Baicalin has been reported to have ameliorative effects on nerve-induced hypoxic ischemia injury; however, its role in the NLRP3 inflammasome-dependent inflammatory response during cerebral ischemia-reperfusion remains unclear. To investigate the molecular mechanisms involved in baicalin alleviating cerebral ischemia-reperfusion injury, we investigated the AMPK signaling pathway which regulates NLRP3 inflammasome activity. SD rats were treated with baicalin at doses of 100 mg/kg and 200 mg/kg, respectively, after middle cerebral artery occlusion at 2 h and reperfusion for 24 h (MCAO/R). MCAO/R treatment significantly increased cerebral infarct volume, changed the ultrastructure of nerve cells, and activated the NLRP3 inflammasome, manifesting as significantly increased expression of NLRP3, ASC, cleaved caspase-1, IL-1β, and IL-18. Our results demonstrated that baicalin treatment effectively reversed these phenomena in a dose-dependent manner. Additionally, inhibition of NLRP3 expression was found to promote the neuroprotective effects of baicalin on cortical neurons. Furthermore, baicalin remarkably increased the expression of p-AMPK following oxygen glucose deprivation/reperfusion (OGD/R). The expression of the NLRP3 inflammasome was also increased when the AMPK pathway was blocked by compound C. Taken together, our findings reveal that baicalin reduces the activity of the NLRP3 inflammasome and consequently inhibits cerebral ischemia-reperfusion injury through activation of the AMPK signaling pathway.

据报道，黄芩苷对神经性缺氧缺血损伤有改善作用；然而，它在脑缺血再灌注过程中 NLRP3 炎症小体依赖性炎症反应中的作用仍不清楚。为了研究黄芩苷减轻脑缺血再灌注损伤的分子机制，我们研究了调节 NLRP3 炎性体活性的 AMPK 信号通路。SD大鼠分别在大脑中动脉闭塞2小时和再灌注24小时（MCAO/R）后，分别以100mg/kg和200mg/kg的剂量给予SD大鼠黄芩苷。MCAO/R 治疗显着增加了脑梗死体积，改变了神经细胞的超微结构，并激活了 NLRP3 炎性体，表现为 NLRP3、ASC、cleaved caspase-1、IL-1β 和 IL-18 的表达显着增加。我们的研究结果表明，黄芩苷治疗以剂量依赖性方式有效地逆转了这些现象。此外，发现抑制 NLRP3 表达可促进黄芩苷对皮质神经元的神经保护作用。此外，黄芩苷在氧葡萄糖剥夺/再灌注 (OGD/R) 后显着增加 p-AMPK 的表达。当 AMPK 通路被化合物 C 阻断时，NLRP3 炎性体的表达也增加。综上所述，我们的研究结果表明黄芩苷降低了 NLRP3 炎性体的活性，从而通过激活 AMPK 信号通路抑制脑缺血再灌注损伤。发现抑制 NLRP3 表达可促进黄芩苷对皮质神经元的神经保护作用。此外，黄芩苷在氧葡萄糖剥夺/再灌注 (OGD/R) 后显着增加 p-AMPK 的表达。当 AMPK 通路被化合物 C 阻断时，NLRP3 炎性体的表达也增加。综上所述，我们的研究结果表明黄芩苷降低了 NLRP3 炎性体的活性，从而通过激活 AMPK 信号通路抑制脑缺血再灌注损伤。发现抑制 NLRP3 表达可促进黄芩苷对皮质神经元的神经保护作用。此外，黄芩苷在氧葡萄糖剥夺/再灌注 (OGD/R) 后显着增加 p-AMPK 的表达。当 AMPK 通路被化合物 C 阻断时，NLRP3 炎性体的表达也增加。综上所述，我们的研究结果表明黄芩苷降低了 NLRP3 炎性体的活性，从而通过激活 AMPK 信号通路抑制脑缺血再灌注损伤。