Effect of Stemona tuberosa Alkaloids on Apoptosis of SMMC-7721 Cells and Expression of Bcl-2， Bax， and Cleaved Caspase-3 / 中国实验方剂学杂志

Objective:To investigate the effect of<italic> Stemona tuberosa</italic> alkaloids on the apoptosis of human hepatoma SMMC-7721 cells and the expression of apoptosis-related proteins including B lymphocytoma-2 （Bcl-2）， Bcl-2-associated X protein （Bax）， and cleaved cysteinyl aspartate-specific protease-3 （cleaved Caspase-3）. Method:SMMC-7721 cells were routinely cultured， passaged， and treated with various concentrations （50， 75， 112， 167， and 250 mg·L^-1） of <italic>S. tuberosa </italic>alkaloids， while those in the blank control group were only treated with 10% fetal bovine serum. The cell proliferation was determined by tetrazolium bromide （MTT） colorimetry and colony assay and the cell apoptosis by Hoechst 33258 staining. The protein expression levels of Bcl-2， Bax， and cleaved Caspase-3 were detected by Western blot. Result:<italic>S. tuberosa</italic> alkaloids inhibited the proliferation of SMMC-7721 cells， and the inhibition rate was significantly increased in comparison with that in the blank control group （<italic>P</italic><0.01）， with the half maximal inhibitory concentrations （IC₅₀） at 24 h， 48 h， and 72 h being （173.36±8.75）， （112.14±16.50）， and （96.41±2.60）mg·L^-1， respectively. The cell colony-inhibitory activity was significantly increased in a dose-dependent manner （<italic>P</italic><0.01）. Compared with the blank control group， <italic>S. tuberosa</italic> alkaloids promoted the apoptosis of SMMC-7721 cells， manifested as increased number of apoptotic cells and elevated apoptotic rate （<italic>P</italic><0.01）. The typical morphological changes such as brightly blue-fluorescent condensed nuclei， cytoplasmic shrinking， and karyopyknosis were found under the upright fluorescence microscope. As revealed by comparison with the blank control group， the expression of Bcl-2 was significantly down-regulated （<italic>P</italic><0.01）， while the protein expression levels of pro-apoptotic protein Bax and cleaved Caspase-3 in the 75， 112， 167， and 250 mg·L^-1 <italic>S. tuberosa</italic> alkaloids groups were significantly up-regulated （<italic>P</italic><0.01）. Conclusion:<italic>S. tuberosa </italic>alkaloids inhibit the proliferation of SMMC-7721 cells and promote their apoptosis possibly by inhibiting Bcl-2 protein expression and promoting Bax and cleaved Caspase-3 protein expression.

Over-expression of miR-144 inhibits invasion of liver cancer SMMC-7721 cells by suppressing TLR/MyD88 pathway / 南方医科大学学报

OBJECTIVE@#To investigate the effects of over-expression of miR-144 on invasion of SMMC-7721 cells and Toll-like receptor (TLR)/myeloid differentiation factor 88 (MyD88) pathway in hepatocellular carcinoma cells.@*METHODS@#The expressions of miR-144 was examined in normal human hepatocyte line HL-7702 and hepatocarcinoma cell line SMMC-7721 using realtime quantitative PCR (qRT-PCR). SMMC-7721 cells were divided into blank group, miR-144 NC group and miR-144 mimics group, and the expressions of miR-144 in each group were detected with qRT-PCR. Cell count kit-8 (CCK8) was used to assess the survival of SMMC-7721 cells, and the cell invasion was evaluated using Transwell assay. The expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and TLR/MyD88 pathway-related proteins in the cells were detected with Western blotting; the effect of 40 μ mol/L MyD88 inhibitor on TLR/MyD88 pathway-related proteins was examined in SMMC-7721 cells.@*RESULTS@#Compared with normal human hepatocytes, SMMC-7721 cells expressed a significantly lower level of miR-144 ( < 0.05). CCK-8 assay showed that test showed that miR-144 over-expression significantly decreased the cell survival rate ( < 0.05), lowered the number of invasive cells, and decreased the expression of MMP-2 and MMP-9 in SMMC-7721 cells ( < 0.05). The expressions of Toll-like receptor 4 (TLR4), MyD88, phosphorylated nuclear factor-kappa B (pNF-κB) and NF-κB protein decreased significantly in miR-144 mimics group and TJ-M2010-2 group ( < 0.05) and were comparable between the two groups ( > 0.05).@*CONCLUSIONS@#Overexpression of miR-144 decreases SMMC-7721 cell survival and invasion by inhibiting TLR/MyD88 pathway.

Effect of Capsaicin on Proliferation and HMGB1 and IL-6 Expressions in Hepatoma SMMC-7721 Cells / 中国实验方剂学杂志

Objective: To investigate the effect of capsaicin on proliferation in human hepatoma SMMC-7721 cells and its possible molecular mechanism. Method: Capsaicin (50,100,150,200,250,300 μmol·L-1) groups and blank group were set up. The cell viability was detected by cell counting kit-8 (CCK-8) assay after SMMC-7721 cells were treated with capsaicin (50,100,150,200,250,300 μmol·L-1) for 24, 48, 72 h. The morphological changes were observed under an inverted microscope after SMMC-7721 cells were treated with capsaicin (150,200,250 μmol·L-1) for 24 h. The mRNA expression levels of high mobility group box 1 (HMGB1) and interleukin-6(IL-6) were measured by Real-time PCR after SMMC-7721 cells were treated with capsaicin (150,200,250 μmol·L-1) for 24 h. The levels of HMGB1 and IL-6 in cell culture supernatant were detected by enzyme-linked immunosorbent assay(ELISA) after SMMC-7721 cells were treated with capsaicin (150,200,250 μmol·L-1) for 24 h. Result: Compared with the blank group, there was no significant difference between 50 and 100 μmol·L-1 capsaicin groups treated for 24, 48, 72 h; after treated with the other concentrations of capsaicin (150, 200, 250, 300 μmo·L-1) at different time points, the proliferation inhibition rate was statistically significant (P-1) groups showed different degrees of morphological changes in SMMC-7721 cells, which became round and wrinkled, with a poor attachment and more exfoliation; compared with the blank group, the mRNA expressions of HMGB1 and IL-6 in SMMC-7721 cells of capsaicin (150, 200, 250 μmol·L-1) groups were significantly down-regulated (PPConclusion: Capsaicin inhibits cell proliferation of SMMC-7721 cells, and the possible mechanism may be related to the down-regulation of HMGB1 and IL-6 at the mRNA and protein levels.

Chrysin promotes SMMC-7721 cell apoptosis by regulating MAPKs signaling pathway / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the effect of chrysin in inducing apoptosis of human hepatic carcinoma cells and explore the possible mechanism.</p><p><b>METHODS</b>Human hepatic carcinoma SMMC-7721 cells treated with DMSO or chrysin at different concentrations (5-200 μg/mL) were examined for changes in the cell proliferation using CCK-8 assay. The morphological changes of SMMC-7721 cells were observed in response to treatment with 5, 10, or 20 μg/mL chrysin, and the changes in the cell nuclei were observed using DAPI nuclear staining. Annexin Ⅴ-FITC/PI flow cytometry was used to determine the cell apoptosis rate. The changes in the apoptosis-related proteins (PARP and caspase-3) and MAPKs signal pathway were detected with Western blotting.</p><p><b>RESULTS</b>Chrysin treatment obviously suppressed the proliferation of SMMC-7721 cells in a dose-dependent manner below the concentration of 60 μg/mL. Chrysin (20 μg/mL) also caused significantly increased cell apoptosis and significant cleavage of PARP and caspase-3. Chrysin significantly activated MAPKs signaling pathway in a time-and dose-dependent manner, with the peak activation level occurring at 15 min. Pretreatment of the cells with specific inhibitors of the MAPKs pathway obviously inhibited the effect of chrysin in inducing cell apoptosis.</p><p><b>CONCLUSIONS</b>Chrysin inhibits the proliferation and promotes apoptosis of SMMC-7721 cells by regulating the activation of MAPKs signaling.</p>

Inhibitory Effects of Emodin on the Proliferation of Human Hepatocellular Carcinoma SMMC7721 Cells / 中国药房

OBJECTIVE:To study the inhibitory effects of emodin on the proliferation of human hepatocellular carcinoma SMMC7721 cells. METHODS:SMMC7721 cells were treated with 0(negative control),25,37.5,50,62.5,75,87.5,100μmol/L emodin solution and 100 μmol/L 5-FU for 24 h,48 h,72 h. The optical density value of cells was detected,and inhibition rate was calculated. SMMC7721 cells were treated with 0 (negative control),25,50,75 μmol/L emodin solution and 100 μmol/L 5-FU for 48 h,and cell apoptosis rate,cell cycle and the expression of Bax and Bcl-2 gene were detected. RESULTS:Compared with negative control,the rate of cell proliferation inhibition increased after treated with 25,37.5,50,62.5,75,87.5,100 μmol/L emodin and 100 μmol/L 5-FU,which was positively associated with the concentration and duration. Compared with negative con-trol,the rate of cell apoptosis increased after treated with 25,50,75 μmol/L emodin solution and 100 μmol/L 5-FU;the expres-sion of Bax increased and that of Bcl-2 dereased;50,75 μmol/L emodin solution and 100 μmol/L 5-FU could arrested cells at G0/G1 phase(P<0.05 or P<0.01). CONCLUSIONS:Emodin can inhibit the proliferation of SMMC7721,promote cell apoptosis and in-hibit cell growth.

Study on the Mechanism of Apoptosis of Hepatoma SMMC7721 Cells Induced by Tetrandrine / 中国药房

OBJECTIVE:To study the mechanism of apoptosis of human liver cancer SMMC7721 cells induced by tetrandrine (Tet). METHODS:MTT assay was used to test the cells activity and calculate the inhibition rate after the cells were cultured by 4, 6,8 and 10 mg/L Tet for 24,48 and 72 h. Flow cytometry was used to test the cells apoptotic ratio after the cells were cultured by 6 mg/L Tet for 24,48 and 72 h;Mitochondrial membrane potential (JC-1) was examined under an inverted fluorescence micro-scope;colorimetric method was used to detect the Caspase-3 activity;the protein expressions of Cyto-C and Pro-caspase-3 were ex-amined by Western blot. All of the tests were operated with blank control (normal culture medium or cultivated for 0 h). RE-SULTS:There was an obvious inhibition on the proliferation of SMMC7721 cells in a time- and dose-dependent manner after cells were cultured by 4,6,8 and 10 mg/L Tet for 24,48 and 72 h. Compared with the blank control,after cells were cultured by 6 mg/L Tet for 24,48 and 72 h,the cells apoptotic ratio was increased,JC-1 was decreased in a dose-dependent manner. There was an in-crease in the Caspase-3 activity after cells were cultured by 6 mg/L Tet for 24 and 48 h. After cells were cultured by 6 mg/L Tet for 24 h,the Cyto-C protein expression was strengthened,and Pro-caspase-3 protein expression was decreased,with statistical differ-ences (P<0.05). CONCLUSIONS:Tet treatment can induce the apoptosis of SMMC7721 cells by a mechanism that is related to the activation of mitochondrial apoptotic pathway.

Apoptosis of SMMC-7721 cells induced by the low-intensity pulsed ultrasound in vitro / 中华物理医学与康复杂志

Objective To explore whether the low-intensity pulsed ultrasound (LIPU) could induce apoptosis on SMMC-7721 cells and to explore the underlying mechanism.Methods The SMMC-7721 cells were randomly divided into 4 groups:a blank control group,which was subject to sham exposure to ultrasound,and 3 ultrasound intervention groups exposed to ultrasound at intensities of 0.5,1.3 and 2.0 W/cm2,respectively.Then they were incubated for 6 h.The cell apoptosis,necrosis and changes of cell cycles were measured using the flow cytometry.The transmission electron microscope (TEM) was used to observe microstructural changes in the cells.The agarose gel electrophoresis (AGE) was used to examine the DNA fragmentation,and Western-blotting was employed to assess the protein expression of caspase-3.Results The average cell apoptosis rate of the 3 intervention groups were 4.66％,8.99％ and 32.41％,respectively.The percentage of cells in G2 phase increased significantly and those in G1 phase decreased significantly in the 3 intervention groups compared to the blank control group at the same time points.In the intervention groups,significant cell apoptosis was observed under TEM,and DNA ladders was seen in AGE,with DNA fragments appearing obviously when cells were incubated for 6 h and 9 h after ultrasound exposure.In intervention groups subject to 1.3 and 2.0 W/cm2 ultrasound exposure,the protein expression of caspase-3 was significantly higher than that of the control group.Conclusion LIPU can inhibit the proliferation and induce apoptosis of SMMC-7721 cells with a dose-dependent feature.The possible mechanism underlying the LIPU-induced cell apoptosis might be related to the activation of the mitochondria pathway,and especially the caspase-3 protein.

Expression of ARK5 in hepatocellular carcinoma tissue and its effect on growth of SMMC-7721 cells / 吉林大学学报(医学版)

Objective To detect the expression of ARK5 in hepatocellular carcinoma (HCC)tissue and hepatoma SMMC-7721 cells,and to investigate its effect on the growth of hepatoma cells.Methods The expression levels of ARK5 mRNA and protein were determined by RT-PCR and Western blotting in 30 cases of HCC tissue, paracarcinoma tissue,SMMC-7721 cells,and hepatic cells LO2.The SiRNA of ARK5 and negative control (NC) siRNA were constructed and transfected into the SMMC-7721 cells,and used as experimental group and negative control group;at the same time blank control group was set up. The proliferation activity and apoptotic rate of transfected cells were detected by MTT assay and flow cytometry (FCM).Results The PCR and Western blotting results showed that the expression levels of ARK5 mRNA and protein in HCC tissue and SMMC-7721 cells were significantly higher than those in paracarcinoma tissue and LO2 cells (P<0.05 ). The MTT assay results demonstrated that the inhibitory rates of growth of transfected cells in experimental group at 24,48 and 72 h were (19.39±5.42)%, (23.19±0.53)%,and (20.74±1.23)%;there were significant differences compared with blank control group and negative control group (P<0.01).The FCM results indicated that the apoptotic rate of the transfected cells in experimental group was (15.017±0.945)%,there were significant differences compared with blank control group (8.770%± 0.656 )% and negative control group (8.763%± 1.201%) (P<0.05 ). Conclusion The ARK5 expression level is significantly increased in HCC tissue and hepatoma SMMC-7721 cells;the inhibition of ARK5 expression could suppress the growth of hepatoma cells and induce apoptosis. So ARK5 maybe act as a cancer-promoting gene and induce hepatocellular carcinogenesis.

Effects of matrine and oxymatrine on apoptosis in human hepatocarcinoma SMMC-7721 / 国际中医中药杂志

Objective To explore the effects of matrine and oxymatrine on apoptosis in human hepatocarcinoma SMMC-7721 cells.Methods The MTT assay and double staining of annexin V-fluorescein isothiocyanate(annexin V-FITC)/propidium iodide(propidium iodide, PI)were used to detect proliferation and apoptosis of SMMC-7721 cells, respectively.Results When the concentrations of matrine and oxymatrine were 0.50 mg/ml, 1.00 mg/ml and 2.00 mg/ml, the proliferation inhibition rates in SMMC-7721 cells was gradually increased in a dose- and time-dependent manner,and the inhibition of matrine on proliferation were greater than that of oxymatrine in the same concentration(1.00 mg/ml)(24 h:42.39%±0.04%vs. 21.36%±0.02%;48 h: 51.69%±0.03%vs. 36.16%±0.02%;72 h: 78.98%±0.05%vs. 61.24%±0.13%;allP<0.05). When the concentrations of matrine and oxymatrine were 0.25 mg/ml, 0.50 mg/ml and 1.00 mg/ml, the apoptosis rates of SMMC-7721 cells were significantly increased;and induction of matrine in apoptosis in SMMC-7721 cells was greater than that of oxymatrine at the same time point(48 h)(apoptosis rates in 0.25 mg/ml, 4.08%±0.20%vs. 2.20%±0.18%;0.50 mg/ml: 4.32%±0.19%vs. 3.08%±0.26%;1.00 mg/ml: 9.93%±0.18%vs. 9.01%±0.20%;allP<0.05).Conclusion Matrine and oxymatrine can inhibit proliferation and promote apoptosis human hepatocarcinoma SMMC-7721 cells.

Study on gallic acid induced human hepatoma SMMC-7721 cells apoptosis and its mechanism / 中国药理学通报

Aim To investigate the proliferative effect and the apoptosis of human hepatoma SMMC-7721 cells induced by gallic acid ( GA ) , and its underlying mechanism. Methods SMMC-7721 cells were cul-tured in vitro. MTT assay was used to observe the pro-liferation of SMMC-7721 cells induced on GA 24 , 48 , 72 h. The morphological and ultra structural changes of the SMMC-7721 cells were observed by inverted micro-scope and transmission electron microscope respective-ly. Annexin V-FITC/PI staining was used to quantify the percentages of apoptosis in the total cell popula-tion. The expression of p53 mRNA was investigated by RT-PCR. Western blot was used to determine the pro-tein expression of p53. Results GA(6. 25~50 μmol ·L-1 ) markedly inhibited the activity of proliferation and induced apoptosis of SMMC-7721 cells after 48 h in a dose-dependent manner. GA significantly induced cell nuclear condensation and fragmentation. RT-PCR and Western blot results showed that GA could improve the expression of p53 mRNA and protein. Conclusion GA can inhibit the proliferation of human hepatoma SMMC-7721 cells and induce cells apoptosis. The mechanism may be associated with improving tumor suppressor gene p53 expression.

Effect of Qishen-Qinggan decoction on proliferation and apoptosis of human hepatocellular carcinoma cellline SMMC-7721 / 国际中医中药杂志

Objective To investigate effect of Qishen-Qinggan decoction on proliferation and apoptosis of human hepatocellular carcinoma cellline SMMC-7721.Methods SMMC-7721 cells were cultivated in vitro.Logarithmic growth phase cells were divided into a drug intervention group and a control group.SMMC-7721 cells were treated with Qishen-Qinggan decoction of 0.135、0.27、0.54、1.08、2.16 g/ml respectively for 12、24、48 hours in the drug intervention group while the control group remained untreated.The inhibition rate of SMMC-7721 cells were detected by MTT assay,cell apoptotic rate were measured by flow cytometry analysis.Results Qishen-Qinggan decoction of 0.135,0.27,0.54,1.08,2.16 g/ml had a significantly inhibitory effect on SMMC-7721 cells in a dose and time dependent manner.OD values of 12 hours were 0.89±0.05,0.85±0.05,0.80±0.06,0.78± 0.02,0.69±0.07,OD values of 24 hours were 0.77±0.07,0.74±0.07,0.59±0.07,0.50±0.09,0.39±0.08,OD values of 48 hours were 0.78±0.05,0.61±0.08,0.44±0.10,0.39±0.08,0.34±0.07 respectively.Each drug intervention group had significant difference compared with control group.Qishen-Qinggan decoction of 0.27,0.54 g/ml could induce apoptosis of SMMC-7721 were 11.19 ± 2.23,15.69 ± 2.51,compared with control group of 1.41 ± 0.22.Apoptotic rates of Qishen-Qinggan decoction of 1.08 g/ml had extremely significant difference with the control group (41.83 ± 7.11 vs 1.41 ± 0.22).Conclusion Qishen-Qinggan decoction could inhibit the proliferation of SMMC-7721 cells probably by inducing cell apoptosis.

The research of compound matrine injection inducing human hepatoma SMMC-7221 cell to apoptosis / 国际中医中药杂志

Objective To explore the compound matrine injection on human hepatoma smmc-7721 cells' proliferation.Methods Human hepatoma smmc-7721 cells were sterilely cultured.Assayed the effects of compound matrine injection on smmc-7721 cells by MTT.The concentrations of the compound matrine injection were 3.34,2.38,1.43 and 0.48 mg/ml; Used the double staining method of annexin V-fluorescein isothiocyanate(Annexin V-FITC)/propidium iodide (propidium iodide,PI) to measure the apoptosis of hepatoma cell.The concentrations of the compound matrine injection were 0.86,1.72,and 3.43 mg/ml.Results The apoptosis rates of compound matrine injection with different concentration of 3.34,2.38,1.43 and 0.48 mg/ml on liver cancer cell SMMC-7721 were51.03％、53.67％、49.83％ and 0.03％ respectively after 24 hours; and 67.14％、65.35％、62.25％ and 0.05％ respectively after 48 hours;and 74.16％、68.77％、66.04％ and 26.02％respectively after 72 hours.The apoptosis rates of compound matrine injection with different concentration of 0.86,1.72 and 3.43 mg/ml on liver cancer cell SMMC-7721 were(2.86±0.35)％,(15.16± 1.15)％and(13.17±0.40)％ respectively after 24 hours; and (8.57±0.44)％,(28.07±0.76)％ and (29.81±8.10)％respectively after 48 hours,which were significantly higher than the control group (1.05±0.09)％(P＜0.05).Conclusion The compound matrine injection has a significant inhibition on human hepatoma smmc-7721 cells' proliferation and the mechanism was its inducing cell apoptosis.

Effects of toxin A from Clostridium difficile on SMMC-7721 cells proliferation and apoptosis / 中国药科大学学报

Aim: To study the effects of Clostridium difficile toxin A on the cytotoxity and apoptosis of human hep-atoma cell line SMMC-7721. Methods: Clone inhibiting experiment and MTT calorimetric assay were used to assay SMMC-7721 proliferation. Morphological changes relevant to the apoptosis and the DNA damage were analyzed by transmission electron microscope and single cell gel assay. The number of apoptosis cells and the expression of Bcl-2 and p53 protein were detected by the flow cytometry. Results: 0. 018- 4. 690 mg/L toxin A significantly decreased the colony information of SMMC-7721 cells, and greatly inhibited SMMC-7721 proliferation in a time- and concentration-dependent manner. Morphological changes related to apoptosis were evident under transmission electron microscope and DNA damage was detected by single cell gel assay when SMMC-7721 cultured with 4. 690 mg/L toxin A for 48 h. Toxin A 0. 0734. 690 mg/L induced apoptosis in SMMC-7721 cells from 6. 8% to 41. 8%. In addition, Toxin A 0. 293-4. 690 mg/L significant decreased Bcl-2 protein expression and increased p53 protein expression in SMMC-7721. Conclusion: These results showed that clostridium difficile toxin A had a significantly cytotoxicity in human SMMC-7721 which was attributed to toxin A induced apoptosis.

Up-expression of peroxisome proliferator-activated receptor-? and of retinoid X receptor-? enhances the inhibitory effect on tumor cells growth / 基础医学与临床

LOVO.PGZ significantly up-regulates the expression of PPAR? in MGC803 and LOVO cells,the expression of PPAR? was higher in combination group than PGZ alone(P

Effects of several Chinese herbal medicines on SMMC-7721 liver cancer cells by FTIR spectroscopy / 第二军医大学学报

Objective:To study the effects of several herbal medicines on SMMC-7721 liver cancer cells with Fourier transform infrared spectrometer(FTIR). Methods: FTIR was employed to determine the infrared spectra(IRs) of SMMC-7721 liver cancer cells cultivated for 20 h with the extracts of Spica prunellae, Herba houttuyniae, Radix bupleuri and Herba artemisiae scopariae. Cluster analysis of IRs was also performed. Results: IR spectral parameters such as band shape, intensity and frequency of the blank, control and herbal-extract-treated cells were compared. There existed obvious blue shift of ? s(PO 2 -), ? as (PO 2 -) bands, red shift of ? as (CH 3), ?(CH 2) bands on the herbal-extract-treated cells IRs. The decreasing ratio of ? as (CH 3) to ? s(CH 2) peak intensity and the increasing ratio of ? s(PO 2 -) to ?(N-H) peak area indicated the destructive effect of herbal extracts on the membrane structure of SMMU-7721 cells and inhibitory effect on the DNA replication respectively. Cluster analysis successfully discriminated the herbal-extract-treated cells from the blank cells and the liver-oriented medicines from the non-liver-oriented medicine. Conclusion: FTIR provides another fast and effective approach to analyze the changes of cells treated with Chinese herbal medicines, which may help to illuminate the functional mechanism of Chinese herbal medicines.

Different inhibition of hepatocarcinoma cell growth by As_2O_3 in SMMC-7721 and BEL-7402 cell lines / 中国病理生理杂志

AIM: To explore the different inhibitory effect of arsenic trioxide (As_2O_3) on hepatocarcinoma cell growth in SMMC-7721 and BEL-7402 cell lines and its mechanism. METHODS: The cell culture and trypan blue staining were used to study the inhibitory effect of arsenic trioxide on cell growth, and the glutathione (GSH) contents in hepatocarcinoma cells treated with arsenic trioxide were detected. RESULTS: Arsenic trioxide inhibited the growth of BEL-7402 cells in a time and dose-dependent manner. The inhibitory effect was significant at a lower dose of 0.50 ?mol/L for 24 h, however, to SMMC-7721 cells, a higher dose of 2.00 ?mol/L for 96 h was needed. The inhibitory rate of arsenic trioxide (0.25-2.00 ?mol/L) on BEL-7402 cell growth was higher than that on SMMC-7721 cells. The content of GSH in SMMC-7721 cells was much higher than that in BEL-7402 cells [(50.8?5.2) (?mol/g) protein and (18.7?1.4) ?mol/g protein, respectively]. CONCLUSION: There was a significant difference in inhibition of hepatocarcinoma cell growth by arsenic trioxide between BEL-7402 and SMMC-7721 cell lines, the cause of which may be due to the difference in GSH content in BEL-7402 and SMMC-7721 cells. [

Effect of spider venom from Macrothele raveni on proliferation and cell cycle of human hepatocellular carcinoma cell line SMMC-7721 / 中草药

Objective To study the effect of spider venom from Macrothele raveni on proliferation and cell cycles of human hepatocellular carcinoma cell line SMMC-7721 and the molecular mechanism of the(effect.) Methods Proliferation of SMMC-7721 cells was determined by MTT assay.DNA synthesis of SMMC-7721 cell pre-and post-treatment with spider venom from M.raveni was tested by -TdR(assay.) The induction of apoptosis and the change of cell cycle in SMMC-7721 cells treated with spider(venom) from M.raveni were investigated by Flow Cytometry.The effect of spider venom from M.raveni on expression of c-myc protein in SMMC-7721 cells was studied by Western Blot.Results MTT assay showed that the proliferation of SMMC-7721 cells in vitro was inhibited by spider venom from M.raveni((P

Effects of new drug of sulfonylurea on the glucose uptake in SMMC7721 cells / 中国病理生理杂志

AIM:To explore the effects of the new drug of sulfonylurea(1-{4-[2-(3-ethyl-4-methyl-2-oxo-3-pyrroline-1-carboxamido)ethyl]-phenylsulfonyl}-3-(1,4-tetramethylene)-urea,BGW) on the glucose uptake and the activation of Akt/PKB in SMMC7721 cells.METHODS:Cultured SMMC7721 cells were divided into control group,glibenclamide group,insulin group,BGW group and BGW+insulin group.Scintillation was used to detect the glucose uptake in SMM7721 cells.The activation of Akt/PKB was tested by Western blotting.RESULTS:Compared to control cells,gibenclamide,insulin,BGW and BGW+insulin significantly increased the glucose uptake(P

Inhibition of VEGF expression and SMMC 7721 cell growth by VEGFsiRNA / 中国病理生理杂志

AIM: To determine the inhibition of VEGF small interfering RNA (siRNA) on expression of VEGF protein and SMMC 7721 cell growth. METHODS: Nine VEGFsiRNA sequences with nineteen nucleotides were designed under the assistance of computer. The inhibitory effect of VEGFsiRNA was analyzed by CCK8. The protein level of VEGF in the media was determined by ELISA. The change of cell cycle was detected by flow cytometry. RESULTS: All the VEGFsiRNA were capable of inhibiting the proliferation of SMMC 7721 cells significantly compared with control and lipofectamine control, while the inhibitory effects of VEGFsiRNA2, VEGFsiRNA4, VEGFsiRNA6, VEGFsiRNA7, VEGFsiRNA8 and VEGFsiRNA9 were better than that of antisense oligodeoxynucleotide. All the VEGFsiRNA reduced the expression of VEGF protein. The effect of VEGFsiRNA7 and VEGFsiRNA2 were the best with the inhibitory rates of 52.65% and 50.43%, respectively. VEGFsiRNAs induced the S arrest in SMMC 7721 cells. The signs of apoptosis in SMMC 7721 cells induced by VEGFsiRNA were not observed. CONCLUSION: VEGFsiRNA sequences were designed and synthesized successfully. VEGFsiRNA effectively inhibited the proliferation of SMMC 7721 cells and reduced the level of VEGF protein.