Heat shock protein 70 inhibited inducible nitric oxide synthase gene expression in infectious cerebral injury in rat

Objective To study the effects of heat shock protein 70 (HSP70) on inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) synthesis in infectious cerebral injury in rat. Methods The infectious cerebral injury model was developed by injection of Pertussis Bacilli (PB) suspension via the left internal carotid artery. A total of 72 rats were divided randomly into 3 groups: normal saline control group (NS group), infection cerebral injury group (PB group) and HSP70 pretreatment group (HSP group). The animals were decapitated at 4 h, 8 h and 24 h after injection of PB or NS. HSP70 expression in brain tissue was detected by using Western blot analysis. iNOS mRNA expression in brain tissue was determined by using in situ hybridization method and NO in the brain homogenate was determined by using Griess method. Results Western blot analysis showed HSP70 in brain tissue elevated after heat shock response (HSR), whereas the level of HSP70 in the HSP group was significantly higher than in the PB group ( P 0.01). The signals of iNOS mRNA expression were observed in NS group, PB group and HSP group at 4th h. Hybridization signals in the PB group were significantly stronger than those in the HSP group at 8th h and 24th h. Similarly, the concentration of NO in the PB group was significantly increased, while decreased in the HSP group ( P 0.01). Conclusion The HSR might inhibit iNOS mRNA expression and the increase of NO, which might be associated with the induction of HSP70 synthesis in brain tissue, suggesting that HSP70 may be protective against infectious cerebral injury. [