RESUMO
Objective To investigate the mechanisms of Pinacidil prec onditioning protection of hemorrhagic shock rats. Methods The rats were divided into 3 groups: a normal group ( n=10), a control group (n=40) and a preconditioning group (n=40). Pinacidil preconditio ning was processed 24 h before making the hemorrhagic shock model. The cPLA 2 expression in myocardium was observed at different time points with western blot; Pinacidil preconditioning was processed 24, 48 and 72 h before making th e hemorrhagic shock model to observe hsp70 expression in myocardium and liver tissue with western blot. Results Pinacidil preconditioning could increase hsp70 expres sion and decrease cPLA2 expression. Conclusions Pinacidil preconditioning protects "shock cell" by inducing hsp70 overexpression and inhibiting cPLA2 expression, which is re sponsible for protecting myocardial and liver tissues of the hemorrhagic shock rats.
RESUMO
AIM: To study the effects of tetrandrine(Tet) and fructose-1,6-diphosphate(FDP) on the elevated intrasynaptosomal [Ca 2+ ] i induced by excitatory amino acids (EAA). METHODS: A rapid method for preparing synaptosomes was used, and intrasynaptosomal free calcium ([Ca 2+ ] i) was measured by using the fluorescent indicator quin-2. RESULTS: L-glutamate (Glu, 100 ?mol/L), aspartate (Asp, 100 ?mol?L -1 ), N-methy1-D-aspartate (100 ?mol/L) and Glu (50 ?mol/L) plus Asp (50 ?mol/L) all elevated intrasynaptosomal [Ca 2+ ] i in a dose-dependent manner. Pretreatment with Tet (10,30,60 ?mol/L) , FDP (15, 30, 75, 150 ?mol/L), MK-801 (10, 20 ?mol/L) and Tet (15, 30 ?mol/L) plus FDP(15, 30 ?mol/L) all attenuated the increase in intrasynaptosomal [Ca 2+ ] i induced by EAAs mentioned as above in a dose-dependent manner, and the effect of Tet plus FDP was most significant. CONCLUSION: Both Tet and FDP inhibited a rise in intrasynaptosomal [Ca 2+ ] i induced by EAAs, which may be one of mechanisms that Tet and FDP pretect cerebral tissues against ischemia injury.