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高压氧对运动性疲劳大鼠肝糖原及肝脏形态结构的影响
引用本文:袁春华,滕进忠,陈艳华,李国印.高压氧对运动性疲劳大鼠肝糖原及肝脏形态结构的影响[J].南昌职业技术师范学院学报,2013(6):21-25.
作者姓名:袁春华  滕进忠  陈艳华  李国印
作者单位:[1]江西科技师范大学生命科学学院,江西南昌330013 [2]解放军第94医院康复科,江西南昌330002
基金项目:江西省卫生厅科技项目(20113141);江西省自然科学基金(20132BAB205064).
摘    要:目的:通过研究高压氧对肝糖原和肝脏形态结构的影响,探讨高压氧消除运动性疲劳的作用机制.方法:4周龄健康雄性SD大鼠30只,随机分为3组:对照组、疲劳模型组、疲劳高压氧暴露组,每组10只.建立大鼠游泳致力竭疲劳模型并通过高压氧暴露进行恢复;8周实验后取每只大鼠两块肝脏组织,其中一块取每只大鼠的肝脏相同部位,光镜观察肝脏组织的病理变化;另一块取肝右叶5g,制备成10%的肝组织匀浆,采用蒽酮法检测肝糖原含量的变化.结果:(1)疲劳高压氧暴露组大鼠游泳时间明显长于疲劳模型组(P<0.05).(2)疲劳模型组与对照组比较,肝糖原含量显著降低(P<0.01);高压氧暴露组与疲劳模型组比较,肝糖原含量显著增高(P<0.05);疲劳高压氧暴露组与对照组比较,肝糖原含量显著降低(P<0.05).(3)光镜观察显示:对照组大鼠肝组织结构正常,疲劳模型组大鼠肝细胞肿胀,核变大,细胞间质模糊,中央静脉扩张淤血,汇管区少量淋巴细胞浸润,胞浆疏松,肝窦内枯否细胞增生肥大.疲劳高压氧暴露组大鼠肝细胞核肿胀有所改善,充血现象消失,肝细胞轮廓较为清晰,细胞间质纹理较疲劳组更清晰,汇管区炎症消退.结论:高压氧消除运动性疲劳的部分作用机制,可能是通过调节肝糖原含量、促进血糖的稳定,并改善肝脏的形态结构、缓解肝组织损伤而实现.

关 键 词:运动疲劳  高压氧  肝糖原  肝脏

Effect of Hyperbaric Oxygen on Hepatic Glycogen and Structure of Exercise-induced Fatigue Rats
Yuan Chun-hua,Teng Jin-zhong,Chen Yan-hua & Li Guo-yin.Effect of Hyperbaric Oxygen on Hepatic Glycogen and Structure of Exercise-induced Fatigue Rats[J].Journal of Nanchang Vocational & Technical Techers' College,2013(6):21-25.
Authors:Yuan Chun-hua  Teng Jin-zhong  Chen Yan-hua & Li Guo-yin
Institution:1 (1. Jiangxi Science & Technology Normal University, Nanchang 330013, P.R. China; 2. The 94th Hospital of the PLA, Nanchang 330000, P.R. China)
Abstract:Objective: to observe the effect of hyperbaric oxygen exposure on hepatic glycogen level and structure changes in exercise-induced fatigue rats. Methods: thirty SD rats were divided into 3 groups randomly: control group, fatigue model group and hyperbaric oxygen (HBO)exposure group of fatigue model. Each group has 10 rats. Establishing rat model of the exhausted swimming to fatigue and giving them hyperbaric oxygen exposure, 8 weeks after the experiment we get two blocks liver tissue from each rat. One is the same part of the liver and the pathological changes of liver tissue were observed by light microscopy. The other which is the right lobe of the liver is prepared in 10% liver homogenates to detect the content of the hepatic glycogen by chromatometry. Result: compared with the fatigue model group, the HBO exposure group had significant difference, the swimming time of rats prolonged ( P 〈 0.05 ). The hepatic glycogen content in the fatigue model group decreased significantly compared with the control group (P〈0.01), and the content in the HBO exposure group was increased compared with the model group (P〈0.05) and was decreased compared with the control group (P〈0.05). Under light microscopy, the hepatic tissue structure is normal in the control group, while in the fatigue model group, liver cell swelling, nuclear enlargement, interstitial cell fuzzy, the central vein congestion, periportal lymphocyte infiltration, cytoplasm osteoporosis, hepatic sinus kupffer cell hyperplasia. After HBO therapy, liver cells swelling were improved, congestion phenomenon disappears, liver cell contour clear, periportal inflammation subsided and interstitial cell texture was more clearly than the fatigue groups. Conclusion: HBO exposure can effectively improve the rat swimming time, reduce the content of MDA and increase the activity of SOD of fatigue rat liver, improve pathological changes of liver tissue. This proved that hyperbaric oxygen exposure can effectively protect the damaged liver of fatigue rat. Hyperbaric oxygen exposure may increase hepatic glycogen content and improve structure of hypatocytes in fatigue rats, which may be part of its mechanism underlying relieving exercise-induced fatigue.
Keywords:exercise-induced fatigue  hyperbaric oxygen  hepatic glycogen  liver
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