长托宁抑制JAK2/STAT3信号通路缓解脑缺血再灌注大鼠脑内炎症反应

Changtonin inhibits JAK2/STAT3 signaling pathway to relieve brain inflammatory response in rats with cerebral ischemia-reperfusion

目的探讨长托宁对脑缺血性再灌注大鼠脑损伤的保护作用及对JAK2/STAT3信号通路的影响。方法采用线栓法制备脑缺血性再灌注(I/R)大鼠模型,随机分为假手术组(sham)、脑缺血再灌注模型组(I/R)、长托宁治疗组(PH);对各组大鼠的神经功能障碍进行评分;检测各组大鼠脑梗死体积以及脑含水量;Nissl染色各组大鼠脑组织神经细胞的数量;ELISA检测各组大鼠脑组织IL-1β、IL-6及TNF-α蛋白的表达;Western blot法检测脑组织p-JAK2、JAK2、p-STAT3和STAT3蛋白表达。结果长托宁明显改善I/R大鼠神经功能障碍,缩小脑梗死体积,降低脑含水量,增强脑内神经元的数量,显著降低IL-1β、IL-6及TNF-α蛋白表达水平,抑制p-JAK2和p-STAT3的蛋白表达。结论长托宁抑制I/R大鼠炎症反应,促进神经元的存活,与抑制JAK2-STAT3信号通路相关。

Objective To explore the protective effect of Changtoning on cerebral ischemia-reperfusion injury in rats and the effect on JAK2/STAT3 signaling pathway. Methods Rat model of cerebral ischemic reperfusion(I/R) was prepared by thread embolization method, and randomly divided into sham operation group(sham), cerebral ischemia reperfusion model group(I/R) and changtoning treatment group(PH);score the neurological dysfunction of each group of rats;detect the cerebral infarction volume and brain water content of each group of rats;Nissl stain the number of nerve cells in the brain tissue of each group of rats;ELISA detect the brain of each group of rats Expression of IL-1β, IL-6 and TNF-α protein in tissues;WB method was used to detect the expression of p-JAK2, JAK2, p-STAT3 and STAT3 protein in brain tissues. Results Changtoning significantly improved neurological dysfunction in I/R rats;reduced the volume of cerebral infarction and lowered the water content of the brain;increased the number of neurons in the brain;significantly reduced the concentration of IL-1β, IL-6 and TNF-α protein;Inhibit p-JAK2 and p-STAT3 protein expression. Conclusion Changtonin can inhibit the inflammatory response of I/R rats and promote the survival of neurons. The mechanism is related to the inhibition of JAK2-STAT3 signaling pathway.