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目的:探讨葛根素在大鼠脑缺血再灌注损伤后的神经保护作用机制以及与JAK2/STAT3信号通路的相关性。方法:将36只SD雄性大鼠随机分为假手术组12只和造模组24只(其中造模组分缺血再灌注组12只及葛根素组12只)。采用线栓法制备大鼠MCAO模型,于脑缺血2h再灌注24h时用Longa评分法进行神经功能缺损评分,TTC染色法测定脑梗死体积,TUNEL法检测海马组织神经细胞凋亡数,免疫组织化学法检测海马组织磷酸化的JAK2(P-JAK2)、STAT3(P-STAT3)的表达。结果:与假手术组比较,造模组神经功能缺损加重,梗死体积增大,凋亡细胞数增多,P-JAK2和P-STAT3表达水平增高,差异具有统计学意义(P<0.05);与缺血再灌注组比较,葛根素组神经功能缺损评分明显下降,梗死体积与凋亡阳性细胞数均见明显减少,P-JAK2及P-STAT3表达水平显著降低,差异均具有统计学意义(P<0.05)。结论:JAK2/STAT3信号通路参与了脑缺血再灌注损伤过程;通过抑制JAK2/STAT3信号通路的异常激活可能是葛根素神经保护作用机制之一。
Aims: To investigate the neuroprotective effect of puerarin on cerebral ischemia-reperfusion injury in rats and its relationship with JAK2 / STAT3 signaling pathway. Methods: Thirty - six male Sprague - Dawley rats were randomly divided into sham operation group (n = 12) and model group (n = 24) (12 in model group and 12 in puerarin group). The rat model of MCAO was established by thread occlusion. The neurological deficits were assessed by Longa score at 2h after cerebral ischemia. The infarct volume was measured by TTC staining. The number of apoptotic neurons in hippocampus was detected by TUNEL. The expression of phosphorylated JAK2 (P-JAK2), STAT3 (P-STAT3) in hippocampus was detected by chemical method. Results: Compared with the sham operation group, the neurological deficit, the volume of infarct and the number of apoptotic cells in the model group increased, the expression of P-JAK2 and P-STAT3 increased (P <0.05), and the difference was statistically significant Compared with the ischemia-reperfusion group, the score of neurological deficit in the Puerarin group was significantly decreased, the infarct volume and the number of apoptotic cells were significantly decreased, and the expression of P-JAK2 and P-STAT3 were significantly decreased (P <0.05). Conclusion: The JAK2 / STAT3 signaling pathway is involved in the process of cerebral ischemia-reperfusion injury. It may be one of the neuroprotective mechanisms of puerarin by inhibiting the activation of JAK2 / STAT3 signaling pathway.