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叶下珠抗肝细胞损伤作用机制 被引量:16
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作者 周世文 徐传福 +5 位作者 周宁 黄永平 黄林清 陈晓红 胡友梅 廖雅琴 《中国中药杂志》 CAS CSCD 北大核心 1997年第2期109-111,共3页
叶下珠能明显降低CCl4引起的小鼠血清ALT的升高,抑制肝脏MDA的生成。叶下珠体外与大鼠肝细胞共同孵育,能抑制CCl4所致肝细胞膜流动性降低,降低〔Ca2+〕i浓度。结果提示,叶下珠保护肝脏损伤作用可能与其抗指质过... 叶下珠能明显降低CCl4引起的小鼠血清ALT的升高,抑制肝脏MDA的生成。叶下珠体外与大鼠肝细胞共同孵育,能抑制CCl4所致肝细胞膜流动性降低,降低〔Ca2+〕i浓度。结果提示,叶下珠保护肝脏损伤作用可能与其抗指质过氧化和膜保护作用有关。 展开更多
关键词 中草药 叶下珠 ALT MDA 抗肝细胞损伤
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从齐墩果酸结构分析抗肝细胞损伤的作用机制 被引量:33
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作者 赵骏 蓝茹 《中草药》 CAS CSCD 北大核心 1998年第12期844-844,共1页
关键词 齐墩果酸 化学结构 抗肝细胞损伤
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青萝卜汁提取物及肝特灵抗肝细胞脂质过氧化损伤作用研究 被引量:6
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作者 高斌 袁桂玉 +3 位作者 梁树仁 奚明 曹武奎 李丽芬 《天津中医》 2000年第4期8-10,共3页
关键词 青萝卜汁提取物 特灵 细胞脂质过氧化损伤
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六棱菊提取物体外抗乙型肝炎的作用 被引量:2
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作者 沈钰明 戴灵豪 +3 位作者 伍义行 俞晓平 张永勇 赵昱 《世界华人消化杂志》 CAS 北大核心 2014年第17期2421-2426,共6页
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
关键词 六棱菊提取物 乙型 抗肝细胞损伤作用 病毒作用
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Estradiol-17β protects against hypoxia-induced hepatocyte injury through ER-mediated upregulation of Bcl-2 as well as ER-independent antioxidant effects 被引量:4
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作者 Min Young Lee Sun Chul Jung +1 位作者 Jang Hem Lee Ho Jae Han 《Cell Research》 SCIE CAS CSCD 2008年第4期491-499,共9页
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
关键词 HYPOXIA estradiol-17β chicken hepatocytes
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Platelet-activating factor in liver injury: A relational scope 被引量:6
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作者 Nikolaos P Karidis Gregory Kouraklis Stamatios E Theocharis 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第23期3695-3706,共12页
The hepatocyte, the main cellular component of the liver, exhibits variable susceptibility to different types of injury induced by endogenous or exogenous factors. Hepatocellular dysfunction or death and regeneration ... The hepatocyte, the main cellular component of the liver, exhibits variable susceptibility to different types of injury induced by endogenous or exogenous factors. Hepatocellular dysfunction or death and regeneration are dependent upon the complicated interactions between numerous biologically active molecules. Platelet- activating factor (PAF) seems to play a pivotal role as the key mediator of liver injury in the clinical and experimental setting, as implied by the beneficial effects of its receptor antagonists. A comprehensive up-to-date overview of the specific functional and regulatory properties of PAF in conditions associated with liver injury is attempted in this review. 展开更多
关键词 PAF PAF-R antagonists Liver INJURY REGENERATION
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