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目的:探讨养阴通脑颗粒(YYTN)对缺血/再灌注损伤大鼠的保护作用及其可能的作用机制。方法:采用线栓法建立大鼠局灶性脑缺血(MCAO)模型,缺血90min后再灌注,分假手术组、MCAO组、YYTN高、中、低剂量组,再灌注后24h灌胃给药,连续7d。在缺血再灌注后第1、3、7天,采用Longa法进行神经功能评分;术后第7天,进行TTC染色、采用免疫荧光双标检测Brd U/Nestin免疫阳性细胞、Western blot检测p-NFκB、p-p65、p-IκBα蛋白表达。结果:缺血再灌注后第3、7天,与假手术组比较,MCAO组Longa评分极显著升高(P<0.01),梗死体积百分比明显升高(P<0.01);与MCAO组比较,YYTN高、中剂量组Longa评分明显降低(P<0.05,P<0.01),且梗死体积的百分比明显减少(P<0.01)。缺血再灌注后第7天,与假手术组比较,MCAO组Brd U/Nestin免疫阳性细胞数量明显增多(P<0.01),p-NFκB、p-p65蛋白表达明显增多(P<0.01),p-IκBα蛋白表达显著减少(P<0.01);与MCAO组比较,YYTN各剂量组Brd U/Nestin免疫阳性细胞数量明显增多(P<0.01),且p-NFκB、p-p65蛋白表达明显减少(P<0.01),p-IκBα蛋白表达显著增多(P<0.01)。结论:YYTN可促进脑缺血再灌注损伤后神经功能恢复、减少梗死体积、促进缺血周边区NSCs增殖进行神经系统自我修复,其作用机制可能与其抑制NF-κB信号通路有关。
Objective: To investigate the protective effect of YYTN on ischemia / reperfusion injury in rats and its possible mechanism. Methods: The model of focal cerebral ischemia (MCAO) was established by thread occlusion in rats. After ischemia 90 min, reperfusion, sham operation group, MCAO group, YYTN high, medium and low dose groups were given intragastrically Administration, continuous 7d. On the 1st, 3rd, 7th day after ischemia-reperfusion, the neurological function score was measured by Longa method. TTC staining was performed on the 7th day after surgery. BrdU / Nestin immunoreactive cells were detected by double immunofluorescence staining. NFκB, p-p65, p-IκBα protein expression. Results: Compared with the sham operation group, the Longa score of MCAO group was significantly increased (P <0.01) and the infarct volume percentage was significantly increased on the 3rd and 7th day after ischemia / reperfusion (P <0.01). Compared with MCAO group, The Longa score of YYTN high and middle dose groups was significantly lower (P <0.05, P <0.01), and the percentage of infarct volume was significantly decreased (P <0.01). On the 7th day after ischemia / reperfusion, the number of BrdU / Nestin immunoreactive cells in MCAO group was significantly increased (P <0.01) and the expression of p-NFκB and p-p65 was significantly increased (P <0.01) (P <0.01). Compared with MCAO group, the number of BrdU / Nestin immunoreactive cells in each dose group of YYTN increased significantly (P <0.01), and the expression of p-NFκB and p-p65 protein decreased significantly (P <0.01), p-IκBα protein expression was significantly increased (P <0.01). CONCLUSION: YYTN can promote neurological recovery, decrease infarct volume, promote the proliferation of NSCs in ischemic peripheral area and repair the nervous system after cerebral ischemia-reperfusion injury. Its mechanism may be related to the inhibition of NF-κB signaling pathway.