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The aim of the present study was to evaluate the in vitro antiproliferative activity of ethanolic extract of leaves and fruits Citrus paradisi plant on HepG-2 liver cell lines by MTT (3-(4, 5-dimethyl-2-thiazolyl)-2,5-diphenyl-2Hterazolium bromide) assay and to isolate and characterize the antiproliferative compounds by TLC (Thin layer chromatography) and FT-IR (Fourier transforms Infrared) spectroscopy. Qualitative phytochemical screening tests were performed to detect phytochemicals compounds from the crude extracts. Antioxidant activity of the plant extracts were characterized by using DPPH (2,2-Diphenyl-1-picrylhydrazyl) free radical scavenging method. The results showed that antioxidant activity using DPPH were found to be increased in a concentration dependent manner and decreased cell viability and cell growth inhibition in a dose dependent manner. The findings from this study indicated that fruit extract exhibited good antiproliferation and antioxidant potential. The seven functional groups of phytocompounds such as carboxylic acid, amine salt, aromatic compounds, cyclic alkene, aldehyde, fluoro compounds and alkene were detected by FT-IR which indicated that fruit extracts of Citrus paradisi possessed vast potential as a medicinal drug especially in liver cancer treatment.
O objetivo do presente estudo foi avaliar a atividade antiproliferativa in vitro do extrato etanólico de folhas e frutos da planta Citrus paradisi em linhagens de células hepáticas HepG-2 por MTT (3- (4, 5-dimetil-2-tiazolil) -2, Ensaio de brometo de 5-difenil-2H-terazólio) e isolar e caracterizar os compostos antiproliferativos por espectroscopia de TLC (cromatografia de camada fina) e FT-IR (infravermelho com transformadas de Fourier). Testes qualitativos de triagem fitoquímica foram realizados para detectar compostos fitoquímicos nos extratos brutos. A atividade antioxidante dos extratos vegetais foi caracterizada pelo método de eliminação de radicais livres DPPH (2,2-difenil-1-picrilhidrazil). Os resultados mostraram que a atividade antioxidante usando DPPH aumentou de uma maneira dependente da concentração e diminuiu a viabilidade celular e a inibição do crescimento celular de uma maneira dependente da dose. Os resultados deste estudo indicaram que o extrato de fruta exibiu bom potencial antiproliferação e antioxidante. Os sete grupos funcionais de fitocompostos, como ácido carboxílico, sal de amina, compostos aromáticos, alceno cíclico, aldeído, compostos de flúor e alceno, foram detectados por FT-IR, o que indicou que extratos de frutas de Citrus paradisi possuíam vasto potencial como medicamento, especialmente no tratamento de câncer do fígado.
Subject(s)
Humans , Citrus paradisi , Liver Neoplasms/drug therapy , Plant Extracts/pharmacology , Cell Line , Spectroscopy, Fourier Transform Infrared , Phytochemicals , AntioxidantsABSTRACT
Abstract The aim of the present study was to evaluate the in vitro antiproliferative activity of ethanolic extract of leaves and fruits Citrus paradisi plant on HepG-2 liver cell lines by MTT (3-(4, 5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-terazolium bromide) assay and to isolate and characterize the antiproliferative compounds by TLC (Thin layer chromatography) and FT-IR (Fourier transforms Infrared) spectroscopy. Qualitative phytochemical screening tests were performed to detect phytochemicals compounds from the crude extracts. Antioxidant activity of the plant extracts were characterized by using DPPH (2,2-Diphenyl-1-picrylhydrazyl) free radical scavenging method. The results showed that antioxidant activity using DPPH were found to be increased in a concentration dependent manner and decreased cell viability and cell growth inhibition in a dose dependent manner. The findings from this study indicated that fruit extract exhibited good antiproliferation and antioxidant potential. The seven functional groups of phytocompounds such as carboxylic acid, amine salt, aromatic compounds, cyclic alkene, aldehyde, fluoro compounds and alkene were detected by FT-IR which indicated that fruit extracts of Citrus paradisi possessed vast potential as a medicinal drug especially in liver cancer treatment.
Resumo O objetivo do presente estudo foi avaliar a atividade antiproliferativa in vitro do extrato etanólico de folhas e frutos da planta Citrus paradisi em linhagens de células hepáticas HepG-2 por MTT (3- (4, 5-dimetil-2-tiazolil) -2, Ensaio de brometo de 5-difenil-2H-terazólio) e isolar e caracterizar os compostos antiproliferativos por espectroscopia de TLC (cromatografia de camada fina) e FT-IR (infravermelho com transformadas de Fourier). Testes qualitativos de triagem fitoquímica foram realizados para detectar compostos fitoquímicos nos extratos brutos. A atividade antioxidante dos extratos vegetais foi caracterizada pelo método de eliminação de radicais livres DPPH (2,2-difenil-1-picrilhidrazil). Os resultados mostraram que a atividade antioxidante usando DPPH aumentou de uma maneira dependente da concentração e diminuiu a viabilidade celular e a inibição do crescimento celular de uma maneira dependente da dose. Os resultados deste estudo indicaram que o extrato de fruta exibiu bom potencial antiproliferação e antioxidante. Os sete grupos funcionais de fitocompostos, como ácido carboxílico, sal de amina, compostos aromáticos, alceno cíclico, aldeído, compostos de flúor e alceno, foram detectados por FT-IR, o que indicou que extratos de frutas de Citrus paradisi possuíam vasto potencial como medicamento, especialmente no tratamento de câncer do fígado.
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Objective:To investigate the effect of pulsed electric field (PEF) combined with low temperature plasma (LTP) on mouse liver cancer cell.Methods:H22 mouse liver cancer cells were divided into liver cancer group, PEF treatment group, LTP treatment group, combined group A (first PEF treatment immediately after LTP treatment), combined group B (first LTP treatment immediately after PEF treatment), combined group C (same as combined group A, but 20 minutes interval) and combined group D (same as combined group B, but 20 minutes interval). Cell viability was detected by cell counting, apoptosis was detected by flow cytometry, intracellular reative oxygen species (ROS) was marked by fluorescence and counted. Twenty healthy female Kunming mouse aged 4-6 weeks without specific pathogens were subcutaneous injected with liver cancer cells, and then were randomly divided into model group, PBS control group, PEF experimental group, LTP experimental group and combined group (LTP+ PEF, no interval) ( n=4). Tumor relative volume and tumor inhibition rate were measured. Results:The survival rates were liver cancer cell group (98.3±0.9)%, PEF treatment group (66.8±4.4)%, LTP treatment group (62.1±3.9)%, combined group A (43.7±3.7)%, combined group B (31.0±1.4)%, combined group C (46.8±2.9)%, combined group D (39.0±2.3)%. Compared with liver cancer cell group, the cell survival rate of all treatment groups was decreased, and the cell survival rate of the four combined treatment group was lower than that of PEF treatment group and LTP treatment group, the differences were statistically significant (all P<0.05). The survival rate of combined B group was the lowest. The results of apoptosis detection were consistent with those of cell survival rate. Under fluorescence microscope, the ROS fluorescence of cells in the combined group B was significantly increased, and the ROS fluorescence of cells in the LTP treatment group was more than that in the PEF treatment group, and the percentage of ROS positive cells in the combined group B was higher than that in the LTP treatment group and the PEF treatment group, with statistical significance (all P<0.05). Tumor relative volume and tumor inhibition rate in the combined group were better than those in the PEF and LTP groups, and the differences were statistically significant (all P<0.05). Conclusion:LTP combined with PEF has a better killing effect on H22 cells than PEF or LTP treatment, which is expected to be a new tumor therapy.
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Objective: To investigate the effect of Clerodendrum bungei-containing serum on liver cancer MHCC97-H cells and its possible mechanism from the perspective of phosphatidylinositol 3-kinase(PI3K)/protein kinase (Akt) signaling pathway. Method: The medicinal serum of 15% C. bungei was used to treat MHCC97-H cells. The effect of serum containing C. bungei on cell proliferation was observed by cell counting kit-8(CCK-8) method, in order to select the best time and concentration. The apoptosis was detected by Annexin V-FITC/PI double staining method. Western blot was used to detect the posphatase and tensin homologous gene deleted from chromosome 10 in key proteins (PTEN), phosphoprotein kinase B (p-Akt) and phosphatidylinositol 3-kinase (PI3K)-related protein expression of PI3K/Akt signaling pathway. Real-time PCR was used to detect C. bungei-containing serum on cells for 72 h after activation of nuclear factor-activated B cell kappa light chain(NF-κB) and tumor necrosis factor-α (TNF-α) mRNA expression. Result: The results of CCK-8 showed an inhibitory effect of the C. bungei-containing serum on the proliferation of tumor cells in a dose and time-dependent manner. Among them, the high-dose group had the most obvious inhibitory effect, and the maximum inhibition rates at 24, 48,72 h were 28%, 32%, and 43%, respectively. The results of flow cytometry showed that with the increase of drug-containing serum concentration, the cell growth was observed. The inhibition rate of cells was increased to different degrees, and the inhibition effect was significantly increased in the 72 h intervention group (PC. bungei-containing serum group was 19.48% and 19.72%, compared with the blank group. The difference was significant (PC. bungei-containing serum (PPC. bungei-containing serum could down-regulate the expression of NF-κB and up-regulate the expression of TNF-α mRNA (PConclusion: The medicinal serum of C. bungei can effectively inhibit the proliferation of MHCC97-H hepatoma cells and promote its apoptosis, which may be related to the PI3K/Akt signaling pathway and its key factors.
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Objectives: To analyze the effect of human placental extracts (HPEx) on hepatocellular carcinoma cells in vitro. Methods: The hepatocellular carcinoma cell lines, namely, HLE and Huh-7, were used. The cells were subjected to a growth assay using the formazan dye method; the effect of combination treatment with sorafenib and HPEx was also assessed. The preventing normal cell damage effect of HPEx was analyzed by virtual therapy where possible; the experimental protocol was constructed on the basis of pre- and post-sorafenib treatment data. Cytotoxicity was measured by lactate dehydrogenase (LDH) assay. Results: HPEx caused significant dose-dependent suppression in the growth of HLE and Huh-7 cells. These tumor cells were significantly suppressed by combination treatment with HPEx and sorafenib. In addition, HPEx potentiated sorafenib sensitivity against tumor cells, and significantly prevented sorafenib-induced cytotoxicity in primary cultured rat hepatocytes under all designed experimental conditions. Specifically, pre-treatment with HPEx had a greater effect than post-treatment with HPEx. Conclusion: HPEx suppresses tumor cell growth, potentiates sorafenib efficacy, and has a preventing normal cell damage effect; this triple functionality of HPEx makes it a useful agent for liver cancer therapy.
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Background and purpose:Low intensity ultrasound (LIUS) can kill cancer cells and promote their apoptosis. However, it is still unknown how it affects the migration and invasion of tumor cells. This study aimed to explore the effect of LIUS on human hepatocellular line MHCC97H in migration and metastasis and the possible mechanismin vitro.Methods:According to the intensity of ultrasonic irradiation, 4 experimental groups were established: control group (0 W/cm2), 0.5 W/cm2, 1.0 W/cm2 and 1.5 W/cm2group. The migration and invasion ability of hepatocellular cells was detected by scratch assay and Transwell migration and invasion assay after the irradiation of LIUS. The changes of cytoskeleton after irradiation were observed by microscope and F-actin green lfuorescence staining. The expressions of MMP-2 and MMP-9 were examined by real-time lfuorescent quantitative polymerase chain reaction (RTFQ-PCR) and Western blot.Results:Low intensity ultrasound (≤1.5 W/cm2) promoted the migration and invasion of hepatocellular line MHCC97H. Scratch assay and Transwell assay showed much more cells under irradiation migrated through membrane than untreated. It was found that morphology of liver cancer cells changed after LIUS irradiation using optical microscope and lfuorescence microscope. The results of RTFQ-PCR and Western blot showed upregulation of MMP-2 expression by LIUS in MHCC97H and high expression of MMP-9 mRNA. Conclusion:Low intensity ultrasound may promote the migration and invasion of MHCC97H through changing cytoskeleton and upregulating protein expression of MMP-2.
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OBJECTIVES@#To build GPC3 gene short hairpin interference RNA (shRNA) slow virus vector, observe expression of Huh-7 GPC3 gene in human liver cell line proliferation apoptosis and the effect of GPC3 gene influencing on liver cancer cell growth, and provide theoretical basis for gene therapy of liver cancer.@*METHODS@#Hepatocellular carcinoma cell line Huh-7 was transfected by a RNA interference technique. GPC3 gene expression in a variety of liver cancer cell lines was detected by fluorescence quantitative PCR. Targeted GPC3 gene sequences of small interfering RNA (siRNA) PGC-shRNA-GPC3 were restructured. Stable expression cell lines of siRNA were screened and established with the help of liposomes (lipofectamine(TM2000)) as carrier transfection of human liver cell lines. In order to validate siRNA interference efficiency, GPC3 siRNA mRNA expression was detected after transfection by using RT-PCR and Western blot. The absorbance value of the cells of blank group, untransfection group and transfection group, the cell cycle and cell apoptosis were calculated, and effects of GPC3 gene on Huh-7 cell proliferation and apoptosis were observed.@*RESULTS@#In the liver cancer cell lines Huh-7, GPC3 gene showed high expression. PGC-shRNA-GPC3 recombinant plasmid was constructed successfully via sequencing validation. Stable recombinant plasmid transfected into liver cancer cell lines Huh-7 can obviously inhibit GPC3 mRNA expression level.@*CONCLUSIONS@#The targeted GPC3 siRNA can effectively inhibit the expression of GPC3.
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Objective To discuss the proliferation inhibition, apoptosis-inducing effects and the mechanism of dihydromyricetin on human liver cancer HepG2. Methods The effects of dihydromyricetin on cell death rate and proliferation in light of MTT test were examined and IC50 was calculated. The effects of dihydromyricetin on liver cancer HepG2 in different cell cycles were observed and analyzed in light of HE fluorescent staining method and Annexin V-PI flow cytometry (FCM). The protein expressions of p34cdc-2、CyclinB1、Bcl-2 and PARP which were related to the cell cycle and apoptosis before and after the use of dihydromyricetin were determined in light of Western blotting. Results The death rate of liver cancer HepG2 were increased with the increasing of dihydromyricetin concentration. The IC50 read (35.22 ± 1.56)μmol/L and displayed dose-response relationship. Dihydromyricetin had significant impacts on liver cancer HepG2 in different cell cycles, the proportion of G2/M cells rose dramatically and that of S cells lowered sharply and that of G0/G1 cell decreased exponentially.The difference was of statistical significance compared with the control group (P < 0.05). Conclusion Dihydromyricetin has distinct medical effects on inhibiting the growth and inducing the apoptosis of liver cancer HepG2. The mechanism is to activate Caspase-3,thus engaged in apoptosis in light of signal transduction of the mitochondrion.
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ObjectiveTo investigate the targeting infection of single chain antibody againstAFP (scFv anti-AFP) directed lentivirus and the inhibitory effects of a dual-growth inhibition systemon hepatocarcinoma cells.MethodsPlasmids WtP53-pPRIME-miR30-shRNA-IGF1R,pMD2G-Anti-AFP,and psPAX2 have previously been constructed to cotransfect to the packaging cell line 293Tusing Lipofectamine2000.The infection results were observed through fluorescence microscopy.PCRand Western blotting were used to demonstrate the successful transduction and transcription of theWtP53-pPRIME-miR30-shRNA-IGF1R gene.The effects of reconstructed lentivirus infected liver cellgrowth were assessed by the cell growth curve of CCK8 cells. Apoptosis was evaluated by theTUNEL assay.ResultsRecombined lentivirus was successfully constructed with the functional PFUtiters of recombined lentivirus at 4.58× 109PFU/ml.This positive result was confirmed by PCR andWestern blotting.ConclusionsThe targeted therapy mediated by anti-AFP scFv could significantlyinhibit the proliferation of HEP3B cells and promote the apoptosis.
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Objective To investigate the effects and possible mechanism of action of inhibiting hepatitis B virus X protein (HBx) expression on liver cancer metastasis. Methods The suppression of HBx expression in MHCC97H cells was performed by siRNA interference technique, and the effects of HBx suppression on the metastasis of MHCC97H cells were detected by Matrigel invasion assays and in a lung-metastasis mouse model. The expression levels of related epithelial-mesenchymal transition (EMT) and apoptosis proteins were examined by Western blotting. Results Introduction of HBx-siRNA into MHCC97H cells inhibited the expression of HBx and the ability to metastasize,downregulated the expression of Twist and N-cadherin, and upregulated E-cadherin expression. These changes resulted in inhibiting EMT of MHCC97H cells. Meanwhile, apoptosis involved in the Twist-P53 pathway was also found. Conclusions Inhibiting expression of HBx can decrease the metastatic a-bility of MHCC97H cells by changing EMT and inducing apoptosis.
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Objective To observe the inhibitory action of annonaceous acetogenins AS-4 on human liver cancer cell line HepG2 in vitro. Method Using different concentration of annonaceous acetagenins group(6.25,12.5,25,50 ?g/mL),control group(25 ?g/mL) of masculine(DDP),control blank group,after routine culture of 24 or 48 hours,the effect of annonaceous acetogenins AS-4 on HepG2 was analyzed by colorimetry assay(MTT) and inverted phase-contrast microscope observing. Result AS-4 had the best inhibitory effect on HepG2,the highest inhibitory rate was 91.68%,and the effect was time-dosage dependent,and the 48 h IC50 was 6.67 ?g/mL. Conclusion AS-4 has lethal effect on HepG2 in vitro,and shows obvious cytotoxic effect.
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[Objective]To study the inhibitory effect of the extract of Rhizoma Amorphophallus,we set up the Kunming mices which were vaccinated with H22 tumor as experimental model,and explore the possibility mechanism of them.[Method]We adopted the mices vaccinated with H22 tumor as experimental model to observe the influence of different extracts on the antitumor ratio,and the cooperating antitumor effect together with 5-Fu.Using flow cytometry to detect the effect of petroleum ether extract on apoptotic cells.Using immunohistochemical method to observe the influence of this extract to the expression of Survivin and Bax(Bcl-2 associated protein x).[Result]The extract of petroleum ether of Rhizoma Amorphophalli had inhibitory effect of the growth on mice vaccinated with H22 tumor,and the possible mechanism was the downregulation of Survivin expression and upregulation of Bax expression to induce apoptosis of tumor cell.
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Objective:To construct recombinant retrovirus expressing human bone morphogenetic protein-7 gene BMP7 and to discuss its apoptosis-inducing activities and the mechanism in liver cancer cell line HepG2. Methods:BMP7 gene was amplified and reconstructed with retroviral plasmid pLP-LNCX by loxP homologous recombination,and then the plasmid pLP-LNCX-BMP7 (pLLBMP7) was transferred into packing cell line PT67 and the supernatant was collected to assay viral titer. MTT assay was adopted to observe HepG2 cells amplification. 48h after pLLBMP7 infection agarose electrophoresis and flow cytometry were used to verify apoptosis of tumor cells,and then the expression of BMP7,caspase-3 and bcl-2 proteins were detected by Western blotting. Results:Recombinant retrovirus pLLBMP7 was justified and transformed into PT67 package cell with supernatant viral titer amounted to 5?109 pfu/ml. In MTT assay retrovirus group had no evident difference from controls in cellular inhibition 72h later (35.1% vs. 5.3%,68.5% vs.18.3%,p
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OBJECTIVE:To study the effect of eriocalyxin B (ER-B) on the proliferation of human umbilical vein endothelial cell (HUVEC) and hepatocelluar carcinoma angiogenesis. METHODS:The effects of ER-B at 6 kinds of concentration on the proliferation of HUVEC cultured in vitro were detected using modified MTT assay. Human hepatic cancer chicken chorioallantoic membrane angiogenesis model was induced to determine the inhibition effect of ER-B against angiogenesis. RESULTS:ER-B showed significant inhibitory effects on the proliferation of HUVEC in a dose and time dependent manner with IC50 about 7.27 ?g?mL-1. The moderate inhibition rate of ER-B in dose of 25 ?g?mL-1,50 ?g?mL-1 and 100 ?g?mL-1 to area of human hepatic cancer chicken chorioallantoic membrane angiogenesis were 14.15%,48.72% and 60.63%,respectively. 50 ?g?mL-1 ER-B has same effect to positive control. CONCLUSION:ER-B significantly inhibits the proliferation of HUVEC and chicken chorioallantoic membrane angiogenesis induced by human liver cancer cell.
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Objective: To study the effects of extremely low frequency (ELF) magnetic field with fixed parameters on human liver cancer cells (SK-HEP-1) at different aspects. Methods: SK-HEP-1 cells were exposed to 50Hz, 20mT magnetic field during the whole culture process, and then proliferation activity, growth kinetics, metabolic profile and cell cycle were analyzed. Results: 50Hz, 20mT magnetic field inhibits the growth and metabolism of SK-HEP-1 cells, and hampers their mitotic division. Conclusion: 50Hz, 20mT magnetic field could be a potential therapy in the treatment of human malignant tumors.
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Objective To investigate whether tumor necrosis factor-? (TNF-?) enhance the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9(MMP-9) in hepatic cancer cell line HepG2 or not. Methods Cultured HepG2 cells were treated by TNF-? with various concentration and time. The morphological changes of HepG2 cells were studied microscopically and the proliferation of HepG2 were detected by methyl thiazolyl tetrazolium (MTT). The expression of VEGF and MMP-9 mRNA in cultured HepG2 were determined by relative quantitative reverse transcription polymerase chain reaction. The VEGF and MMP-9 protein level in supernatants and in cytoplasm were determined by enzyme-linked immunosorbent assay (ELISA) and by immunocytochemical staining, respectively.Results There was a little morphological changes in HepG2 with TNF-? treatment, but no change of cell proliferation in corresponding time. The expression of VEGF and MMP-9 mRNA was enhanced gradually with the TNF-? concentration increasing, the VEGF and MMP-9 protein level in supernatants and in cytoplasm was elevated gradually with the concentration increasing. There was a dependance on the concentration when the concentration of TNF-? was lower than or equal to 10~4 U/L. Furthermore, the effect of promotion was close to peak when the TNF-? concentration up to 10~4 U/L; but no time-effect pattern observed. Conclusion TNF-? can enhance the expression of VEGF and MMP-9 at the level of mRNA and protein in hepatic cancer cell line.
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Objectives:To investigate in vitro tumor killing effect of recombinant human perforin C terminal truncated 125 amino acid polypeptide (rhPFP C) and N terminal truncated 118 amino acid polypeptide (rhPFP N, 22 139aa) using liver cancer cell line SMMC 7721 as target cells. Methods:Recombinant human PFP C and PFP N peptide were expressed by E.coli in fusion form with glutathione S transferase(GST), and were purified by affinity chromatography with glutathione agarose. Liver cancer cell line SMMC 7721 was treated with fusion proteins in different concentrations for 24 h before surviving cells were measured with microscopy and colorimetric MTT assay. Results:After treatment with rhPFP C or rhPFP N, SMMC 7721 cell membrane damaged, appeared lysis. In MTT assay, optical density values in test group were significantly lower than those in control group. At concentration of 2.5 ?g/ml, the killing activity of rhPFP C and rhPFP N were 33.38% and 5.90% respectively. Conclusions:Both rhPFP C and rhPFP N showed obvious killing effect on liver cancer cell line SMMC 7721.The activity of rhPFP C was great higher than that of rhPFP N.
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Objective To observe the anti-tumor effect of ethaselen on transplanted liver cancer(H22)and Lewis lung cancer mice.Methods The transplanted liver cancer(H22)and Lewis lung cancer mice models were established.Each genus consisted of 60 mice,which were divided into control,CTX,and three ethaselen dose groups,respectively,with 12 mice in each.Intraperitoneal injection(ip.)of three dosages was performed once a day through the abdominal wall separately,from the second to the eighth day after cancer was transplanted.On the eleventh day,six mice in each group were killed to calculate the tumor inhibition ratio and observe the cell cycle by flow cytometry,and the others were observed for the life extension ratio.Results When ethaselen was given at the dosage of 25,12.5 and 6.3 mg/kg,the tumor inhibition ratio was 52.5%,43.6% and 30.2%,and the life extension ratio was 56.6%,38.7% and 14.2% in the transplanted liver cancer(H22)mice,respectively.The tumor inhibition ratio was 43.8%,29.6% and 18.9%,and the life extension ratio was 47.3%,17.9% and 6.3% in the transplanted Lewis lung cancer mice,respectively.Compared with that of the control,the apoptosis ratio was obviously increased in each group,and there was obviously induced S phase arrest in 25.0 mg/kg(P