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牛樟叶水提物对D-半乳糖致衰老模型小鼠的作用机制研究 被引量:4

Effect and Mechanism of Aqueous Extracts of Cinnamomum Kanehirae Leaves on D-Galactose-Induced Aging Model Mice
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摘要 目的探讨牛樟叶水提物(AECL)对D-半乳糖致衰老模型小鼠的作用机制。方法取KM小鼠,于颈背部皮下注射D-半乳糖(100 mg/kg,连续20 d),建立衰老小鼠模型。另取10只同批健康小鼠作为正常对照组(A组);模型小鼠随机分为模型组(B组),阳性对照组(C组,维生素E 200 mg/kg),AECL高、中、低剂量组(D1组、D2组、D3组,生药20,10,5 g/kg),各10只。C组、D1组、D2组、D3组小鼠灌胃给药,每日2次,连续30 d;A组和B组给予等体积生理盐水。末次给药2 h后,剖取肝脏、心脏、肾脏和脑,制备成10%组织匀浆,以酶联免疫吸附(ELISA)法检测上述组织、器官匀浆中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)、一氧化氮(NO)和总抗氧化能力(T-AOC)的水平。结果与A组比较,B组小鼠血清中SOD,GSH-Px,T-AOC水平均显著降低(P<0.05);与B组比较,C组、D1组、D2组小鼠血清中SOD和GSH-Px水平均显著升高(P<0.05),C组、D1组T-AOC水平均显著升高(P<0.05)。与A组比较,B组小鼠肝组织匀浆中SOD和CAT水平均显著降低(P<0.05);与B组比较,C组、D1组、D2组、D3组肝组织匀浆中SOD和CAT水平均显著升高(P<0.05)。与A组比较,B组小鼠肾脏组织匀浆中SOD水平显著降低(P<0.05);与B组比较,C组、D2组SOD水平均显著升高(P<0.05)。与A组比较,B组小鼠心脏组织匀浆中SOD显著降低(P<0.05);与B组比较,C组和D2组SOD均显著升高,D1组CAT水平均显著升高(P<0.05)。与A组比较,B组小鼠脑组织匀浆中SOD,GSH-Px,NO水平均显著降低(P<0.05);与B组比较,C组、D1组NO水平均显著升高(P<0.05)。结论AECL具有延缓衰老的作用,其作用机制可能与改善机体心、脑、肝、肾等器官的抗氧化能力有关。 Objective To investigate the effect and mechanism of aqueous extracts of Cinnamomum Kanehirae Leaves(AECL)on D-galactose-induced aging model mice.Methods KM mice were subcutaneously injected with D-galactose(100 mg/kg,20 d)at the neck and back to establish the aging model mice.Ten healthy mice in the same batch were selected as normal control group(group A),and the model mice were randomly divided into model group(group B),positive control group(group C,200 mg/kg of vitamin E),AECL high-dose,medium-dose and low-dose groups(groups D1,D2 and D3,20,10,5 g/kg of herb-drug),10 rats in each group.The mice in groups C,D1,D2 and D3 were given intragastric administration,twice a day for 30 d,the mice in group A and group B were given the equal volume of normal saline.2 h after the last administration,the liver,heart,kidney and brain were dissected to prepare10%tissue homogenate,and the levels of superoxide dismutase(SOD),catalase(CAT),glutathione peroxidase(GSH-Px),nitric oxide(NO)and total antioxidant capacity(T-AOC)were detected by enzyme-linked immunosorbent assay(ELISA).Results Compared with those in group A,the levels of SOD,GSH-Px and T-AOC in group B were significantly decreased(P<0.05).Compared with those in group B,the levels of SOD and GSH-Px in groups C,D1 and D2 were significantly increased(P<0.05),and the level of T-AOC in groups C,D1 was significantly increased(P<0.05).Compared with those in group A,the levels of SOD and CAT in liver homogenate in group B were significantly decreased(P<0.05).Compared with those in group B,the levels of SOD and CAT in liver homogenate in groups C,D1,D2,D3 were significantly increased(P<0.05).Compared with that in group A,the level of SOD in renal homogenate in group B was significantly decreased(P<0.05).Compared with that in group B,the level of SOD in renal homogenate in groups D1,D2 was significantly increased(P<0.05).Compared with those in group A,the level of SOD in heart homogenate in group B was significantly decreased(P<0.05).Compared with those in group B,the level of SOD in heart homogenate in group C,D2 was significantly increased,and the level of CAT in heart homogenate in group D1 was significardly increased(P<0.05).Compared with those in group A,and the levels of SOD,GSH-Px and NO in brain homogenate in group B were significantly decreased(P<0.05).Compared with that in group B,the level of NO in brain homogenate in groups C,D1 was significantly increased(P<0.05).Conclusion AECL has an anti-aging effect,and its mechanism may be related to improving the antioxidant capacity of heart,brain,liver,kidney and other organs.
作者 张蓓 余潇苓 万永艳 梁学政 覃开羽 ZHANG Bei;YU Xiaoling;WAN Yongyan;LIANG Xuezheng;QIN Kaiyu(Liuzhou Traditional Chinese Medical Hospital,Guangxi,China 545026;The First Affiliated Hospital of Zhejiang Chinese Medical University,Hangzhou,Zhejiang,China 310006)
出处 《中国药业》 CAS 2021年第3期18-21,共4页 China Pharmaceuticals
基金 国家自然科学基金[81460549] 广西壮族自治区柳州市柳北区应用技术研究与开发计划项目[LB201801] 广西壮族自治区柳州市阳和工业新区应用技术研究开发与科技创新项目[2019007]。
关键词 牛樟叶 水提物 衰老 D-半乳糖 小鼠 作用机制 Cinnamomum Kanehirae Leaves aqueous extracts aging D-galactose mice mechanism
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