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1.
目的:研究五子衍宗丸对男性老年肾虚者外周血白细胞线粒体DNA缺失、线粒体呼吸链酶复合体活力的影响。方法:38例男性老年肾虚者采用单盲法,随机分为五子衍宗丸治疗组和安慰剂对照组,服药3个月。分别用聚合酶链反应(PCR)和酶动力学方法检测治疗前后外周血白细胞线粒体DNA缺失及线粒体呼吸链酶复合体的活力。结果:五子衍宗丸可提高男性老年肾虚者外周血白细胞线粒体呼吸链酶复合体I、Ⅳ活力,减少线粒体DNA缺失(P<0.05,P<0.01)。结论:五子衍宗丸对男性老年肾虚者白细胞线粒体DNA氧化损伤有保护作用。  相似文献
2.
目的 :研究五子衍宗丸及其拆方对线粒体DNA缺失、线粒体呼吸链酶复合体及三磷酸腺苷(ATP)合成的影响。方法 :用聚合酶链反应 (PCR)、酶动力学和生物发光技术进行检测。结果 :五子衍宗丸及其拆方的枸杞子、菟丝子可减少老年大鼠脑组织线粒体DNA缺失 (P <0 0 1) ,提高脑线粒体呼吸链复合酶Ⅰ、Ⅳ活力和ATP的合成 (P <0 0 5,P <0 0 1) ;枸杞子、菟丝子还可减少老年大鼠心线粒体DNA缺失 (P<0 0 5,P <0 0 1)。结论 :五子衍宗丸、枸杞子、菟丝子对老年大鼠线粒体DNA的氧化损伤有保护作用。  相似文献
3.
消炎利胆片提取物对小鼠应激性肝损伤的影响   总被引:1,自引:0,他引:1  
摘要 目的研究消炎利胆片提取物(XLP)对拘束负荷诱发小鼠应激性肝损伤的影响。方法 实验动物随机分为正常对照组, 拘束应激模型组, 硫普罗宁组(80 mg/kg)、XLP 低、中、高剂量(XLP 125、250、500 mg/kg)组, 共6组, 每组10只小鼠。分别用赖氏法测定小鼠血浆丙氨酸氨基转移酶(ALT)活性、硫代巴比妥酸法测定肝组织丙二醛(MDA)含量、Griess化学法测定一氧化氮(NO)含量,荧光酶标仪测定肝组织抗氧化能力指数(ORAC)、HPLC法测定谷胱甘肽(GSH)含量,比色法测定谷胱甘肽过氧化物酶(GPX-Px)、谷胱甘肽硫转移酶(GST)活性,紫外分光光度法测定肝线粒体呼吸链复合酶活性、氧化还原差光谱测定细胞色素(Cyt)a、b、c和c1含量。结果 与模型组比较, XLP可以明显降低拘束负荷小鼠血浆ALT活性、肝组织MDA和NO含量, 有效提高肝组织的ORAC指数、GSH含量、GPX-Px和GST活性;同时XLP可以显著增加拘束小鼠肝线粒体呼吸链复合酶Ⅱ活性, 明显降低肝细胞色素含量。结论 消炎利胆片提取物对拘束负荷诱发小鼠应激性肝损伤有一定的减轻作用, 其作用可能与缓解拘束负荷小鼠的氧化应激状态相关。  相似文献
4.
目的研究五子衍宗丸及其拆方对线粒体DNA缺失、线粒体呼吸链酶复合体及三磷酸腺苷(ATP)合成的影响。方法用聚合酶链反应(PCR)、酶动力学和生物发光技术进行检测。结果五子衍宗丸及其拆方的枸杞子、菟丝子可减少老年大鼠脑组织线粒体DNA缺失(P<0.01),提高脑线粒体呼吸链复合酶Ⅰ、Ⅳ活力和ATP的合成(P<0.05,P<0.01);枸杞子、菟丝子还可减少老年大鼠心线粒体DNA缺失(P<0.05,P<0.01)。结论五子衍宗丸、枸杞子、菟丝子对老年大鼠线粒体DNA的氧化损伤有保护作用。  相似文献
5.
目的:探讨丁基苯酞(butylphthalide,NBP)对原代培养神经元在低糖低氧损伤下的保护作用及线粒体作用机制。方法:采用Hoechst 33342和PI共染的方法,观察NBP对低糖低氧损伤造成神经细胞坏死和凋亡的影响,并用荧光探针标记以及分光光度法检测NBP对神经细胞线粒体膜电位、线粒体膜流动性及线粒体呼吸链复合酶IV活性的影响。结果:NBP(10-6~10-4mol/L)能显著减少低糖低氧引起的神经细胞坏死和凋亡;机制研究表明它能明显改善由损伤引起的神经细胞线粒体膜电位、线粒体膜流动性及线粒体呼吸链复合酶IV活性的降低。结论:NBP对低糖低氧损伤导致的神经细胞坏死和凋亡具有良好的保护作用,而线粒体保护可能是其作用机制之一。  相似文献
6.

Objective

To investigate the protective role of Sijunzi decoction in neuromuscular junction (NMJ) and muscle cell mitochondria ultrastructure; as well as its effects on the amount of adenosine triphosphate (ATP) and the activities of mitochondrial respiratory chain complexes I, II, III, and IV in autoimmune myasthenia gravis rats.

Methods

An experimental autoimmune myasthenia gravis (EAMG) rat model was established by inoculating rats with acetylcholine receptors extracted from Torpedo. Rats were divided into three groups: model, prednisone, and Sijunzi decoction, and were fed physiological saline, prednisone, or Sijunzi decoction, respectively. NMJ and muscle cell mitochondria ultrastructure were observed by transmission electron microscope. The amount of ATP was assessed by high performance liquid chromatography. The activities of mitochondrial respiratory chain complexes I, II, III, and IV was determined using the Clark oxygen electrode method.

Results

In the model group, there were sparse muscle fibers, with decreased mitochondria, and sparse, diffluent, or absent NMJ folds. After intervention with Sijunzi decoction, the above pathology changes were improved: muscle fiber structure was clear and complete; the mitochondria count was higher; and the NMJ structure was close to normal. Gastrocnemius muscle mitochondria in the model group produced significantly less ATP than those in the prednisone group (P<0.01). Conversely, the ATP of Sijunzi decoction group was significantly higher than prednisone group (P<0.01). The activities of gastrocnemius muscle mitochondrial respiratory chain complexes I, II, III, and IV in both the prednisone and Sijunzi decoction groups was dramatically higher compared with the model group (P<0.05). The activities of complexes I and III in the Sijunzi decoction group were significantly higher than those in the prednisone group (P< 0.05), but there was no obvious difference in complex II or IV activities between the two groups (P>0.05).

Conclusion

Sijunzi decoction improved pathological changes in muscle mitochondria and NMJ, enhanced the amount of ATP in gastrocnemius muscle mitochondria, and improved the activities of respiratory chain complexes I, II, III, and IV (especially I and III) of the EAMG rats.  相似文献
7.
OBJECTⅣE: To investigate the protective role of Sijunzi decoction in neuromuscular junction(NMJ)and muscle cell mitochondria ultrastructure; as well as its effects on the amount of adenosine triphosphate(ATP) and the activities of mitochondrial respiratory chain complexes I, Ⅱ, Ⅲ, and Ⅳ in autoimmune myasthenia gravis rats.METHODS: An experimental autoimmune myasthenia gravis(EAMG) rat model was established by inoculating rats with acetylcholine receptors extracted from Torpedo. Rats were divided into three groups: model, prednisone, and Sijunzi decoction, and were fed physiological saline, prednisone, or Sijunzi decoction, respectively. NMJ and muscle cell mitochondria ultrastructure were observed by transmission electron microscope. The amount of ATP was assessed by high performance liquid chromatography. The activities ofmitochondrial respiratory chain complexes I, Ⅱ, Ⅲ,and Ⅳ was determined using the Clark oxygen electrode method.RESULTS: In the model group, there were sparse muscle fibers, with decreased mitochondria, and sparse, diffluent, or absent NMJ folds. After intervention with Sijunzi decoction, the above pathology changes were improved: muscle fiber structure was clear and complete; the mitochondria count was higher; and the NMJ structure was close to normal. Gastrocnemius muscle mitochondria in the model group produced significantly less ATP than those in the prednisone group(P0.01). Conversely, the ATP of Sijunzi decoction group was significantly higher than prednisone group(P0.01). The activities of gastrocnemius muscle mitochondrial respiratory chain complexes I, Ⅱ, Ⅲ, and Ⅳ in both the prednisone and Sijunzi decoction groups was dramatically higher compared with the model group(P0.05). The activities of complexes I and Ⅲ in the Sijunzi decoction group were significantly higher than those in the prednisone group(P0.05), but there was no obvious difference in complex Ⅱ or Ⅳ activities between the two groups(P0.05).CONCLUSION: Sijunzi decoction improved pathological changes in muscle mitochondria and NMJ,enhanced the amount of ATP in gastrocnemius muscle mitochondria, and improved the activities of respiratory chain complexes I, Ⅱ, Ⅲ, and Ⅳ(especially I and Ⅲ) of the EAMG rats.  相似文献
8.
目的:从线粒体角度探讨电针治疗阿尔茨海默病(AD)的作用机制.方法:选取8月龄SAMP8小鼠12只,随机分为模型组6只,电针组6只,另选取6只8月龄的SAMR1小鼠为对照组.电针组电针“百会”“大椎”“肾俞”“太溪”穴,每日1次,每次20 min,10次为一疗程,共治疗3个疗程;其他两组不做治疗干预,只进行相同方式、相同时间和相同程度的抓取和小鼠固定器固定.疗程结束后,采用Morris水迷宫检测小鼠学习记忆能力,分光光度法检测海马线粒体呼吸链酶复合物的活性,反相高效液相色谱法检测细胞三磷酸腺苷(ATP)水平.结果:与对照组相比,模型组小鼠平均逃避潜伏期明显延长,原平台象限停留时间缩短,海马线粒体呼吸链酶复合物Ⅰ、Ⅱ、Ⅲ和Ⅳ活性降低,细胞ATP含量减少;与模型组比较,电针组平均逃避潜伏期缩短,原平台象限停留时间延长,海马线粒体呼吸链酶复合物Ⅰ、Ⅱ、Ⅲ和Ⅳ活性升高,细胞ATP含量增加.结论:电针能够提高小鼠海马线粒体呼吸链酶复合物活性及细胞ATP含量,改善线粒体功能,可能是治疗AD的机制之一.  相似文献
9.
目的:探讨脾虚型功能性消化不良(FD)大鼠胃组织线粒体呼吸链复合物IV亚单位(COX VA)蛋白和mRNA表达及脾虚一号方对其的干预作用。方法: 70只7 d龄雄性SD大鼠随机分为正常组,FD模型组(单模型组),脾虚型FD模型组(双模型组),多潘立酮组,脾虚一号方低、中、高剂量组,每组10只。FD模型组、脾虚证FD模型组给予0.1%蔗糖碘乙酰胺蔗糖溶液灌胃,连续6 d。脾虚证FD模型组正常饲料喂养至6周龄后叠加改良小平台站立,连续14 d。造模结束后分别给予蒸馏水10 mL·kg-1·d-1,多潘立酮3.125 mg·kg-1·d-1,脾虚一号方1.275,2.55,5.1 g·kg-1·d-1,灌胃14 d。采用实时荧光定量聚合酶链式反应(Real-time PCR),蛋白质免疫印迹(Western blot)和免疫组化法检测胃窦组织COX VA mRNA与蛋白表达量。结果:与正常组比较,脾虚一号方高剂量组COX VA蛋白平均积分吸光度升高(P<0.05);多潘立酮组、脾虚一号方低、中剂量组COX VA蛋白表达量均有不同程度降低(P<0.01),而脾虚一号方高剂量组COX VA蛋白表达量则升高(P<0.01);单模型组COX VA mRNA表达量升高最明显(P<0.01)。与双模型组比较,多潘立酮组、脾虚一号方低、中剂量组COX VA蛋白表达量均有不同程度降低(P<0.01),多潘立酮组、脾虚一号方低、中剂量组COX VA mRNA表达量均有不同程度降低,而脾虚一号方高剂量组、单模型组则升高,差异均无统计学意义。结论:脾虚型FD大鼠存在COX VA蛋白的表达量降低,脾虚一号方能够增加COX VA蛋白的表达量,改善能量代谢。  相似文献
10.
目的:从线粒体角度探讨电针治疗阿尔茨海默病(AD)的作用机制。方法:选取8月龄SAMP8小鼠12只,随机分为模型组6只,电针组6只,另选取6只8月龄的SAMR1小鼠为对照组。电针组电针"百会""大椎""肾俞""太溪"穴,每日1次,每次20min,10次为一疗程,共治疗3个疗程;其他两组不做治疗干预,只进行相同方式、相同时间和相同程度的抓取和小鼠固定器固定。疗程结束后,采用Morris水迷宫检测小鼠学习记忆能力,分光光度法检测海马线粒体呼吸链酶复合物的活性,反相高效液相色谱法检测细胞三磷酸腺苷(ATP)水平。结果:与对照组相比,模型组小鼠平均逃避潜伏期明显延长,原平台象限停留时间缩短,海马线粒体呼吸链酶复合物Ⅰ、Ⅱ、Ⅲ和Ⅳ活性降低,细胞ATP含量减少;模型组比较,电针组平均逃避潜伏期缩短,原平台象限停留时间延长,海马线粒体呼吸链酶复合物Ⅰ、Ⅱ、Ⅲ和Ⅳ活性升高,细胞ATP含量增加。结论:电针能够提高小鼠海马线粒体呼吸链酶复合物活性及细胞ATP含量,改善线粒体功能,可能是治疗AD的机制之一。  相似文献
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