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作 者:刘红梅[1] 李清楚[1] 康志强[1] 李蕾 何丽[1] 罗方[1] LIU Hongmei;LI Qingchu;KANG Zhiqiang(Department of Endocrinology,Zhengzhou Central Hospital,Zhengzhou 450007,China)
机构地区:[1]郑州市中心医院内分泌科
出 处:《中国糖尿病杂志》2019年第10期764-770,共7页Chinese Journal of Diabetes
基 金:河南省医学科技攻关计划项目(201503228)
摘 要:目的建立糖尿病周围神经病变(DPN)大鼠模型,探讨血糖波动对DPN大鼠的影响及相关机制。方法将45只SD大鼠随机分为正常对照(NC)组、持续高糖组(SHG)及波动血糖组(IHG),每组各15只。注射STZ诱发糖尿病,每天定时注射胰岛素及灌服葡萄糖建立血糖波动模型。12周后通过检查大鼠一般情况、血糖水平及波动性、坐骨神经传导速度(MNCV)、足底热敏反应时间、坐骨神经的超微结构改变以验证造模成功,同时检测坐骨神经的核因子κB(NF-κB)表达水平、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性及IL-1β、IL-6、TNF-α相关蛋白表达水平。结果NC、SHG、IHG组MNCV、SOD依次降低(P<0.05),足底热敏反应时间、平均光密度、MDA含量、IL-1β、IL-6、TNF-α蛋白表达依次升高(P<0.05)。结论血糖波动可加重DPN病情,其机制可能与增加氧化应激水平、NF-κB及IL-1β、IL-6、TNF-α等炎性因子相关蛋白表达水平有关。Objective To explore the effect of blood gluocose fluctuation on diabetic peripheral neuropathy(DPN)and its related mechanism by establishing DPN rat model.Methods 45 SD rats were randomly divided into normal control group(NC,n=15),continuous hyperglycemia group(SHG,n=15)and fluctuating blood glucose group(IHG,n=15).Diabetes mellitus was induced by STZ injection.Blood glucose fluctuation model was established by regular injection of insulin and administration of glucose every day.After 12 weeks,the success of the model was verified by examining the general condition,blood glucose level fluctuation,sciatic nerve conduction velocity(MNCV),plantar thermosensitive reaction time and ultrastructural changes of sciatic nerve.At the same time,the expression level of nuclear factorκB(NF-κB),malondialdehyde(MDA)content and superoxide dismutase(SOD)in sciatic nerve were detected.Activity of SOD and expression of IL-1β,IL-6 and TNF-αrelated proteins were measured.Results MNCV and SOD decreased in turn in NC,SHG and IHG groups(P<0.05),while the time of plantar thermal response,average optical density,MDA content,IL-1β,IL-6 and TNF-αprotein expression increased in turn(P<0.05).Conclusion Blood glucose fluctuation can aggravate DPN,and its mechanism may be related to the increase of oxidative stress,and related to the increased expression of NF-κB and inflammatory factors such as IL-1β,IL-6 and TNF-α.
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