| Objective:Explore the hypoxic preconditioning on cerebral infarction when Toll-like receptor 5(TLR5)expression;further study the relationship between TLR5 and p-p38,Bax and their possible roles in ischemic stroke.Methods:50 healthy male Sprague Dawley(SD)rats were randomly divided into five groups,namely normal control group(N,n=10),sham-operated group(S,n=10),middle cerebral artery occlusion group(M,n=10),hypoxia-preconditioned group(H,n=10),hypoxia-preconditioned+middle cerebral artery occlusion group(HM,n=10).We assessed the animal models by Longa’5 points neurological deficit score,after 24 hours ’ surgery;through measured infarct size with TTC.Immunohistochemical was used to verify the target protein of TLR5,phosphorylation of p38 mitogen-activated protein kinase(P-p38)and pro-apoptotic factor Bax protein.Results:1.Neurological deficit score: neurological deficit symptoms of group HM improved significantly(P<0.05).2.Infarction size: the area of group HM with cerebral infarction was significantly reduced(P<0.01).3.Rats in each group by immunohistochemistry results: group H compared with group N,TLR5,P-p38 and Bax expression were reduced(P<0.05).group M compared with group N,TLR5,P-p38 and Bax levels were significantly higher(P<0.01),expression of group HM remained increased(P<0.01),but the increment in group M was significantly(P<0.01);group HM compared with group M,expression of TLR5,P-p38 and Bax was significantly decreased(P<0.01).Conclusions:Through the endogenous mechanism of brain protection,hypoxic preconditioning can reduce the area of cerebral infarction,improve the symptom of neurological deficits after cerebral infarction in rats,reduce ischemic brain injury and play an important protective role to neuron;Hypoxic preconditioning by regulating the expression of TLR5,inhibition of p38 phosphorylation,decrease the expression of Bax to exert neuroprotective effect.It may be one part of the mechanisms with the protective effect in the brain. |
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