研究石菖蒲和α-细辛醚抵抗大鼠疲劳运动后学习记忆下降的RGS14/MEK/ERK信号通路作用机制。80只SD大鼠按完全随机法分为:正常组(normal,Nor)、运动组(exercise,E)、运动+石菖蒲组(exercise+Acorus tatarinowii Schott,EAT)、运动+α-细辛醚组(exercise+α-asarone,EαA)、运动+石菖蒲+RGS14拮抗剂CCG-63802组(EATC)、运动+α-细辛醚+RGS14拮抗剂CCG-63802(EαAR)、运动+石菖蒲+MEK拮抗剂U0126组(EATU)、运动+α-细辛醚+MEK拮抗剂U0126组(EαAU),每组10只。开展水迷宫实验进行学习记忆检测;利用免疫组化、免疫印迹(Western blot)和荧光实时定量PCR(RT-PCR)等方法检测G蛋白信号调节蛋白14(regulator of G protein signaling 14,RGS14)、Raf-1、磷酸化丝裂原活化蛋白激酶激酶(phosphorylated mitogen-activated protein kinase kinase,p-MEK)和磷酸化细胞外信号调节激酶1/2(phosphorylated extracellular signal-regulated kinase 1/2,p-ERK1/2)表达水平。结果表明EAT和EαA组大鼠逃避潜伏期显著低于E组;穿越平台次数显著高于E组(P<0.01)。EATC和EαAR组大鼠逃避潜伏期最短,穿越平台次数最多(P<0.01)。EATU和EαAU大鼠逃避潜伏期最长,穿越平台次数最少(P<0.01)。EAT和EαA组RGS14蛋白和mRNA表达水平显著低于E组,Raf-1、p-MEK和p-ERK1/2表达水平则显著高于E组(P<0.01)。EATC和EαAR组RGS14蛋白和mRNA表达水平最低,显著低于其他各组,Raf-1、p-MEK和p-ERK1/2表达水平最高,显著高于其他各组(P<0.01或P<0.05)。EATU和EαAU组p-MEK、p-ERK1/2表达水平最低,显著低于其他各组(P<0.01)。以上实验结果表明石菖蒲和α-细辛醚能够基于对海马RGS14/MEK/ERK信号通路的调节,从而显著提高疲劳运动大鼠的学习记忆。
Objectives:This study is to investigate the effects of new anti-tumor formular(NAF)on expression of PCNA,P21 ras and NF-KB P65 in liver precancerous lesions of HBV large envelope transgenic mice injected by aflatoxin B1(AFB1).Methods:The precancerous HBV large envelope transgenic mouse injected by AFB1 liver model was used.Mice was given water,NAF concentrated water solution throughout the whole experiment(48 weeks).PCNA,P21 ras and NF-KB P65 protein expression were detected by immunohistochemical method.Results: PCNA,P21 ras and NF-KB P65 expressions were significantly inhibited by NAF treatment.Conclusion NAF inhibited PCNA,P21 ras and NF-KB P65 protein expressions,therefore,NAF could show obvious effects on protecting against synergistic hepatoearcinogenesis of HBV and AFB1.
目的:观察有氧游泳运动对Ⅱ型糖尿病大鼠肾脏损伤的改善效果,并探讨其可能的机制。方法:45只4周龄健康雄性SD大鼠,随机抽取10只为正常对照组,基础饲料喂养;其余35只经高糖高脂喂养5周后,配合腹腔注射STZ(35 mg/kg.bw)诱导建立Ⅱ型糖尿病大鼠模型;7周后,将成模大鼠随机分为糖尿病安静组和糖尿病运动组,每组14只。3组大鼠均采用基础饲料喂养;糖尿病运动组大鼠进行8周有氧游泳运动;正常对照组、糖尿病安静组2组大鼠均自由活动,不施加任何干预。结果:(1)8周有氧游泳运动后,糖尿病运动组肾脏在电镜下的形态表现为肾小球三层结构较清晰,基底膜增厚不明显,足突融合减少,溶酶体增多现象等均有一定程度减少,较糖尿病安静组有明显改善;(2)糖尿病运动组血糖浓度和24 h UA排泄量较糖尿病安静组显著降低(分别为P<0.05或P<0.01);(3)糖尿病运动组肾皮质Jagged-1、Val1744NICD和Hes-1蛋白的表达较糖尿病安静组均显著降低(P<0.05或P<0.01)。结论:运动可提高Ⅱ型糖尿病大鼠肾功能,改善大鼠肾脏损伤,可能与其下调Ⅱ型糖尿病状态下激活的Notch-1信号通路有关。
