Objective:To explore effect of 5-AZn-2'-deoxycytidine on proliferation of human lung adenocarcinoma cell line A549 in vitro.Methods:Superoxide dismutase(SOD)activity was measured by hydroxylamine colorimetric meth...Objective:To explore effect of 5-AZn-2'-deoxycytidine on proliferation of human lung adenocarcinoma cell line A549 in vitro.Methods:Superoxide dismutase(SOD)activity was measured by hydroxylamine colorimetric method.Inhibition effect of 5-AZn-2'deoxycytidylic acid at different concentration and different time on growth of A549 cell was determined by MTT assay.Methylene dioxyamphetamine(MDA)was measured by throbarbituric acid colorimetric method.Effect of 5-AZn-2'deoxycytidylic acid on apoptosis of A549 cell was determined by Hoechst 33258 dyeing detection.Results:5-AZn-2'deoxycytidylic acid had significant inhibition effect on proliferation of A549 cells in vitro,and the inhibition was notably dependent on time and dosage during 48-72 h;SOD level was significantly lower than those of control group(P<0.05,P<0.01),MDA level was significantly higher than those in the control group(P<0.05,P<0.01).A549 cells began to be in apoptosis after using 5-AZn-2'deoxycytidylic acid.Conclusions:5-AZn-2'deoxycytidylic acid has significant inhibition effect on growth of A549 cell,and can lead the change of lipid peroxidation.It indicates that the mechanism has relationship with A549 cell cycle tissue and induction factor of apoptosis.展开更多
AIM: To examine the protective effect of estradiol on the cultured hepatocytes under oxidative stress. METHODS: Hepatocytes of rat were isolated by using perfusion method, and oxidative stress was induced by a serum-f...AIM: To examine the protective effect of estradiol on the cultured hepatocytes under oxidative stress. METHODS: Hepatocytes of rat were isolated by using perfusion method, and oxidative stress was induced by a serum-free medium and FeNTA. MDA level was determined with TBA method. Cell damage was assessed by LDH assay. Apoptosis of hepatocytes was assessed with cytoflowmetric analysis. Expression of Bcl-xl in cultured hepatocytes was detected by Western blot. The radical-scavenging activity of estradiol was valued by its ability to scavenge the stable free radical of DDPH. RESULTS: Oxidative stress increased LDH from 168 +/- 25 x 10(-6)IU.cell(-1) to 780 +/- 62 x 10(-6)IU.cell(-1) and MDA(from 0.28 +/- 0.07 x 10(-6)nmol.cell(-1) to 1.35 +/- 0.12 x 10(-6)nmol.cell(-1)) levels in cultured hepatocyte, and estradiol inhibited both LDH and MDA production in a dose dependent manner. In the presence of estradiol 10(-6)mol.L(-1), 10( -7 )mol.L(-1) and 10(-8)mol.L(-1),the LDH levels are 410 +/- 53 x 10(-6)IU.cell(-1) (P【0.01 vs oxidative group), 530 +/- 37 X 10(-6)IU.cell(-1 ) (P【0.01 vs oxidative group), 687+/-42 x 10(-6)IU.cell(-1) (P【0.05 vs oxidative group) respectively, and the MDA level are 0.71+/-0.12 x 10(-6)nmol.cell(-1) (P【0.01 vs oxidative group),0.97+/-0.11 x 10(-6)nmol.cell(-1 )(P【0.01 vs oxidative group) and 1.27+/-0.19 x 10(-6)nmol.cell(-1) respectively. Estradiol suppressed apoptosis of hepatocytes induced by oxidative stress, administration of estradiol(10(-6)mol/L)decreased the apoptotic rate of hepatocytes under oxidative stress from 18.6 +/- 1.2% to 6.5 +/-2.5%, P【0.01. Bcl-xl expression was related to the degree of liver cell damage due to oxidative stress, and estradiol showed a protective action. CONCLUSION: Estradiol protects hepatocytes from oxidative damage by means of its antioxidant activity.展开更多
基金supported by the grants from National Natural Science Foundation of China(No.81300015)Qianjiang Talent Program(No.2013R10050) of Zhejiang Province,China
文摘Objective:To explore effect of 5-AZn-2'-deoxycytidine on proliferation of human lung adenocarcinoma cell line A549 in vitro.Methods:Superoxide dismutase(SOD)activity was measured by hydroxylamine colorimetric method.Inhibition effect of 5-AZn-2'deoxycytidylic acid at different concentration and different time on growth of A549 cell was determined by MTT assay.Methylene dioxyamphetamine(MDA)was measured by throbarbituric acid colorimetric method.Effect of 5-AZn-2'deoxycytidylic acid on apoptosis of A549 cell was determined by Hoechst 33258 dyeing detection.Results:5-AZn-2'deoxycytidylic acid had significant inhibition effect on proliferation of A549 cells in vitro,and the inhibition was notably dependent on time and dosage during 48-72 h;SOD level was significantly lower than those of control group(P<0.05,P<0.01),MDA level was significantly higher than those in the control group(P<0.05,P<0.01).A549 cells began to be in apoptosis after using 5-AZn-2'deoxycytidylic acid.Conclusions:5-AZn-2'deoxycytidylic acid has significant inhibition effect on growth of A549 cell,and can lead the change of lipid peroxidation.It indicates that the mechanism has relationship with A549 cell cycle tissue and induction factor of apoptosis.
文摘AIM: To examine the protective effect of estradiol on the cultured hepatocytes under oxidative stress. METHODS: Hepatocytes of rat were isolated by using perfusion method, and oxidative stress was induced by a serum-free medium and FeNTA. MDA level was determined with TBA method. Cell damage was assessed by LDH assay. Apoptosis of hepatocytes was assessed with cytoflowmetric analysis. Expression of Bcl-xl in cultured hepatocytes was detected by Western blot. The radical-scavenging activity of estradiol was valued by its ability to scavenge the stable free radical of DDPH. RESULTS: Oxidative stress increased LDH from 168 +/- 25 x 10(-6)IU.cell(-1) to 780 +/- 62 x 10(-6)IU.cell(-1) and MDA(from 0.28 +/- 0.07 x 10(-6)nmol.cell(-1) to 1.35 +/- 0.12 x 10(-6)nmol.cell(-1)) levels in cultured hepatocyte, and estradiol inhibited both LDH and MDA production in a dose dependent manner. In the presence of estradiol 10(-6)mol.L(-1), 10( -7 )mol.L(-1) and 10(-8)mol.L(-1),the LDH levels are 410 +/- 53 x 10(-6)IU.cell(-1) (P【0.01 vs oxidative group), 530 +/- 37 X 10(-6)IU.cell(-1 ) (P【0.01 vs oxidative group), 687+/-42 x 10(-6)IU.cell(-1) (P【0.05 vs oxidative group) respectively, and the MDA level are 0.71+/-0.12 x 10(-6)nmol.cell(-1) (P【0.01 vs oxidative group),0.97+/-0.11 x 10(-6)nmol.cell(-1 )(P【0.01 vs oxidative group) and 1.27+/-0.19 x 10(-6)nmol.cell(-1) respectively. Estradiol suppressed apoptosis of hepatocytes induced by oxidative stress, administration of estradiol(10(-6)mol/L)decreased the apoptotic rate of hepatocytes under oxidative stress from 18.6 +/- 1.2% to 6.5 +/-2.5%, P【0.01. Bcl-xl expression was related to the degree of liver cell damage due to oxidative stress, and estradiol showed a protective action. CONCLUSION: Estradiol protects hepatocytes from oxidative damage by means of its antioxidant activity.
