Résumé
Objective To observe the interfering effect of different doses of penehyclidine hydrochloride (PHC) on the mRNA expressions of nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) in the lung tissue of rats with traumatic shock so as to investigate the protective role of PHC in secondary long injury following traumatic shock and the underlying mechanism.Methods The traumatic shock model was established.A total of 104 Wistar rats were randomly divided into four groups:control group,shock group,low dose PHC group ( P1 group) and high dose PHC group ( P2 group).At the beginning of resuscitation,the rats in P1 and P2 groups were given transjugular intravenous injection of 2 ml/kg isotonic saline containing 0.15 mg/kg and 0- 45 mg/kg PHC respectively,while the rats in shock and control groups were injected only isometric isotonic saline.The rats in the four groups were killed at 2 h,6 h,12 h and 24 h after resuscitation respectively to detect the mRNA expressions of NF-κB and iNOS by using RT-PCR and determine the lung wet/dry weight (W/D) ratio,lung permeability index (LPI) and lung injury score (LIS).Results The mRNA expressions of NF-κB and iNOS,lung W/D ratio,LPI and LIS at all the time intervals in the shock,P1 and P2 groups were all significantly increased as compared with those in the control group (P<0.05).Howerver,the P2 group showed significant reduction in aspects of the mRNA expressions of NF- κB and iNOS,lung W/D ratio,LPI and LIS at all time points and P1 group also had significant decrease regarding the mRNA expressions of NF-κB and iNOS,lung W/D ratio at2 h,6 h,and LPI and LIS at 2 h,6 h,12 h,as compared with the shock group.Meanwhile,P2 group showed evident decrease at 6 h concerning the mRNA expressions of NF-κB and iNOS,lung W/D ratio,LPI and LIS as compared with P1 group (P < 0.05 ).Conclusions PHC,especially at a large dosage,can significantly mitigate the long injury secondary to traumatic shock,and the mechanism may be associated with the inhibition of mRNA expressions of NF-κB and iNOS.
Résumé
Objective To investigate the effects of glycine on the expression of HSP70 and TNF-α mRNA in the liver tissue of rats with traumatic shock and explore the protective mechanism of glycine a-gainst secondary liver injury after traumatic shock. Methods The traumatic shock model was established and 120 Wistar rats were divided randomly into three groups: treatment group, shock group and control group. At the beginning of resuscitation, the rats in the treatment were injected with 0.5 ml isotonic saline containing 100 mg/kg glycine, those rats in the shock group were injected only with 0.5 ml isotonic saline. The rats in three groups were killed at 3, 6, 12, 24 and 48 hours after resuscitation respectively. The ex-pression of HSP70 and TNF-α mRNA in the liver tissue were detected by RT-PCR, pathological changes were observed and serum ALT and AST were measured. Results The expressions of HSP70 and TNF-α mRNA in the liver tissue of rats in the shock group began to increase at 3 hours and both reached the peak value at 6 hours after resuscitation, but the expression of HSP70 mRNA in the treatment group reached the peak value at 12 hours after resuscitation. Compared with the control group, the expression of HSP70 mR-NA in the treatment group increased significantly and that of TNF-α mRNA decreased siganicantly, serum ALT and AST decreased and pathological damage was relieved significantly (all P < 0.05). Conclusion By enhancing the expression of HSP70 mRNA and decreasing the expression of TNF-α mRNA, glycine may play a protective role against the secondary damage of liver after traumatic shock.