Influence of Paeonol on neuroinflammation in ischemic stroke rats by regulating p38 mitogen-activated protein kinase signaling pathway
Objective To investigate the influence of Paeonol on neuroinflammation in ischemic stroke rats and its mechanism.Methods Male SD rats with SPF level were used to establish a rat model of ischemic stroke.Rats were devided into Sham group,Model group,Paeonol group(20 mg/kg Paeonol),and Paeonol combined with p38 mitogen-activated protein kinase(p38 MAPK)activator group(Paeonol+Anisomycin group,20 mg/kg Paeonol+2 mg/kg Anisomycin).After modeling for 48 hours,neurological function deficit score were observed,cerebral infarction volume was detected,neuronal apoptosis and microglia activation were assessed by TUNEL staining and immunofluorescence staining.The levels of tumor necrosis factor α(TNF-α),interleukin(IL)-1β and IL-6 in the brain tissue of the ischemic penumbra were detected by enzyme linked immunosorbent assay(ELISA).The expression of p-p38 MAPK and p38 MAPK was measured by Western blot.Results Compared to the Sham group,rats in the Model group had severe neurological damage,white infarct lesions in the brain tissue,increased neurological function deficit score,cerebral infarct volume,neuron apoptosis rate,microglia cell count and levels of TNF-α,IL-1β,IL-6,and p-p38 MAPK protein expression,the differences were statistically significant(all P<0.05).Compared to the Model group,rats in the Paeonol group exhibited reduced neurological function deficit score,cerebral infarct volume,neuron apoptosis rate,microglia cell count and levels of TNF-α,IL-1β and IL-6,and p-p38 MAPK protein expression,the differences were statistically significant(P<0.05).Compared to the Paeonol group,rats in the Paeonol+Anisomycin group showed increased neurological function deficit score and cerebral infarct volume,and the protective effect of Paeonol on ischemic stroke-induced brain injury and inflammatory response could be reversed by Anisomycin(P<0.05).Conclusion Paeonol may alleviate ischemic stroke-induced brain injury by inhibiting the p38 MAPK pathway,suppressing microglia activation and inflammatory response.
PaeonolIschemic strokeNeuroinflammationP38 mitogen-activated protein kinase signaling pathway
国家科技期刊平台
NSTL
万方数据
维普
