2010Shiyong yixue zazhiRequires access

Effects of heat stress on HSP72 expression and proinflammatory cytokine secretion in cirrhotic rats with endotoxemia

Ren Guang-yua

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Abstract

Objective To explore the effects of heat stress on the expression of heat shock protein 72 (HSP72) and TNF-αsecrection 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- αsecrection 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-α 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.

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Objective To explore the effects of heat stress on the expression of heat shock protein 72 (HSP72) and TNF-αsecrection 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- αsecrection 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-α 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.

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Available abstract

Objective To explore the effects of heat stress on the expression of heat shock protein 72 (HSP72) and TNF-αsecrection 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- αsecrection 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-α 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.

Key concepts: Lipopolysaccharide, Heat shock protein, Proinflammatory cytokine, Secretion, Endocrinology, Internal medicine, Tumor necrosis factor alpha, Cytokine

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