CN109771428B - Application of tripterine and erastin in medicine for treating non-small cell lung cancer - Google Patents
Application of tripterine and erastin in medicine for treating non-small cell lung cancer Download PDFInfo
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Abstract
The invention discloses application of tripterine and erastin in a medicine for treating non-small cell lung cancer. Experiments prove that after 1-5 mu M tripterine and 1.25-5 mu M erastin are combined to treat the non-small cell lung cancer cells, the cell death of the cancer cells can be obviously induced, and the survival rate of the lung cancer cells is reduced, so that the effect of treating the lung cancer is achieved, and an important thought is provided in the aspect of clinical treatment of the lung cancer.
Description
Technical Field
The invention relates to application of tripterine and erastin in medicaments for treating non-small cell lung cancer, belonging to the field of medicaments.
Background
Lung cancer is one of the most common malignant tumors in the world, and has become the 1 st cause of death of malignant tumors in urban population in China. Non-small cell lung cancers include squamous cell carcinoma (squamous cell carcinoma), adenocarcinoma, large cell carcinoma, which have slower growth and division of cancer cells and relatively late metastasis compared to small cell carcinoma. Non-small cell lung cancer accounts for about 80% of all lung cancers, with about 75% of patients finding a very low 5-year survival rate at the middle and advanced stages.
In 2012, scientists discovered a new pattern of cell death, called iron death (ferroptosis), that was dependent on iron ions. Iron death differs from apoptosis, cellular necrosis and autophagy in morphology, biochemistry and genetics, and is mainly characterized by reduced mitochondrial shrinkage, increased density of bilayer membranes, reduced or eliminated mitochondrial cristae, and concomitant increase in cytoplasm and lipid Reactive Oxygen Species (ROS). It is now demonstrated that iron death is closely related to a variety of physiological and pathological processes such as tumor suppression, neuronal degeneration, antiviral immune response, and ischemia-reperfusion injury. Therefore, the deep research on the signaling pathway and the regulation mechanism of iron death has important significance for the treatment of related diseases, on one hand, cancer cells can be directly eliminated by triggering or intensifying iron death, or the sensitivity of the cancer cells to chemotherapy is increased; on the other hand, the iron death can be inhibited, and the pathological processes of ischemia-reperfusion injury, neurodegenerative diseases and the like can be inhibited or delayed.
Erastin, a classical inducer of iron death (ferroptosis), reduces GSH synthesis by inhibiting System Xc "in cells, reducing intracellular cystine uptake. Decreased GSH levels cause decreased intracellular GPX4 activity, leading to increased lipid peroxidation, accumulation of lipid ROS, and ultimately, cell iron death. Therefore, erastin induced iron death in cancer cells is also a new strategy for cancer treatment.
Tripterine is a quinone methyl triterpene substance, is red needle crystal, and has molecular formula of C29H38O4The relative molecular mass was 450.61. Tripterine, together with artemisinin, triptolide, capsaicin and curcumin, was listed by the Cell journal in 2007 as five traditional natural drug compounds most likely to be developed into modern drugs. In 1936, tripterine was first extracted and separated from radix Tripterygii Wilfordii by scientists, which initiated the research of tripterine. According to reports of a large number of documents, the tripterine has a plurality of remarkable pharmacological activities, such as anti-inflammatory and anti-oxidation, anti-atherosclerosis, anti-virus and neurodegenerative diseases (such as Parkinson's disease, Huntington's disease and Alzheimer's disease) and the like. Has potential prospect in the treatment of allergic asthma, amyotrophic lateral sclerosis, rheumatoid arthritis and other diseases. 2006, scientists have tried to elucidate the anticancer mechanism of tripterine after discovering the anticancer effect thereof, and since then, have triggered a hot tide in the research on the anticancer effect and mechanism of tripterine.
Tripterine as a natural proteasome inhibitor can affect multiple signal pathways and protein functions in cells, such as NF-kappa B, HSP 90, proteasome, c-Jun, AKT/mTOR, VEGFR and the like, and can induce apoptosis of multiple tumor cells. It is commonly used for treating leprosy, rheumatic arthritis and other autoimmune diseases in clinic. However, according to clinical observation and literature reports, the main toxic and side effects of tripterine are represented by damages to reproductive, endocrine and digestive systems, especially damages to blood systems and skin mucosa. The clinical application of tripterine is limited by the large toxic and side effects of tripterine. However, at low concentrations, tripterine is not likely to produce toxic side effects, and its significant activity in inducing tumor cell apoptosis is being continuously confirmed by experiments.
Therefore, how to improve the antitumor effect of tripterine within the biological safety dose has become a research hotspot, and the research on the effect and mechanism of the tripterine on the erastin-induced iron death is very little.
Disclosure of Invention
In view of the above, the invention provides an application of tripterine and erastin in a medicine for treating non-small cell lung cancer. The invention uses non-small cell lung cancer cells as experimental materials, focuses on the tumor iron death, deeply studies the action and molecular mechanism of tripterine with different concentrations on the iron death induced by erastin, and simultaneously promotes the cancer cell death by reducing the toxic and side effect of the tripterine, thereby providing theoretical basis and new approach for the treatment of cancer.
The medicine composition for treating non-small cell lung cancer comprises the following raw materials: tripterine and erastin, wherein the effective concentration of tripterine is 1-5 μ M, and the effective concentration of erastin is 1.25-5 μ M.
Further, the composition also comprises one or more pharmaceutically acceptable pharmaceutical excipients, wherein the pharmaceutical excipients are one or more of cosolvent, emulsifier, solubilizer, osmotic pressure regulator, binder, filler, disintegrant, lubricant, preservative and antioxidant.
The tripterine is used as a natural proteasome inhibitor, can influence various signal pathways and protein in cells to play roles, is not easy to generate toxic or side effect due to low-concentration tripterine, and has obvious activity in the aspect of inducing tumor cell apoptosis. erastin decreases GSH synthesis by inhibiting the cystine/glutamate antiporter System Xc "on the cell membrane, reducing intracellular cystine uptake. Decreased GSH levels cause decreased intracellular GPX4 activity, leading to increased lipid peroxidation, accumulation of lipid ROS, and ultimately, cell iron death. After 1-5 mu M tripterine and 1.25-5 mu M erastin are combined to treat the non-small cell lung cancer cells, the cell death of the cancer cells can be obviously induced, and the survival rate of the lung cancer cells is reduced, so that the effect of treating the lung cancer is achieved.
The invention has the following advantages:
(1) the medicinal composition has simple use mode and better medicinal effect, and the proliferation inhibition effect of the non-small cell lung cancer cells is enhanced along with the prolonging of the action time;
(2) the safety is high, the side effect is low, the cell death of cancer cells can be obviously induced, the survival rate of lung cancer cells is reduced, and no damage is caused to other functions of an organism;
(3) low cost and suitability for large-scale production.
Drawings
FIG. 1 is a diagram showing the effect of the CCK-8 method of the present invention in detecting the activity of erastin with different concentrations on human NSCLC cells in example 1;
FIG. 2 is a diagram illustrating the effect of the CCK-8 method of detecting tripterine of different concentrations on the activity of human NSCLC cells in example 2 of the present invention;
FIG. 3 is a graph showing the effect of CCK-8 method for detecting erastin and tripterine on the viability of human NSCLC cells;
FIG. 4 is a graph showing the effect of flow cytometry for detecting the simultaneous treatment of erastin and tripterine on the ROS level in human NSCLC cells in example 4 of the present invention;
FIG. 5 is a graph showing the effect of observing the simultaneous treatment of erastin and tripterine on the morphology of human NSCLC cells in example 5 of the present invention;
FIG. 6 is a graph showing the effect of erastin in combination with tripterine on the growth of non-small cell lung cancer transplanted tumors in nude mice in example 6 of the present invention;
FIG. 7 is a bar graph showing the observation that erastin in combination with tripterine inhibited the growth of non-small cell lung cancer nude mouse transplanted tumors in example 6 of the present invention;
Detailed Description
The technical solutions in the embodiments of the present invention will be clearly and completely described below with reference to the drawings in the embodiments of the present invention, and it is obvious that the described embodiments are only a part of the embodiments of the present invention, and not all of the embodiments. All other embodiments, which can be derived by a person skilled in the art from the embodiments given herein without making any creative effort, shall fall within the protection scope of the present invention.
Example 1
CCK-8 method for detecting influence of erastin on human non-small cell lung cancer cell viability
Principle of experiment
The reagent CCK-8 containing WST-8 (chemical name: 2- (2-Methoxy-4-nitrophenyl) -3- (4-nitrophenyl) -5- (2, 4-disulfonic acid benzene) -2H-tetrazole monosodium salt) is a compound similar to MTT, which can be reduced by intramitochondrial dehydrogenases in the presence of an electron coupling reagent 1-Methoxy-5-methylphenazinium dimethyl sulfate (1-Methoxy PMS) to Formazan (refer to FIG. 1), which is a highly water-soluble orange-yellow Formazan product, and the amount of Formazan produced is proportional to the number of living cells. Therefore, the cell proliferation and toxicity analysis can be directly carried out by utilizing the characteristic, and the more the cell proliferation is faster, the darker the color is; the more cytotoxic, the lighter the color. The absorbance was measured at a wavelength of 450nm using a microplate reader and the Formazan product Formazan was formed in an amount proportional to the number of cells. The number of living cells was judged from the measured absorbance value (OD value), and the larger the OD value, the stronger the cell activity.
Laboratory instruments and materials
Cell culture incubator (Thermo Fisher), ELX-800 microplate reader (BioTek), inverted microscope (LEICA DMIRB), fetal bovine serum (Biological Industries), DMEM (high sugar) medium (GIBCO), CCK-8(MCE), dmso (sigma), erastin (selleck), 96-well cell culture plate (NEST), non-small cell lung cancer cell (HCC827 cell, shanghai cell institute of the chinese academy of sciences).
Experimental procedure
Non-small cell lung cancer cells were seeded at a density of about 8000 cells/well in 96-well plates at 37 ℃ with 5% CO2And culturing in a cell culture box containing DMEM high-sugar culture solution containing 10% fetal calf serum. When the cell density reaches 70-80%, adding erastin with final concentration of 0, 0.625, 1.25, 2.5, 5, 10, 20 μ M gradient to pass through DMSOThe treated cells were negative control groups, each cell was plated with three duplicate wells. After further culturing for 24 hours, the morphology was observed under an inverted microscope. Preparing a culture medium containing 10% of CCK-8, adding the culture medium into each hole in a liquid changing mode, incubating in an incubator for a certain time, measuring the absorbance at 450nm, and detecting the influence of erastin with different concentrations on the activity of the human non-small cell lung cancer cells, wherein the result is shown in figure 1.
Cell viability was calculated as follows: the cell survival rate is equal to the OD value of the experimental group/the OD value of the blank control group multiplied by 100 percent; data statistics are expressed as mean ± standard deviation (x ± s) using the t-test.
As shown in FIG. 1, the survival rate of non-small cell lung cancer cells gradually decreased with the increase of erastin concentration, and the IC 50 value was 6.263. mu.M. The results indicate that erastin can reduce the survival rate of the non-small cell lung cancer cells, and the survival rate is reduced in a concentration-dependent manner.
Example 2
CCK-8 method for detecting influence of tripterine on human non-small cell lung cancer cell activity
Principle of experiment same as example 1
Laboratory instruments and materials
Cell culture incubator (Thermo Fisher), ELX-800 microplate reader (BioTek), inverted microscope (LEICA DMIRB), fetal bovine serum (Biological Industries), DMEM (high sugar) medium (GIBCO), CCK-8(MCE), dmso (Sigma), celastrol (Sigma), 96-well cell culture plate (NEST), non-small cell lung cancer cell (HCC827 cell, shanghai cell institute of the chinese academy).
Experimental procedure
Non-small cell lung cancer cells were seeded at a density of about 8000 cells/well in a 96-well plate and cultured at 37 ℃ in a cell culture chamber containing 5% CO2 in DMEM high-glucose medium containing 10% fetal bovine serum. When the cell density reaches 70-80%, tripterine with final gradient concentration of 0, 0.625, 1.25, 2.5, 5, 10, 20 μ M is added, and DMSO-treated cells are used as negative control group, and each cell is provided with three multiple wells. After further culturing for 24 hours, the morphology was observed under an inverted microscope. Preparing a culture medium containing 10% of CCK-8, adding the culture medium into each hole in a liquid changing mode, incubating in an incubator for a certain time, and then measuring the absorbance at 450 nm. The results of detecting the effect of tripterine with different concentrations on the activity of human non-small cell lung cancer cells are shown in fig. 2.
Cell viability was calculated as follows: the cell survival rate is equal to the OD value of the experimental group/the OD value of the blank control group multiplied by 100 percent; data statistics are expressed as mean ± standard deviation (x ± s) using the t-test.
As shown in FIG. 2, the survival rate of the NSCLC cells gradually decreased with the increase of the tripterine concentration, and the IC 50 value was 3.812 μ M. The results show that the tripterine can reduce the survival rate of the non-small cell lung cancer cells, and the survival rate is reduced in a concentration dependence way.
Example 3
CCK-8 method for detecting influence of erastin and tripterine on human non-small cell lung cancer cell activity
Principle of experiment same as example 1
Laboratory instruments and materials
Cell culture incubator (Thermo Fisher), ELX-800 microplate reader (BioTek), inverted microscope (LEICA DMIRB), fetal bovine serum (Biological Industries), DMEM (high sugar) medium (GIBCO), CCK-8(MCE), dmso (Sigma), erastin (selleck), tripterine (Sigma), 96-well cell culture plate (NEST), non-small cell lung cancer cell (HCC827 cell, shanghai cell institute of the chinese academy of sciences).
Experimental procedure
Non-small cell lung cancer cells were seeded at a density of about 8000 cells/well in a 96-well plate and cultured at 37 ℃ in a cell culture chamber containing 5% CO2 in DMEM high-glucose medium containing 10% fetal bovine serum. When the cell density reaches 70-80%, 2.5 μ M erastin and tripterine with final gradient concentrations of 0, 0.3, 0.625, 1.25, 2.5, and 5 μ M are added, and DMSO-treated cells are used as negative control group, and each cell is provided with three wells. After further culturing for 24 hours, the morphology was observed under an inverted microscope. Preparing a culture medium containing 10% of CCK-8, adding the culture medium into each hole in a liquid changing mode, incubating in an incubator for a certain time, and then measuring the absorbance at 450 nm. The results of detecting the effect of simultaneous treatment of erastin and tripterine on the activity of human non-small cell lung cancer cells are shown in fig. 3.
Cell viability was calculated as follows: the cell survival rate is equal to the OD value of the experimental group/the OD value of the blank control group multiplied by 100 percent; data statistics are expressed as mean ± standard deviation (x ± s) using the t-test.
As shown in FIG. 3, when 2.5. mu.M of erastin and 1.25-5. mu.M of tripterine were used to treat non-small cell lung cancer cells simultaneously, the cell death rate was increased in a tripterine concentration-dependent manner.
Example 4
Flow cytometry for detecting influence of erastin and tripterine on ROS level in human non-small cell lung cancer cells
Principle of experiment
Reactive Oxygen Species (ROS) are partial reduction products of oxygen during the metabolism of the body. ROS play an important role in vital activities, and low levels of ROS help to suppress inflammatory responses and promote cell proliferation. However, high levels of ROS can promote anti-tumor signaling and induce tumor cell senescence and death. Since tumor cells need to maintain higher levels of ROS homeostasis, anticancer therapies that modulate ROS have potential utility.
DCFH-DA (2, 7-dichlorofluorescein protein acetate) is a cell permeable, non-labeled, oxidation sensitive fluorescent probe. DCFH-DA (2, 7-dichlorofluorescein protein acetate) is hydrolyzed by cellular esterase to 2, 7-dichlorotetrafluorodioxane (2, 7-dichlorofluorescein protein, DCFH.) DCFH is unable to permeate the cell membrane, thereby loading the probe into the cell. Reactive oxygen species in the cell can then oxidize non-fluorescent DCFH to produce fluorescent DCF, thereby determining the level of intracellular ROS as a function of fluorescence intensity. The probe is widely used for detecting cell redox reaction.
Laboratory instruments and materials
Cell culture chamber (Thermo Fisher), DCFH-da (Sigma), flow cytometer facscalibur (bd), fetal bovine serum (Biological Industries), DMEM (high sugar) medium (GIBCO), dmso (Sigma), erastin (selleck), tripterine (Sigma), 10cm cell culture plate (NEST), non-small cell lung cancer cell (HCC827 cell, shanghai cell institute of chinese academy).
Experimental procedure
Non-small cell lung cancer cells are treated at a rate of about 2X 106The cells were plated at a density of 10cm cell culture dish at 37 ℃ in 5% CO2And culturing in a cell culture box containing DMEM high-sugar culture solution containing 10% fetal calf serum. When the cell density reached 70-80%, 2.5. mu.M erastin and 1.25. mu.M tripterine were added for 24h, and DMSO-treated cells were used as negative control groups, with three replicates for each cell. After the treatment, the cells were gently washed 2-3 times with 1 XPBS. PBS was discarded and appropriate dilutions of DCFH-DA ROS probe at a final concentration of 10uM were added. The cells were returned to 37 ℃ and incubated in a 5% CO2 incubator protected from light. After 30min the supernatant was discarded, followed by gentle washing 2 times with 1 × PBS to wash off excess ROS probe. The cells were then digested with pancreatin and centrifuged at 800rpm at 4 ℃ for 3 min. After collecting cells, gently washing 1 time with 1 × PBS, then adding 500ul of 1 × PBS to each centrifuge tube, after resuspending the cells with a pipette, transferring to BD Calibur flow-type loading tube, and detecting DCFH-DA staining positive cells with a flow cytometer FL1 channel. At least 10,000 cells were detected in each sample, and the intracellular ROS level changes were analyzed by flow Jo calculation in combination with flow cytometry analysis software and ROS profiles were generated as shown in FIG. 4.
As can be seen in FIG. 4, while a single treatment of 2.5 μ M erastin and 1.25 μ M tripterine slightly increased intracellular ROS levels, the combined treatment of erastin and tripterine significantly increased intracellular ROS levels.
Example 5
Influence of erastin and tripterine on human non-small cell lung cancer cell morphology during simultaneous treatment
The experimental principle is as follows:
observing the morphological change of the non-small cell lung cancer cell after the combined treatment of erastin and tripterine.
Laboratory instruments and materials
Cell culture incubator (Thermo Fisher), inverted microscope (Olympus), fetal bovine serum (Biological Industries), DMEM (high-sugar) medium (GIBCO), CCK-8(MCE), dmso (Sigma), erastin (seleck), celastrol (Sigma), 10cm cell culture dish (NEST), non-small cell lung cancer cell (HCC827 cell, shanghai cell institute of chinese academy of sciences).
Experimental procedure
Non-small cell lung cancer cells are treated at a rate of about 2X 106The density of each cell was seeded in 10cm cell culture dishes at 37 ℃ in 5% CO2And culturing in a cell culture box containing DMEM high-sugar culture solution containing 10% fetal calf serum. When the cell density reached 70-80%, 2.5. mu.M erastin and 1.25. mu.M tripterine were added, and DMSO-treated cells were used as negative control. After further culturing for 24 hours, the morphology was observed under an inverted microscope.
The effect of simultaneous treatment of erastin and tripterine on the morphology of non-small cell lung cancer cells was observed under an inverted microscope, and the results are shown in FIG. 5.
As shown in FIG. 5, when 2.5. mu.M of casein and 1.25. mu.M of tripterine were simultaneously used to treat cells, the cell morphology was significantly changed, inducing cell death.
The result shows that the combination treatment of the tripterine with small concentration and the erastin with small concentration can remarkably induce the cancer cells to generate cell death and reduce the survival rate of the lung cancer cells, thereby achieving the effect of treating the lung cancer.
Example 6
erastin combined with tripterine for inhibiting growth of non-small cell lung cancer nude mouse transplanted tumor
The experimental principle is as follows:
the nude mouse xenograft tumor model has the characteristics of short modeling period, high success rate, and the shape and biological functions of the original human cancer still remained in the tumor tissue, so the nude mouse xenograft tumor model is widely applied to the screening of anti-tumor drugs and the clinical research of cancer occurrence and development. In the experiment, HCC827 cells are selected as objects, a humanized non-small cell lung cancer xenograft tumor model is established, and the in vivo inhibition effect of low-concentration erastin and tripterine combined treatment on lung cancer is investigated.
Laboratory instruments and materials
Cell culture incubator (Thermo Fisher), fetal bovine serum (Biological Industries), DMEM (high glucose) medium (GIBCO), erastin (selleck), tripterine (Sigma), 10cm cell culture dish (NEST), non-small cell lung cancer cell (HCC827 cell, shanghai cell institute of chinese academy), BALB/c nude mouse (beijing huafukang).
Experimental procedure
The cell culture step is repeated, culturing a sufficient number of cells for seeding. On the day of inoculation, all cells were collected, diluted to 1X 10 with PBS60.2 ml. Before preparation for inoculation, 6 male nude mice of each group were equally distributed according to body weight (SPF grade, body weight 20. + -.2 g). Non-small cell lung cancer HCC827 cells are cultured at a temperature of about 1 × 106The number of individuals was inoculated subcutaneously into the right hind limb of nude mice, and then the growth state and tumor volume of the nude mice were measured in time. When the tumor size of the experimental nude mice reaches 50mm3In the meantime, nude mice with similar tumor size and body weight were selected and divided into 4 groups: (1) a model control group; (2)5mg/kg erastin treatment group; (3)1mg/kg tripterine treatment group; (4)5mg/kg erastin +1mg/kg tripterine combined treatment group. The model group was administered with the mixed solution of the dissolved drug, and the latter three groups were administered by intraperitoneal injection once a day in accordance with the body weight. The body weight and the tumor volume of the nude mice were measured every 3 days, and the analysis data was recorded. After 2 weeks of drug treatment, nude mice were euthanized, tumor tissue was dissected out, and volume recordings were made with the results shown in fig. 6-7.
Tumor volume in nude mice was calculated as follows: tumor volume (mm)3) Long diameter x short diameter2×0.5。
As can be seen from FIGS. 6-7, the tumor size was reduced in the nude mice of the single-treatment group of 5mg/kg erastin or 1mg/kg tripterine, as compared with the model group; compared with the model group and the drug single treatment group, the tumor inhibition rate is obviously increased when 5mg/kg of erastin and 1mg/kg of tripterine are treated in a combined way, and the tumor size of the nude mice is obviously reduced (p is less than 0.001).
The results show that the combined treatment of small concentrations of erastin and tripterine can significantly inhibit the tumor growth of HCC827 tumor-bearing mice.
Claims (1)
1. The application of the tripterine and the erastin in preparing the medicine for treating the non-small cell lung cancer is characterized in that:
the medicine for treating the non-small cell lung cancer comprises the following raw materials: tripterine and erastin, wherein the effective concentration of tripterine is 1.25 or 2.5 μ M, and the effective concentration of erastin is 2.5 μ M;
the medicine also comprises one or more pharmaceutically acceptable medicinal excipients, wherein the medicinal excipients are one or more of cosolvent, emulsifier, solubilizer, osmotic pressure regulator, adhesive, filler, disintegrant, lubricant, preservative and antioxidant.
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| CN101352444A (en) * | 2008-09-11 | 2009-01-28 | 中国科学院广州生物医药与健康研究院 | New use of tripterine in pharmacy |
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| CN101352444A (en) * | 2008-09-11 | 2009-01-28 | 中国科学院广州生物医药与健康研究院 | New use of tripterine in pharmacy |
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| Title |
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| Upregulation and activation of p53 by erastin-induced reactive oxygen species contribute to cytotoxic and cytostatic effects in A549 lung cancer cells;CHAOLI HUANG 等;《ONCOLOGY REPORTS》;20181031;第40卷(第4期);第2363-2370页 * |
| 雷公藤红素对非小细胞肺癌细胞株H1299增殖与凋亡的影响;陈国柱 等;《生物技术通讯》;20081131;第19卷(第6期);第826-829页 * |
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