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1Nanjing University of Traditional Chinese Medicine, Nanjing 210046, China.2Apothecary of Changzhou Seventh Peoples Hospital of Jiangsu, Changzhou 213011, China.3Key Laboratory for Modern Research of Traditional Chinese Medical Formula of Jiangsu, Nanjing 210046, China.

机译:1南京中医药大学,南京210046,中国江苏常州七人民医院,常州213011,中国江苏南京南京南京现代医疗公式的现代化研究实验室,南京210046。

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This study aims to investigate the effects of clausenamide on streptozotocin (STZ)-induced diabetes in rats. The diabetic rat model was established via an intraperitoneal STZ injection. The rats were randomly divided into five groups, the normal control group, the model group, the insulin treatment group, the high-dose clausenamide treatment group, and the low-dose clausenamide treatment group. Three months after drug administration, reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry were carried out to measure the?Cyclooxygenase-2?(COX-2) expression in the hippocampus of the rats in each group. The RT-PCR results indicate that the hippocampal COX-2 mRNA levels significantly increased in diabetic rats compared with those in the other groups. However, the hippocampal mRNA COX-2 levels in the clausenamide treatment groups significantly decreased, which indicates an inhibitory role of clausenamide on COX-2 mRNA in the diabetic rats. The immunohistochemistry results demonstrate that COX-2 expression in the hippocampus of the diabetic rats significantly increased, which suggests that an abnormal COX-2 expression is involved in the pathogenesis of learning and memory deficiencies, and that clausenamide exerts a protective role by inhibiting COX-2 expression in diabetic rats. Clausenamide has several protective effects on the brain injury induced by long-term diabetes, and significantly reduces diabetes-related learning and memory deficiency. The mechanism correlated well with the inhibition of COX-2 expression in the hippocampus.
机译:本研究旨在探讨Clausenamide对大鼠链脲佐菌素(STZ)诱导的糖尿病的影响。糖尿病大鼠模型通过腹膜内的STZ注射建立。将大鼠随机分为五组,正常对照组,模型组,胰岛素治疗组,高剂量氏菌酰胺处理组,以及低剂量氏菌酰胺处理组。药物给药后三个月,进行逆转录聚合酶链反应(RT-PCR)和免疫组化,以测量每组大鼠大鼠海马的α环氧酶-2?(COX-2)表达。 RT-PCR结果表明,与其他组中的那些,糖尿病大鼠的海马COX-2 mRNA水平显着增加。然而,克劳诺酰胺处理基团中的海马mRNA COX-2水平显着降低,这表明克劳诺酰胺在糖尿病大鼠中COX-2 mRNA上的抑制作用。免疫组织化学结果表明,糖尿病大鼠海马中的COX-2表达显着增加,这表明异常的COX-2表达参与了学习和记忆缺陷的发病机制,并且Clausenamide通过抑制COX施加保护作用2糖尿病大鼠表达。 Clausenamide对长期糖尿病诱导的脑损伤具有几种保护作用,并显着降低了糖尿病相关的学习和记忆缺乏。该机制与海马中COX-2表达的抑制良好。

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