Study on the Mechanism of Action of MicroRNA-140-5p in the Treatment of Autism by Regulating the Nuclear Factor Kappa B Signaling Pathway

To study the effect and mechanism of microRNA-140-5p on inflammatory factors in autistic rats induced by valproate. 50 Sprague-dawley rats at 12.5 d of pregnancy were randomly selected and divided into groups. The valproate group (10 rats) was intraperitoneally injected with valproate (600 mg/kg); the valproate+microRNA-negetive control group was intraperitoneally injected with valproate (600 mg/kg) and microRNA-negetive control; valproate+microRNA-140-5p group, intraperitoneal injection of valproate (600 mg/kg) and microRNA-140-5p; valproate+microRNA-140-5p+phorbol 12-myristate 13-acetate group was intraperitoneally injected with valproate (600 mg/kg) and microRNA-140-5p and phorbol 12-myristate 13-acetate. The control group (10 rats) was intraperitoneally injected with the same amount of normal saline. The impact of injury, polymerase chain reaction and enzyme-linked immunosorbent assay methods to detect the impact of inflammation-related and nuclear factor kappa B-related genes and proteins expression. The results showed that valproate-induced autistic rats may cause death or malformation, microRNA-140-5p may alleviate the death or malformation caused by it and phorbol 12-myristate 13-acetate may reverse the therapeutic effect of microRNA-140-5p; valproate modeling will cause the weight loss of rats and the high expression of microRNA-140-5p can effectively alleviate the weight loss and the use of phorbol 12-myristate 13-acetate will cause weight loss; microRNA-140-5p can shorten the time of opening eyes for the first time in valproate mice and can improve the learning and memory ability of valproate rats and the pathological damage of brain tissue; microRNA-140-5p can also inhibit the activation of nuclear factor kappa B signal to achieve the effect of inhibiting the expression of inflammatory factors. MicroRNA-140-5p reduces the secretion of inflammatory factors in valproate-induced autistic rats by regulating the nuclear factor kappa B signaling pathway.