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作 者:赵伟成[1] 李晓芸[2] 张文璇[1] 廖美娟[1] 杨承祥[1] 罗刚健[2]
机构地区:[1]广东省佛山市第一人民医院麻醉科,528000 [2]中山大学附属第三医院麻醉科,广州市510630
出 处:《实用医学杂志》2015年第1期20-23,共4页The Journal of Practical Medicine
基 金:广东省自然科学基金项目(编号:S2011010003506);广东省佛山市科技局项目(编号:20111021010025;201208025)
摘 要:目的:评价脊髓缝隙连接细胞间通讯在糖尿病大鼠神经病理性痛维持中的作用。方法:雄性SD大鼠,2个月龄,体重180-220g,采用腹腔注射1%链脲佐菌素(STZ)方法制备糖尿病模型,注射STZ后48h血糖〉16.7mmol/L的大鼠作为糖尿病大鼠。采用随机数字表法将16只糖尿病大鼠分为糖尿病组(D组)和甘珀酸治疗组(G组),每组8只,另取8只同月龄的雄性SD大鼠为正常对照组(C组)。G组于注射STZ后28d鞘内注射缝隙连接阻滞剂甘珀酸25μg,1次/d,连续7d;而D组大鼠则鞘内注射相同容量的甘珀酸溶剂。分别于注射STZ前(T1)、注射STZ后7、14、21、28、35d时(T2~T6)测定机械缩足反应阈(PWT)。于T6时处死大鼠.取腰段脊髓组织检测Cx43的表达。结果:与C组比较,D组、G组T4~T6时PWT降低(P〈0.05),T6时脊髓Cx43的表达增加(P〈0.05);与D组比较,G组T1~T5时PWT无显著变化(P〉0.05),T6时PWT升高(P〈0.05),脊髓Cx43的表达减少(P〈0.05)。结论:脊髓缝隙连接细胞间通讯可能参与糖尿病大鼠神经病理性痛的维持。Objective To evaluate the role of spinal gap junction cellar communication in the rat model with diabetic neuropathy pain. Methods Diabetic rat model was induced by intraperitoneal injection with 1% streptozotocin (STZ, 60 mg/kg) in sprague-dawley rats. Those with Glucose level 〉16.7 mmol/L after 48 h were as diabetic model, and were randomly allocated to diabetic group (D group, n = 8) and carbenoxolone treatment group (G group, n = 8). Another 8 age-matched normal rats served as controlled group (C group, n = 8). 28 days after STZ injection, the rats in G group received daily intraperitoneal carbenoxolone (25 μg) whereas those in D group received the same volume of vehicle for 7 consecutive days. Responses to the mechanical stimulus were measured with von Frey filament, and paw withdraw threshold (PWT) was recorded before STZ injection, 7,14,21,28, and 35 days after STZ injection(T1 to T6). At T6 the rats were killed and lumbar segments of spinal cord were removed. Spinal gap junction subunit connexin 43 (Cx43) were determined by Western blotting assay. Results Compared to C group, both D and G groups showed lower PWT at T4 to T6. Compared to D group, G group had higher PWT at T6(P 〈 0.05). G group showed higher PWT at T6 than at T5 (P 〈 0.05). Compared with C group, the spinal Cx43 expression significantly increased in D and G groups at T6 (P 〈 0.05). A reduction of spinal Cx43 expression were seen in G group when compared with D group at T6 (P 〈 0.05). Conclusion Spinal gap junction cellar communication might play a role in maintaining diabetic neuropathic pain in rats.
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