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重组人生长激素对内毒素致肝细胞凋亡效应的抑制作用 被引量:17

Recombinant human growth hormone downregulates the apoptosis of HepG2 cells induced by LPS
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摘要 目的 观察内毒素(LPS)对肝细胞的直接作用及重组人生长激素(rhGH)的干预效果。方法 内毒素诱导肝细胞损害,HepG2细胞传代培养24h后,换用含内毒素(20μg/ml)和/或rhGH、肝细胞生长因子(HGF)的新鲜培养液继续培养16h,观察药物对LPS作用的干预效果。结果  HepG2细胞经LPS作用16h,透射电镜观察既有形态正常的细胞,同时也出现典型的凋亡细胞:表现为胞浆浓缩核凝聚成块状,凋亡小体形成,细胞器(包括线粒体)结构基本正常;TUNEL标记后胞核呈棕褐色染色,而对照细胞无阳性染色信号,证实LPS作用16h后HepG2细胞已发生凋亡。将rhGH与 LPS同时加入培养液中共同作用16h,rhGH可明显减少HepG2细胞经LPS诱导的细胞凋亡数量对照组为(99±0.8)%,rhHG处理组为(36±5.6)%,P<0.001。结论 重组人生长激素可以抑制LPS致肝细胞凋亡作用。 Objective: To investigate the effect of LPS on human hepatocytes and study whether recombinant human growth hormone (rhGH) could protect hepatocytes from apoptosis induced by LPS. Methods HepG2 cells were treated with LPS (20 μg/ml) or LPS and rhGH for 16 hours. The apoptosis of HepG2 cells was detected by terminal deoxynucleotide transferas-mediated dUTP nick end labeling (TUNEL) or electron microscopy. Results HepG2 cells treated with LPS exhibited some specific morphological features of typical apoptosis. the percentage of apoptotic cells in HepG2 cells treated with LPS and hrGH was significantly lower than that treated with LPS (36 ± 5.6)% vs (99 ± 0.8)%, P<0. 001). Conclusions LPS can induce apoptosis of HepG2 cells, and hrGH can downregulate the apoptotic role of LPS on HePG2 cells.
出处 《中华肝脏病杂志》 CAS CSCD 2001年第2期100-102,共3页 Chinese Journal of Hepatology
关键词 内毒素类 生长激素 细胞凋亡 肝细胞 Lipopolysaccharides Human growth hormone Apoptosis Hepatocytes
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