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AIM:To examine the protective effect of estradiol on thecultured hepatocytes under oxidative stress.METHODS:Hepatocytes of rat were isolated by usingperfusion method,and oxidative stress was induced by aserum-free medium and FeNTA.MDA level was determinedwith TBA method.Cell damage was assessed by LDHassay.Apoptosis of hepatocytes was assessed withcytoflowmetric analysis.Expression of Bcl-xl in culturedhepatocytes was detected by Western blot.The radical-scavenging activity of estradiol was valued by its ability toscavenge the stable free radical of DDPH.RESULTS:Oxidative stress increased LDH(from 168±25×10~(-6)IU.cell~(-1)to 780±62×10~(-6)IU.cell~(-1))and MDA(from 0.28±0.07×10~(-6)nmol.cell~(-1)to 1.35±0.12×10~(-6)nmol.cell~(-1))levelsin cultured hepatocyte,and estradiol inhibited both LDH andMDA production in a dose dependent manner.In thepresence of estradiol 10~(-6)mol.L~(-1),10~(-7)mol.L~(-1)and 10~(-8)mol.L~(-1),the LDH levels are 410±53×10~(-6)IU.cell~(-1)(P<0.01 vsoxidative group),530±37×10~(-6)IU.cell~(-1)(P<0.01 vsoxidative group),687±42×10~(-6)IU.cell~(-1)(P<0.05 vsoxidative group)respectively,and the MDA level are 0.71±0.12×10~(-6)nmol.cell~(-1)(P<0.01 vs oxidative group),0.97±0.11×10~(-6)nmol.cell~(-1)(P<0.01 vs oxidative group)and 1.27×0.19×10~(-6)nmol.cell~(-1)respectively.Estradiol suppressedapoptosis of hepatocytes induced by oxidative stress,administration of estradiol(10~(-6)mol/ L)decreased theapoptotic rate of hepatocytes under oxidative stress from 18.6±1.2% to 6.5±2.5%.P<0.01.Bcl-xl expression wasrelated to the degree of liver cell damage due to oxidativestress,and estradiol showed a protective action.CONCLUSION: Estradiol protects hepatocytes from oxidative damage by means of its antioxidant activity
AIM: To examine the protective effect of estradiol on the cultured hepatocytes under oxidative stress. METHODS: Hepatocytes of rat were isolated by usingperfusion method, and oxidative stress was induced by aserum-free medium and FeNTA. MDA level was determined with TBA method. Cell damage was assessed by LDHassay. 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 toscavenge the stable free radical of DDPH.RESULTS: Oxidative stress increased LDH from 168 ± 25 × 10 -6 IU.cell -1 to 780 ± 62 × 10 -6 IU.cell -1 and MDA from 0.28 ± 0.07 × 10 ~ (-6) nmol.cell ~ (-1) to 1.35 ± 0.12 × 10 ~ (-6) nmol.cell ~ (-1)) levels of 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 ~ LDH levels were 410 ± 53 × 10 ~ (-6) IU.cell ~ (-1) (P <0.01 vsoxi (P <0.01 vsoxidative group) and (68 ± 42 × 10 ~ (-6)) IU.cell ~ (-1) P (530 ± 37 × 10 -6) (P <0.01 vs oxidative group), 0.97 ± 0.11 × 10 ~ (-6) nmol, respectively, and the MDA levels were 0.71 ± 0.12 × 10 ~ (-6) nmol.cell -1 (P <0.01 vs oxidative group) and 1.27 × 0.19 × 10 ~ (-6) nmol.cell ~ (-1) respectively.Estradiol suppressedapoptosis of hepatocytes induced by oxidative stress, administration of estradiol (10 ~ (-6) mol / L) decreased theapoptotic rate of hepatocytes under oxidative stress from 18.6 ± 1.2% to 6.5 ± 2.5% .P <0.01.Bcl-xl expression wasrelated 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