摘要
目的:研究寒冷应激对大鼠肝脏损伤的诱导作用及其分子机制.方法:将雄性SD大鼠置于(-15±1)℃自动控温低温实验舱内每日进行冷暴露6 h,按照寒冷应激暴露时间的不同分为1,3,5,7,10,14 d组.取各组大鼠肝脏组织石蜡切片,采用HE染色观察不同寒冷暴露时间下对大鼠肝脏的损伤程度.采用Western Blot方法检测大鼠肝脏组织c-Jun氨基末端激酶(JNK)和细胞外信号调节激酶(ERK)信号分子的表达及磷酸化水平.结果:寒冷应激对大鼠肝脏可产生明显的损伤作用,冷应激7 d时肝脏损伤有暂时性恢复,但随后再次加重.寒冷应激后肝组织JNK1/2(P-JNK1/2)磷酸化水平显著增高,而且这种增高与肝组织细胞损伤程度存在显著的相关性,但ERK1/2的表达及磷酸化水平没有明显的改变.结论:寒冷应激可以引起大鼠肝脏的损伤,肝脏组织JNK1/2的磷酸化水平的增高可能是其重要分子机制之一.
Abstract
AIM: To study the impairment of chronic cold stress on rat liver and the involvement of c-Jun N-terminal kinase(JNK) pathway. METHODS: Adult male SD rats were placed in the re-frigerator( 6 h for 1,3,5,7,10 and 14 d,respectively) and the exposure temperature was( - 15 ± 1 )℃. The impairment of liver was observed by HE staining (hematoxylin and eosin stain) and the expression and activation of c-Jun N-terminal kinase ( JNK ) and extracellular signal-regulated kinase (ERK) were determined by Western blot. RESULTS: Cold stress induced significant pathological impairment of the rat liver. Although partially recovered at 7 d,the impairment aggravated again thereafter. Western blot showed that the level of phosphorylated JNK increased after the cold exposure and the increase was significantly correlated to the impairment of the rat liver. But no significant changes were observed in the expression and activation of ERK. CONCLUSION: Cold stress leads to impairment of the rat liver and the increased phosphorylation of JNK may contribute to the cold-induced liver impairment.
基金项目
国家科技支撑计划专项项目(2006BAI19B07)
NETL
NSTL
维普
万方数据