摘要
研究虾青素通过PI3K/Akt存活途径增强大鼠海马神经元对心搏骤停诱发的全脑缺血的耐受性及调节机制。构建大鼠窒息性全脑缺血模型,60只SPF级Wistar大鼠随机分为空白对照组(KB组,n=20)、抑制剂组(YB组,n=20)、虾青素组(XB组,n=20)。通过测定细胞活性,采用Ed U(5-Ethynyl-2’-de0xyuridine)标记具有增值能力细胞的方法,观察全脑缺血后海马DG和CAI区的神经干细胞增值情况。采用RT-PCR法、Western blot方法分别检测各组大鼠海马神经细胞内JNK3 mRNA表达及蛋白表达情况。与对照组相比(1. 107±0. 121),虾青素剂量组细胞活性增强(1. 468±0. 302)。DG和CAI区的双标阳性细胞数,与对照组相比,YB组是正常组Ed U阳性细胞数量的1. 2倍。RT-PCR结果分析可得:与对照组相比,YB组凝胶电泳JNK3 mRNA表达上升,与YB组相比,虾青素剂量组细胞内JNK3 mRNA表达降低。JNK3蛋白表达与对照组比较,抑制剂组JNK3蛋白表达降低(P <0. 05);与抑制剂组比较,虾青素组JNK3蛋白表达升高(P <0. 05)。试验表明虾青素可通过PI3K/Akt信号通路增强大鼠海马神经元活化从而发挥对心搏骤停诱发的全脑缺血的耐受性作用。
To investigate the tolerance and regulation mechanism of astaxanthin in rat hippocampal neurons induced by cardiac arrest induced by cardiac arrest by PI3 K/Akt survival pathway,the model was used to observe the effect of astaxanthin on hippocampal neurogenesis by acute cerebral ischemia through PI3 K/Akt survival pathway. Sixty SPF wistar rats were randomly divided into blank control group( KB group,n = 20),inhibitor group( YB group,n = 20),and astaxanthin group( XB group,n = 20). By measuring cell activity,the cells with value-adding ability were labeled with Ed U( 5-Ethynyl-2’-de0 xyuridine). To observe the increase of neural stem cells in hippocampal DG and CAI areas after global cerebral ischemia. The expression of JNK3 mRNA and protein in hippocampal neurons of each group were detected by RT-PCR and Western blot. Compared with the control group( 1. 107 ± 0. 121),the cell viability of the astaxanthin dose group was enhanced( 1. 468 ± 0. 302). The number of double-labeled positive cells in the DG and CAI regions,the YB group was 1. 2 times the number of Ed U-positive cells in the normal group compared with the control group. The results of RTPCR analysis showed that compared with the control group,the expression level of JNK3 mRNA in the YB group was increased. Compared with the YB group,the expression level of JNK3 mRNA in the astaxanthin dose group was decreased. JNK3 protein expression level compared with the control group,the expression level of JNK3 protein in the inhibitor group was lower( P < 0. 05). The expression level of JNK3 protein in the astaxanthin group was higher than that in the inhibitor group( P < 0. 05). Astaxanthin can enhance the activation of rat hippocampal neurons through PI3 K/Akt signaling pathway exerting its tolerance to global cerebral ischemia induced by cardiac arrest.
作者
柴林
刘春艳
方志成
杨贤义
肖敏
李昌盛
夏俊琳
CHAI Lin;LIU Chun-yan;FANG Zhi-cheng;YANG Xian-yi;XIAO Min;LI Chang-sheng;XIA Jun-lin(Shiyan Taihe Hospital,Shiyan 442000,China;Shiyan Maternal and Child Health Hospital,Shiyan 442000,China)
出处
《药物生物技术》
CAS
2019年第6期485-489,共5页
Pharmaceutical Biotechnology
