基于TXNIP/NLRP3通路探讨天麻素对宫内炎症致早产大鼠脑损伤及炎症反应的影响OA

Objective:To explore the effects of Gastrodin(Gas)on neuroinflammation and brain injury in premature rats induced by intrauterine inflammation via regulating the TXNIP/NLRP3 pathway.Methods:Premature rats were randomly divided into the Control group,the Model group,the low-dose and high-dose gastrodin(Gas-L,Gas-H)groups,the high-dose gastrodin+TXNIP activator negative control group(Gas-H+OE-NC),and the high-dose gastrodin+TXNIP activator(Gas-H+OE-TXNIP)group,with 8 rats in each group.The levels of inflammatory factors in brain tissue was measured by ELISA experiment,and the patho-logical changes of brain tissue were measured by HE staining.The level of ROS in brain tissue was detected by DCFH-DA fluorescence probe method,and the positive expression of NeuN and Iba-1 were measured by im-munohistochemistry.The protein expression of the TXNIP/NLRP3 pathway in brain tissue was measured by Western blot,and the co-localization of TXNIP and NLRP3 was detected by immunofluorescence.Results:Compared with the Control group,severe pathological brain injury was observed in the Model group.The lev-els of TNF-α,IL-6 and IL-18 in the brain tissue,the content of ROS,the number of Iba-1 positive cells,the expression level of TXNIP/NLRP3 pathway proteins,and the co-localization coefficient of TXNIP and NL-RP3 were significantly increased,while the level of IL-10 and the number of NeuN-positive cells were markedly decreased(P<0.05).Compared with the Model group,the pathological brain injury in the Gas-L group and the Gas-H group was alleviated.The levels of TNF-α,IL-6 and IL-18 in the brain tissue,the content of ROS,the number of Iba-1 positive cells,the expression level of TXNIP/NLRP3 pathway proteins,and the co-localization coefficient of TXNIP and NLRP3 were markedly decreased,while the level of IL-10 and the number of NeuN-positive cells were notably increased(P<0.05).Moreover,the improvement of all indicators in the Gas-H group was better than that in the Gas-L group(P<0.05).Compared with the Gas-H+OE-NC group,the pathological brain injury in the Gas-H+OE-TXNIP group was aggravated.The levels of pro-inflammatory factors in brain tissue,the level of ROS,the number of Iba-1 positive cells,the expres-sion level of TXNIP/NLRP3 pathway proteins,and the co-localization coefficient of TXNIP and NLRP3 were markedly increased,while the level of IL-10 and the number of NeuN-positive cells were notably decreased(P<0.05).Conclusions:Gas can improve inflammatory imbalance and oxidative stress,alleviate pathologi-cal brain injury,and exert neuroprotective effects by inhibiting oxidative stress,blocking the interaction and pathway activation between TXNIP and NLRP3.