目的:探讨六棱菊(Laggera alata,L.alata)提取物对乙型肝炎病毒(hepatitis B virus,HBV)感染影响.方法:采用D-氨基半乳糖(D-galactosamine,D-GalN)致人源HL-7702肝细胞损伤模型,研究六棱菊提取物对类似乙型肝炎引起的肝细胞损伤的影响;...目的:探讨六棱菊(Laggera alata,L.alata)提取物对乙型肝炎病毒(hepatitis B virus,HBV)感染影响.方法:采用D-氨基半乳糖(D-galactosamine,D-GalN)致人源HL-7702肝细胞损伤模型,研究六棱菊提取物对类似乙型肝炎引起的肝细胞损伤的影响;采用HBV基因转染的HepG2.2.15细胞模型,评价六棱菊提取物的体外抗HBV作用.通过MTT法检测细胞毒性和细胞活力;通过ELISA和荧光定量PCR法分别检测乙型肝炎表面抗原(hepatitis B virus surface antigen,HBsAg)/乙型肝炎e抗原(hepatitis B e antigen,HBeAg)和HBV DNA水平.结果:六棱菊提取物在25-100μg/mL浓度时,对D-GalN致肝细胞损伤均具有显著保护作用,而在100μg/mL浓度时展示了其最高保护率为45.66%.六棱菊提取物作用HepG2.2.15细胞3d,在10-100μg/mL浓度下对HBsAg有显著抑制作用,其最高抑制率为45.92%;在100μg/mL下能显著抑制HBeAg分泌,其抑制率为50.5%.六棱菊提取物作用HepG2.2.15细胞6 d,在10-100μg/mL浓度下对HBsAg有显著抑制作用,其最高抑制率为84.31%;在25-100μg/mL浓度下能显著抑制HBeAg分泌,最高抑制率为88.45%;同时,在100μg/mL时对HBV DNA复制有显著抑制作用.结论:六棱菊提取物具有较强的体外抗肝细胞损伤作用和抗HBV作用,其抗乙型肝炎作用可能与所含咖啡酰奎宁酸类活性成分有关.展开更多
Although many previous studies have suggested that estrogen functions as a cytoprotective agent under oxidative stress conditions, the underlying mechanism by which this effect is exerted remains to be elucidated. Thi...Although many previous studies have suggested that estrogen functions as a cytoprotective agent under oxidative stress conditions, the underlying mechanism by which this effect is exerted remains to be elucidated. This study assessed the effects of estradiol-17β （E2） （10^-8s M） on hypoxia-induced cell injury and its related signaling in primary cultured chicken hepatocytes. Hypoxic conditions were found to augment the level of DNA damage and to reduce cell viability and the level of [^3H]-thymidine incorporation, and these phenomena were prevented through treatment with E2. Hypoxia also increased caspase-3 expression, but showed no evidence of an influence on the expression of Bcl-2. However, E2 induced an increase in the level of Bcl-2 expression under hypoxic conditions and reduced the level of caspase-3 expression. The effects of E2 on Bcl-2 and caspase expression were blocked by ICI 182780 （E2 receptor （ER） antagonist, 10＂7 M）. In addition, hypoxia resulted in an increase in the intracellular reactive oxygen species （ROS） generated. These effects were blocked by E2, but not by E2-BSA and ICI 182780. Hypoxia also activated p38 mitogen-activated protein kinase （MAPK）, c-JUN N-terminal kinase/stress-activated protein kinase （JNK/SAPK） and nuclear factor-kB （NF-kB）. These effects were blocked by E2, but not by ICI 182780. The inhibition of p38 MAPK and JNK/SAPK blocked NF-kB activation. In conclusion, E2 was found to protect against hypoxia-induced cell injury in chicken hepatocytes through ER-mediated upregulation of Bcl-2 expression and through reducing the activity of ROS-dependent p38 MAPK, JNK/ SAPK and NF-kB.展开更多
文摘目的:探讨六棱菊(Laggera alata,L.alata)提取物对乙型肝炎病毒(hepatitis B virus,HBV)感染影响.方法:采用D-氨基半乳糖(D-galactosamine,D-GalN)致人源HL-7702肝细胞损伤模型,研究六棱菊提取物对类似乙型肝炎引起的肝细胞损伤的影响;采用HBV基因转染的HepG2.2.15细胞模型,评价六棱菊提取物的体外抗HBV作用.通过MTT法检测细胞毒性和细胞活力;通过ELISA和荧光定量PCR法分别检测乙型肝炎表面抗原(hepatitis B virus surface antigen,HBsAg)/乙型肝炎e抗原(hepatitis B e antigen,HBeAg)和HBV DNA水平.结果:六棱菊提取物在25-100μg/mL浓度时,对D-GalN致肝细胞损伤均具有显著保护作用,而在100μg/mL浓度时展示了其最高保护率为45.66%.六棱菊提取物作用HepG2.2.15细胞3d,在10-100μg/mL浓度下对HBsAg有显著抑制作用,其最高抑制率为45.92%;在100μg/mL下能显著抑制HBeAg分泌,其抑制率为50.5%.六棱菊提取物作用HepG2.2.15细胞6 d,在10-100μg/mL浓度下对HBsAg有显著抑制作用,其最高抑制率为84.31%;在25-100μg/mL浓度下能显著抑制HBeAg分泌,最高抑制率为88.45%;同时,在100μg/mL时对HBV DNA复制有显著抑制作用.结论:六棱菊提取物具有较强的体外抗肝细胞损伤作用和抗HBV作用,其抗乙型肝炎作用可能与所含咖啡酰奎宁酸类活性成分有关.
文摘Although many previous studies have suggested that estrogen functions as a cytoprotective agent under oxidative stress conditions, the underlying mechanism by which this effect is exerted remains to be elucidated. This study assessed the effects of estradiol-17β （E2） （10^-8s M） on hypoxia-induced cell injury and its related signaling in primary cultured chicken hepatocytes. Hypoxic conditions were found to augment the level of DNA damage and to reduce cell viability and the level of [^3H]-thymidine incorporation, and these phenomena were prevented through treatment with E2. Hypoxia also increased caspase-3 expression, but showed no evidence of an influence on the expression of Bcl-2. However, E2 induced an increase in the level of Bcl-2 expression under hypoxic conditions and reduced the level of caspase-3 expression. The effects of E2 on Bcl-2 and caspase expression were blocked by ICI 182780 （E2 receptor （ER） antagonist, 10＂7 M）. In addition, hypoxia resulted in an increase in the intracellular reactive oxygen species （ROS） generated. These effects were blocked by E2, but not by E2-BSA and ICI 182780. Hypoxia also activated p38 mitogen-activated protein kinase （MAPK）, c-JUN N-terminal kinase/stress-activated protein kinase （JNK/SAPK） and nuclear factor-kB （NF-kB）. These effects were blocked by E2, but not by ICI 182780. The inhibition of p38 MAPK and JNK/SAPK blocked NF-kB activation. In conclusion, E2 was found to protect against hypoxia-induced cell injury in chicken hepatocytes through ER-mediated upregulation of Bcl-2 expression and through reducing the activity of ROS-dependent p38 MAPK, JNK/ SAPK and NF-kB.
