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作 者:包春茶 李红丽 舒彬 杨忠 李倩 Bao Chuncha;Li Hongli;Shu Bin;Yang Zhong;Li Qian(Department of Rehabilitation Medicine,University Town Hospital,Chongqing Medical University,Chongqing 401331,China;Department of Histology and Embryology,Army Medical University,Chongqing 400038,China;Department of Clinical Hemopathy Teaching and Research,Army Medical University,Chongqing 400038,China)
机构地区:[1]重庆医科大学附属大学城医院康复中心,重庆401331 [2]陆军军医大学基础医学院组胚教研室,重庆400038 [3]陆军军医大学临床血液教研室,重庆400038
出 处:《中华物理医学与康复杂志》2019年第11期801-806,共6页Chinese Journal of Physical Medicine and Rehabilitation
基 金:国家自然科学基金项目(31571242)。
摘 要:目的探讨有氧耐力运动对老年小鼠肾组织纤维化的影响及其可能的分子机制。方法将36只健康雄性C57小鼠分为青年对照组(2月龄)、老年对照组(19月龄)、老年运动组(19月龄),每组12只。老年运动组给予连续有氧耐力运动。7周后取各组小鼠肾脏组织,采用HE染色、天狼星红染色、RT-PCR、免疫组织化学等技术检测肾组织病理结构改变和纤维化指标的表达情况。结果与青年对照组比较,老年对照组肾组织中胶原纤维沉积量显著增加(P<0.05);与老年对照组比较,老年运动组肾组织中胶原纤维沉积量明显减少(P<0.05)。与青年对照组比较,老年对照组肾组织中上皮细胞表面标志物E-cadherin mRNA和蛋白表达量明显减少(P<0.05);与老年对照组比较,老年运动组肾组织中E-cadherin mRNA和蛋白表达量明显增加(P<0.05)。与青年对照组比较,老年对照组成纤维细胞表面标志物α-平滑肌肌动蛋白(α-SMA)、转化生长因子β1(TGF-β1)mRNA和蛋白表达量明显减少(P<0.05);与老年对照组比较,老年运动组α-SMA、TGF-β1的mRNA和蛋白表达明显增加(P<0.05)。结论有氧耐力运动能减少胶原纤维沉积,延缓老年性肾组织纤维化发生,其机制可能与有氧耐力运动抑制了TGF-β1和α-SMA信号、上调了E-cadherin表达水平有关。Objective To explore the effect of aerobic endurance exercise on renal fibrosis in elderly mice and its possible mechanism.Methods Thirty-six healthy,male C57 mice were sorted into a young control group(2 months old),a senile control group(19 months old)and a senile exercise group(also 19 months old).The senile exercise group underwent aerobic endurance exercise for 7 weeks.Then all of the mice were sacrificed and any changes of in their renal tissues were recorded,especially the expression of fibrosis indicators using HE staining,Sirius red staining,RT-PCRs and immunohistochemical methods.Results Collagen fibers deposited in the kidney tissue of the senile groups were significantly more numerous than in the young control group,but their number had decreased significantly after the exercise.Conclusion Aerobic endurance exercise can inhibit collagen deposition and delay the formation of renal fibrosis,at least in rats.This may be related to its inhibition of TGF-β1 andα-SMA expression and up-regulation of E-cadherin expression.
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