[Mechanism of Butylphthalide in Treating Delayed Encephalopathy After Carbon Monoxide Poisoning Based on Activation of Microglia].

Objective To explore the mechanism of butylphthalide (NBP) in regulating microglia activation and inflammatory cytokine expression in the hippocampus of the mouse model of delayed encephalopathy after carbon monoxide poisoning (DEACMP). Methods Wild-type C57 adult mice with normal cognitive function were selected,and DEACMP was modeled by static inhalation of carbon monoxide.The mice were randomized into three groups:DEACMP,control,and NBP.The NBP group was administrated with NBP suspension at 6 mg/kg by gavage for 21 days,and the DEACMP and control groups were administrated with the same amount of vegetable oil by gavage.The hippocampal injury was observed by HE staining.The protein level of ionized calcium-binding adapter molecule 1 (IBA1) was determined by Western blotting,and the levels of downstream inflammatory cytokines were measured by ELISA. Results Compared with the control group,the DEACMP and NBP groups showed prolonged escape latency (=0.001,=0.029),reduced nerve cells (=0.001,=0.035),up-regulated expression of IBA1 (=0.001,=0.042),increased mean fluorescence intensity of IBA1 (=0.001,=0.021),and elevated levels of tumor necrosis factor-α (TNF-α) (=0.002,=0.024),interleukin (IL)-6 (=0.001,=0.015),and IL-1β (=0.001,=0.023).Compared with the DEACMP group,the NBP group showed shortened escape latency (=0.025),increased nerve cells (=0.039),down-regulated expression of IBA1 (=0.035),decreased average fluorescence intensity of IBA1 (=0.031),and lowered levels of TNF-α (=0.028),IL-6 (=0.037),and IL-1β (=0.034). Conclusion NBP can inhibit the activation of microglia and reduce the expression of inflammatory factors,thereby alleviating cognitive dysfunction and brain tissue damage caused by DEACMP.