乳酸通过抑制NLRP3/caspase-1信号通路减轻大鼠创伤性脑损伤OA

Aim To explore the mechanism by which lactate acid(Lac)alleviates traumatic brain injury(TBI)in rats.Methods Fifty SPF grade male SD rats were randomly divided into a sham surgery(Sham)group,a TBI group,a Lac group,a nu-cleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3(NLRP3)inhibitor(MCC950)group,and a Lac+MCC950 group.The modified Neurological Severity Score(mNSS),pathological changes in brain tissue,neuronal apoptosis rate,as well as the co-expression of neuronal nucleir protein(NeuN)and NLRP3,levels of inflammatory factors,and expression levels of NLRP3/cysteine aspartic acid specific protease-1(caspase-1)signaling pathway related proteins in brain tissue were compared among different groups of rats.Results Compared with the Sham group,the TBI group showed significant pathological damage to brain tissue,obvious infiltration of inflammatory cells,enhanced fluorescence intensity of NeuN and NLRP3 co-expression,the mNSS,cell apoptosis rate,and the levels of inflammatory factors and NLRP3/caspase-1 signaling pathway related protein in brain tissue were all increased(P<0.05).Compared with the TBI group,the Lac group,MCC950 group,and Lac+MCC950 group reversed the changes of the above indicators(P<0.05);Compared with the Lac group,the MCC950 group and the Lac+MCC950 group further reversed the alterations of the above indicators(P<0.05).Conclusion Lac can effectively alleviate neurological deficits and histopathological damage in rats after TBI,inhibit neuronal apoptosis,and its mechanism of action may be related to the inhibition of the NLRP3/caspase-1 signaling pathway.