, sulfate, sodium alginate and silicon dioxide.
The binder is at least one selected from starch slurry, sodium carboxymethyl cellulose, povidone, hydroxypropyl cellulose, methyl cellulose and ethyl cellulose.
The preservative is at least one selected from benzoic acid and salts thereof, sorbic acid and salts thereof and parabens.
The diluent is at least one selected from starch, saccharide, cellulose and inorganic salts.
The solubilizer is one of tween, polyoxyethylene fatty alcohol ether, sulfate and sulfonate.
The disintegrating agent is at least one selected from starch, sodium carboxymethyl starch, crosslinked povidone, low-substituted hydroxypropyl cellulose and crosslinked polyvinylpyrrolidone.
The antioxidant is at least one selected from ascorbic acid, sulfite, bisulfite, gallic acid and lipid thereof.
The wetting agent is at least one selected from water and ethanol.
The lubricant is at least one selected from magnesium stearate, talcum powder, hydrogenated vegetable oil, polyethylene glycol and micropowder silica gel.
The invention also provides a medicine for treating breast cancer, which comprises cyclovirobuxine D or a derivative or pharmaceutically acceptable salt thereof and pharmaceutically acceptable auxiliary materials.
The dosage form of the medicine is granule, tablet, capsule, pill, suspension, solution, injection or infusion.
The medicaments of the present invention may be administered in a variety of known ways, for example orally, by injection, by inhalation spray. The medicine of the invention can be used alone or in combination with other medicines. The oral composition may be any orally acceptable dosage form including, but not limited to, granules, tablets, capsules, pills, suspensions, and solutions.
Sterile injectable compositions can be formulated according to techniques known in the art using suitable dispersing or wetting agents and suspending agents. Pharmaceutically acceptable carriers and solvents that can be used include water, sodium chloride solution, and the like.
The medicine of the invention can be prepared into common preparations, and also can be prepared into sustained release preparations, controlled release preparations, targeted preparations and various microparticle administration systems.
The actual dosage level of the active ingredient in the medicament of the present invention may be varied to obtain an amount of active ingredient that is effective to achieve the desired therapeutic response for the particular patient, composition and mode of administration, which is non-toxic to the patient. The dosage level selected will depend on a variety of factors including the route of administration, the time of administration, the rate of excretion, the duration of the treatment, other drugs, compounds and/or materials used in combination with cyclovirobuxine D, the age, sex, weight, general health and past medical history of the patient being treated, and like factors well known in the medical arts.
The beneficial effects are that:
the cyclovirobuxine D can be used as an active ingredient, is applied to treating breast cancer, exploits a new application of cyclovirobuxine D, and provides a new choice for preparing medicaments for treating breast cancer. The research of the invention finds that: cyclovirobuxine D can obviously inhibit proliferation and migration of human breast cancer cells MCF-7 and induce apoptosis, and has the effect of resisting breast cancer. Therefore, cyclovirobuxine D can be used for preparing medicines for treating breast cancer.
Drawings
FIG. 1 is a graph showing experiments of cyclovirobuxine D inhibiting proliferation of human breast cancer cells MCF-7.
FIG. 2 is a graph showing the cloning experiments of cyclovirobuxine D acting on human breast cancer cells MCF-7.
FIG. 3 is a graph showing cell cycle distribution experiments of flow cytometry analysis of human breast cancer cells MCF-7.
FIG. 4 is a graph showing a scratch experiment of cyclovirobuxine D acting on human breast cancer cells MCF-7.
FIG. 5 is a chart showing the hoechst33342 staining experiment of cyclovirobuxine D acting on human breast cancer cells MCF-7 cells.
FIG. 6 is a graph showing the mitochondrial membrane potential test of cyclovirobuxine D acting on human breast cancer cells MCF-7.
Detailed Description
The technical scheme of the present invention is described in detail below through specific examples, but the scope of the present invention is not limited to the examples.
The specific techniques or conditions are not identified in the examples and are described in the literature in this field or are carried out in accordance with the product specifications. The reagents or equipment used were conventional products available for purchase through regular channels, with no manufacturer noted.
The experimental methods in the following examples are conventional methods unless otherwise specified. The test materials used in the examples described below, unless otherwise specified, are all commercially available products.
The specifications and sources of reagents used in the examples: cyclovirobuxine D with purity of 98.5% is prepared by laboratory (refer to CN112521440, a purification method of cyclovirobuxine D); 4% paraformaldehyde was purchased from Biosharp corporation; crystal violet, purchased from alaa Ding Gongsi.
DMEM high sugar medium and foetal calf serum were purchased from Gibco,
penicillin-streptomycin (double antibody), PBS buffer solution, pancreatin cell digestion solution, cell cryopreservation solution, hoechst33342 living cell staining solution (100×) are all purchased from Biyun Tian biological reagent company;
thiazole blue (MTT) was purchased from Sigma, usa;
cell cycle kits were purchased from Kaiyi organisms;
c2006 mitochondrial membrane potential detection kit (JC-1) was purchased from the bi yun tian biological reagent company and included: JC-1 (200X), JC-1 staining buffer (5X), CCCP (10 mM), ultrapure water.
Cell culture broth (10% fetal bovine serum, 1% diabody): adding 50mL of fetal bovine serum and 5mL of diabody into a 500mL sterile container, and fixing the volume to 500mL by using a DMEM high-sugar culture medium to obtain the feed;
low serum cell culture broth (2% fetal bovine serum, 1% diabody): adding 10mL of fetal bovine serum and 5mL of diabody into a 500mL sterile container, and fixing the volume to 500mL by using a DMEM high-sugar culture medium to obtain the feed;
MTT working solution (5 mg/mL): under the condition of avoiding light, 0.6g of MTT powder is completely dissolved in 12mL of 1 XPBS in a sterile super clean bench, filtered and sterilized by a 0.22 mu m filter, and then split-packed in a 1.5mL centrifuge tube (wrapped with tin foil) and preserved in a dark place at-20 ℃;
crystal violet staining solution: 0.05g of crystal violet powder is weighed and dissolved in 10mL of absolute methanol to prepare 0.5% crystal violet stock solution, and the stock solution is stored in a refrigerator at 4 ℃ in a dark place. The working concentration of crystal violet is 0.1%, and the crystal violet is diluted by PBS when in use;
hoechst33342 (1×): taking 0.1mL of cell culture solution, and adding 0.9ml Hoechst33342 living cell staining solution (100X) to obtain the cell culture solution;
JC-1 dyeing working solution: diluting JC-1 by adding 8mL of ultrapure water into 50 mu L of JC-1 (200X), vigorously swirling to mix the JC-1 evenly, then adding 2mL of JC-1 dyeing buffer solution (5X), and mixing evenly to obtain JC-1 dyeing working solution; relates to a reagent derived from a mitochondrial membrane potential detection kit.
CCCP working fluid (10 μm): taking 2 mu L of 10mM CCCP, and adding 998 mu L of cell culture solution to obtain the compound;
JC-1 staining buffer (1×): 1mL of JC-1 staining buffer (5X) is taken, and 4mL of distilled water is added to be uniformly mixed to obtain the dye.
MCF-7 cell line (human breast cancer cell) was purchased from the cell bank of the national academy of sciences.
The test detection instrument used in the examples:
flow cytometer, FACSCalibur, BD company, usa;
fluorescent inverted microscope, TS2, NOKON company;
the enzyme-labeled instrument, tecan Sunrise, austria.
EXAMPLE 1MTT assay for detection of cyclovirobuxine D anti-tumor Activity
Selecting human breast cancer MCF-7 cells in logarithmic growth phase, discarding old culture solution, respectively washing the cells twice with 1mL of PBS buffer solution, adding 1mL of pancreatin cell digestive solution to eliminate cell clusters into single cells, adding 3mL of cell culture solution to stop digestion, centrifuging for 5min, discarding supernatant, adding 1mL of cell culture solution to blow the precipitate again into single cell suspension, and diluting to proper cell concentration.
The 96-well plate, control group and experimental group are adopted, 3000 MCF-7 cells (100 mu L) in logarithmic growth phase are added in each well, only 100 mu L of fresh cell culture solution is added in blank group, three parallel groups are arranged in control group, experimental group and blank group, after the cells grow overnight, 100 mu L of fresh cell culture solution is respectively added in blank group and control group, and the cell culture solution is respectively added in experiment group to dilute to the final concentration of 20 mu mol/L, 40 mu mol/L, 60 mu mol/L, 80 mu mol/L, 100 mu mol/L, 120 mu mol/L, 140 mu mol/L and 160 mu mol/L cyclobuxine D liquid respectively, only 100 mu L of fresh culture solution is added in blank group, and the solution contains 5% CO at 37 DEG C 2 Incubating for 24, 48 and 72 hr, adding 20 μl of MTT (5 mg/ml) working solution into each group, standing 96-well plate in incubator for 4 hr, sucking supernatant, adding 200 μl of LDMSO to dissolve precipitate, oscillating at 37deg.C for 10min, and measuring with enzyme-labeled instrumentAbsorbance at 492 nm.
Cell viability = [ (experimental OD value-blank OD value)/control OD value-blank OD value ] ×100%.
FIG. 1 is a graph showing experiments of cyclovirobuxine D inhibiting proliferation of MCF-7 cells. As can be seen from fig. 1: cyclovirobuxine D has 24, 48 and 72h of IC effect on MCF-7 cells 50 The values were 159.4. Mu. Mol/L, 48.9. Mu. Mol/L and 13.1. Mu. Mol/L, respectively.
Experimental results show that the survival rate of MCF-7 cells is gradually reduced along with the increase of the concentration of cyclobuxine D, and the MCF-7 cells are in a dose-response relationship.
Example 2 cloning experiments to test the antiproliferative Capacity of cyclovirobuxine D
2000 MCF-7 cells in logarithmic growth phase are added to each well of a 6-well plate, and placed at 37 ℃ and 5% CO 2 Culturing in an incubator. After the cells are attached, the original culture medium is discarded, 2mL of fresh cell culture solution is added into a control group, 2mL of cyclovirobuxine D liquid which is diluted by the cell culture solution to the final concentration of 20 mu mol/L, 40 mu mol/L, 60 mu mol/L and 80 mu mol/L is respectively added into an experiment group, and the experiment group is placed into an incubator at 37 ℃ and contains 5% CO 2 After 24h incubation, the liquid was discarded, washed twice with 1mL of PBS buffer, and 2mL of cell culture medium was added to each well for further culture. The fluid was changed every 3d and the proliferation of the cell clone was observed.
After 14d, sufficient colonies have formed in each well of the 6-well plate (a plurality of cell masses greater than 10 cells have formed under microscopic observation). After the medium is discarded, 1mL of PBS buffer solution is used for carefully washing twice, 1mL of 4% paraformaldehyde is used for fixing cells for 10min in each hole, 1mL of 0.5% crystal violet staining solution is added in each hole, the staining solution is sucked and removed after the light-shielding staining for 10min, the residual staining solution is washed by tap water, and after the cells are naturally dried, a digital camera is used for photographing and recording.
FIG. 2 is a graph showing the cloning experiments of cyclobuxine D acting on MCF-7 cells.
The experimental results show that: with the increase of the concentration of the cyclobuxine D, the cloning number of the MCF-7 cell community is reduced, and the cloning capacity is gradually weakened, which shows that the cyclobuxine D has an inhibition effect on the growth and proliferation of MCF-7 cells and has the characteristic of concentration dependence.
Example 3 flow cytometry to determine the Effect of cyclovirobuxine D on MCF-7 cell cycle
Taking MCF-7 cells in logarithmic growth phase, centrifuging at 1000rpm for 3min, removing supernatant, adding 1mL cell culture solution, gently blowing to uniform cell suspension, counting with microscope, and collecting 1×10 cells 5 The density of each/mL was evenly added to a 6-well plate with 2mL per well and placed in an incubator overnight. Discarding the original culture medium, washing twice with 1mL PBS buffer solution, adding 2mL cell culture solution into control group, adding 80 μmol/L cyclovirobuxine D liquid medicine into drug group, and standing at 37deg.C with 5% CO 2 After incubation in an incubator for 24h under the conditions, the culture medium was discarded, washed twice with 1mL of PBS buffer, and after digestion of the cells with 500 μl of EDTA-free pancreatin per well, 1mL of cell culture medium was added to gently blow the cells, and the cell suspension was transferred to a 2mL centrifuge tube, placed in 4 ℃, and centrifuged at 2000rpm for 5min. Cells were washed 2 times with pre-chilled 1mL pbs each, the supernatant was discarded, 1mL of 70% absolute ethanol was used to re-suspend the cells, and the cells were left overnight at-20 ℃.
Before testing, at 4 ℃,2000rpm, centrifuging for 5min to remove the fixing solution, adding 500 mu L of PI/RNase A staining working solution (before using, the PI/RNase A working solution is prepared into the staining working solution according to the volume of 9:1 and is derived from a cell cycle kit) into each sample, incubating for 15min at room temperature in a dark place, filtering the cell suspension by a 200-mesh filter screen, and detecting the sample by a flow cytometer.
FIG. 3 is a graph of cell cycle distribution experiments of flow cytometry analysis of MCF-7 cells.
The results of fig. 3 show that: compared with the control group, the cyclovirobuxine D group has statistical difference * P < 0.05). Experiments show that: under the action of cyclobuxine D, the mitotic cycle of MCF-7 cells is changed and is S phase retardation. Thus, the cell S-phase retardation may be the mechanism of action of cyclovirobuxine D in inhibiting cancer cell proliferation.
Example 4 scratch assay to determine the Effect of cyclovirobuxine D on the ability to migrate breast cancer cells
Five lines are drawn on the back of each hole of the six-hole plate at uniform intervals along the ruler by using a marker.
MCF-7 cells in logarithmic growth phase were taken according to 1X 10 5 The density of each/mL was evenly added to a 6-well plate with 2mL per well and placed in an incubator overnight. After the cell wall had grown full, a 200. Mu.L gun head was used to scratch vertically along the line drawn (note that the gun head remained vertical during this process). Slowly washing with 1mL PBS for 2 times, washing away the scratched cells, adding 2mL cyclobuxine D liquid medicine with final concentration of 20 mu mol/L, 40 mu mol/L, 60 mu mol/L and 80 mu mol/L diluted by low serum culture solution into the medicine group, adding the same amount of low serum culture solution into the control group, continuously placing into an incubator for culturing, observing the scratch condition among the cells under a fluorescent inverted microscope at 0h, 24h and 48h respectively, and photographing and recording the experimental result.
FIG. 4 is a graph showing a scratch test of cyclovirobuxine D acting on MCF-7 cells.
FIG. 4 shows that cyclovirobuxine D can inhibit the migration of MCF-7 cells and has a dose-dependent effect on the inhibition of migration capacity.
The experimental results show that: the decrease of wound healing ability of MCF-7 cells after treatment with cyclobuxine D indicates that cyclobuxine D can inhibit the migration of MCF-7 cells, and the migration inhibition effect is related to the drug action concentration.
Example 5hoechst 33342 staining experiment to determine the Effect of cyclovirobuxine D on the ability to induce apoptosis in breast cancer cells
Taking MCF-7 cells in logarithmic growth phase, 5×10 4 Each cell/mL was inoculated into 6-well plates at 2mL per well, and placed at 37℃in 5% CO 2 Culturing in an incubator. After the cells are attached, the original cell culture solution is discarded, 2mL of cell culture solution is added into the medicine group to dilute the medicine group to obtain the cyclobuxine D medicine liquid with the final concentration of 20 mu mol/L, 40 mu mol/L, 60 mu mol/L and 80 mu mol/L, the equivalent cell culture solution is added into the control group, and the mixture is placed at 37 ℃ and contains 5% of CO 2 After incubation for 24h in an incubator under the condition, the liquid medicine is discarded, after washing twice with 1mL of PBS respectively, 2mL of 1 Xhoechst 33342 staining solution is added into each well, the mixture is placed in the incubator for incubation for 10min, the culture solution containing the dye is sucked, after washing twice with 1mL of PBS respectively, each well is added withAfter 1mL of the cell culture solution, the change of the cell nucleus morphology can be observed under a fluorescence microscope, and the result is recorded by photographing.
FIG. 5 is a chart showing the experiment of staining of MCF-7 cells with cyclovirobuxine D by hoechst 33342.
The results of fig. 5 show that: with the increase of the concentration of cyclobuxine D, chromatin in cells is condensed, brightness is improved, nucleus is split, which indicates that the cyclobuxine D can induce MCF-7 cells to die, and the higher the drug concentration is, the more the number of the apoptotic cells is increased.
Example 6 mitochondrial membrane potential detection experiments to determine the effects of cyclovirobuxine D on the ability to induce apoptosis in breast cancer cells
Taking MCF-7 cells in logarithmic growth phase, 1×10 5 Each cell/mL was inoculated into a 6-well plate at 2mL per well and placed in an incubator overnight. The original cell culture solution is discarded, 2mL of cyclobuxine D liquid medicine with the final concentration of 20 mu mol/L, 40 mu mol/L and 60 mu mol/L which is diluted by the cell culture solution is added into the medicine group, the equivalent cell culture solution is added into the control group, and the equivalent cell culture solution is added into the positive control group. Placing at 37deg.C, containing 5% CO 2 After 24h in an incubator under the condition, the positive control group is washed twice with 1mL of PBS, 2mL of CCCP working solution is added, and the temperature is 37 ℃ and the concentration of CO is 5% 2 Incubating in incubator under dark condition for 20min, discarding old cell culture solution in six-well plate, washing with 1mL PBS twice, adding 1mL cell culture solution and 1mL JC-1 staining working solution, and adding 5% CO at 37deg.C 2 Incubating in an incubator for 20min in dark under the condition, sucking the supernatant after the incubation, washing with 1mL of 1 XJC-1 staining buffer solution at 4 ℃ twice, adding 2mL of cell culture solution into each well, and observing under a fluorescence microscope.
When the mitochondrial membrane potential is high, JC-1 gathers in the matrix of mitochondria to form a polymer, and red fluorescence can be generated; at low mitochondrial membrane potential, JC-1 cannot be accumulated in the matrix of mitochondria, and JC-1 is a monomer and can generate green fluorescence. This allows for a very convenient detection of changes in mitochondrial membrane potential by fluorescence color transitions. The decrease in cell membrane potential can be readily detected by the transition of JC-1 from red to green fluorescence, and the transition of JC-1 from red to green fluorescence can also be used as a detection indicator for early apoptosis.
FIG. 6 is a graph showing the mitochondrial membrane potential test of cyclobuxine D acting on MCF-7 cells.
As the results in FIG. 6 show, MCF-7 cells treated with the positive control CCCP showed weaker red fluorescence (FIG. 6-a) and high density green fluorescence in the field of view (FIG. 6-b); high-density red fluorescence was observed after JC-1 staining of control cells (FIG. 6-c), and green fluorescence intensity was weaker (FIG. 6-d); as the concentration of cyclobuxine D increases, the red fluorescence of MCF-7 cells treated by cyclobuxine D is reduced (FIG. 6-e, FIG. 6-g, FIG. 6-i), the green fluorescence intensity is enhanced (FIG. 6-f, FIG. 6-h, FIG. 6-j), indicating that the membrane potential of MCF-7 cells treated by cyclobuxine D decreases to a degree related to the drug concentration.
The results of MTT experiment, cell cycle experiment, scratch experiment, hoechst33342 staining experiment and mitochondrial membrane potential detection experiment show that: cyclovirobuxine D can obviously inhibit proliferation and migration of human breast cancer MCF-7 cells, induce apoptosis, has the effect of resisting breast cancer, and can be used for preparing medicaments for treating breast cancer.
As described above, although the present invention has been shown and described with reference to certain preferred embodiments, it is not to be construed as limiting the invention itself. Various changes in form and details may be made therein without departing from the spirit and scope of the invention as defined by the appended claims.
Claims (10)
1. The application of cyclovirobuxine D in preparing medicine for treating breast cancer is provided.
2. The use according to claim 1, wherein cyclovirobuxine D inhibits proliferation and migration of MCF-7 cells of human breast cancer cells.
3. The use according to claim 1, wherein cyclovirobuxine D induces apoptosis in breast cancer cells.
4. The use according to claim 1, wherein cyclovirobuxine D acts on 24h, 48h and 72h IC of breast cancer cells MCF-7 cells 50 The values were 159.4. Mu. Mol/L, 48.9. Mu. Mol/L and 13.1. Mu. Mol/L, respectively.
5. The use according to claim 1, wherein the medicament comprises cyclovirobuxine D or a derivative or pharmaceutically acceptable salt thereof.
6. The use according to claim 5, wherein the pharmaceutically acceptable salt comprises a hydrochloride, phosphate, oxalate, sulfate or citrate salt.
7. The use according to claim 5, wherein the medicament further comprises pharmaceutically acceptable excipients.
8. The medicine according to claim 7, wherein the auxiliary materials comprise one or more of an emulsifier, a binder, a preservative, a diluent, a solubilizer, a disintegrant, an antioxidant, a wetting agent and a lubricant.
9. A medicament for treating breast cancer, which is characterized by comprising cyclovirobuxine D or a derivative or pharmaceutically acceptable salt thereof and pharmaceutically acceptable auxiliary materials.
10. The medicament according to claim 9, wherein the medicament is in the form of granules, tablets, capsules, pills, suspensions, solutions, injections or infusions.
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