实用肝脏病杂志2017，Vol.20Issue(4)：397-401,5.DOI:10.3969/j.issn.1672-5069.2017.04.005
Oridonin对急性肝衰竭小鼠肝细胞凋亡的影响及其机制研究
Suppression of TNF-α and JNK- related pro-apoptotic signaling expression of oridonin in mice with LPS/D-Gal-induced acute liver failure
摘要
Abstract
Objective To investigate the anti-apoptosis effect of oridonin in mice with lipopolysaccharide (LPS)/D-galactosamine(D-Gal)-induced acute liver failure (ALF). Methods 25 mice were randomly divided into five groups (5 in each),e.g.,normal,model,oridonin-intervened and oridonin-intervened at different doses,and oridonin for 12 days. ALF model was established in C57BL/6 mice by intraperitoneal injection of LPS/D-Gal. TUNEL,real-time PCR and Western blot were applied to related detection. Results Hepatocyte apoptosis rate in mice in model group was (36.4±1.8)%,significantly higher than that in oridonin-intervened groups [(19.4±3.3)%and (11.4±0.3)%,respectively,P<0.01];administration of oridonin significantly decreased hepatic TNF-α mRNA level in model group (P<0.01);the expressions of mitochondrial-dependent pro-apoptotic protein such as JNK, bax,cytochrome C,cleaved caspase8/9/3 were upregulated in the model group as compared to in the control group;Pretreatment with oridonin significantly reversed the changes of apoptosis signal pathway induced by LPS/D-Gal, the expression of caspase 8 was not significantly changed and the expression of anti-apoptotic protein bcl-xl increased. Conclusion Oridonin has an anti-apoptosis effect on LPS/D-Gal-induced ALF in mice,and its mechanism may be related to the suppression of pro-apoptotic cytokine TNF-α and JNK-related pro-apoptotic signaling.关键词
急性肝衰竭/D-氨基半乳糖氨/冬凌草甲素/凋亡/小鼠Key words
Acute liver failure/D-galactosamine/Oridonin/Apoptosis/Mice引用本文复制引用
邓怡林,于合国,施敏,石翠翠,范建高,李光明..Oridonin对急性肝衰竭小鼠肝细胞凋亡的影响及其机制研究[J].实用肝脏病杂志,2017,20(4):397-401,5.基金项目
国家自然科学基金资助项目(编号:81400631/81570549) （编号:81400631/81570549）
