Aim To probe the possible mechanisms of the main active components combinations between Astragalus and Panax notoginseng antagonizing on ischemia-reperfusion (I/R) injury from the perspective of the inflammatory response.Methods C57BL/6mice were divided randomly into:sham, model, Astragaloside IV (ASTIV), Ginsenoside Rgl (Rgl), Ginsenoside Rbl (Rbl), Notoginsenoside R1(R1), four active components combination, AST IV+Rg1, ASTIV+Rbl, ASTIV+R1and Edaravone, pretreated for3d. After1h of the last administration, the model of cerebral I/R injury was established by bilateral common carotid artery (CCA) ligation for20min followed by reperfusion for24h. The expression of TNF-a, IL-1β, ICAM-1mRNA in brain tissues were detected by RT-PCR, the expression of p-IκBα as well as NF-κB proteins of cytoplasm and nucleus in brain tissues were tested by western-blot, then, NF-κB nuclear translocation rate was caculated.Results①After cerebral I/R, the expression of TNF-α, IL-1β,ICAM-1mRNA in brain tissues were increased. ASTIV remarkably decreased the expression of TNF-α mRNA,Rg1significantly down-regulated ICAM-1mRNA expression, R1could decrease both TNF-a and ICAM-1mRNA expressions, ASTIV combined with Rg1, Rb1,1Rl had different degree suppression on TNF-α, IL-1β, ICAM-1mRNA, moreover, the inhibitory effects of four active components combination and ASTFV+R1on the inflammatory cytokines were more obvious.②fter cerebral I/R, the expression of p-IκBα protein in brain tissues was notablely increased, NF-κB protein was significantly down-regulated in cytoplasm while up-regulated in nucleus, nuclear translocation rate was raised. ASTIV, Rg1, R1and the active components combinations could prevent the phosphorylation of IκB, relieve the translocation of NF-κB nuclear, furthermore, the effects of the combinations were greater than those of the active components alone. The effects of four active components combination were better than those of ASTIV+Rbl and ASTIV+Rgl.Conclusion The main active components combinations between Astragalus and Panax notoginseng can decrease the productions of the inflammatory cytokines by restraining the activation of NF-κB signaling pathway, thus relieving secondary inflammatory reaction after cerebral ischemia, contributing to the protective effects on brain tissues. |