摘要
目的:探讨热应激诱导肝硬化内毒素血症大鼠热休克蛋白72(HSP72)表达及对致炎细胞因子TNF-α分泌的影响。方法:CCl4诱导的肝硬化SD大鼠及正常饮食的SD大鼠先后给予热应激处理及腹膜腔内注入脂多糖(LPS),另外两组肝硬化SD大鼠及正常饮食SD大鼠仅腹腔内注入LPS作为对照。ELISA检测并比较各组大鼠血浆内毒素、HSP72、TNF-α的含量,RT-PCR检测肝组织HS72mRNA表达,评价HSP72表达对TNF-α分泌的影响。结果:外源给予LPS能加重肝硬化大鼠内毒素血症。热处理及LPS注入后,肝硬化大鼠及正常大鼠血浆及肝组织HSP72表达均较未热处理组增强,而未热处理的两组大鼠LPS注入后血浆TNF-α含量明显高于热处理组。结论:热应激能促进肝硬化内毒素血症大鼠肝组织及血浆HSP72表达,而抑制TNF-α分泌。
Objective To explore the effects of heat stress on the expression of heat shock protein 72 (HSP72) and TNF-α secrection in cirrhotic rats with endotoxemia. Methods Cirrhotic SD rats induced by CCl4 and the rats with normal diets were first treated with heat stress and then injected peritoneally with lipopolysaccharide (LPS). The cirrhotic rats and the rats with normal diets in another two groups only received LPS as control. Plasma levels of endotoxin, HSP72, and TNF-α were detected by ELISA and then compared among all the groups. The expression of Hsp72 mRNA in the liver tissues was detected by RT-PCR. The effect of Hsp72 expression on TNF-α secrection was assessed. Results Extraneous administration of LPS exacerbated endotoxemia in the rats. As compared with those receiving no heat stress, plasma levels of HSP72 and HSP72 mRNA expression in the liver tissue were higher in the cirrhotic rats and healthy rats after they were treated with heat stress and administrated LPS, but plasma TNF-ot levels were markedly lower. Conclusions Heat stress can promote HSP72 expresion in liver tissue and plasma, suppressing TNF-α secretion in cirrhotic rats with endotoxemia.
出处
《实用医学杂志》
CAS
北大核心
2010年第16期2908-2910,共3页
The Journal of Practical Medicine
基金
浙江省科技计划项目(编号:2009C33129)
绍兴市科技计划项目(编号:2008A23014)