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作 者:何建华[1] 徐黎[1] 沈羽[1] 孔明建 石林玉 马正良[1]
机构地区:[1]南京医科大学附属鼓楼临床学院麻醉科,江苏南京210008
出 处:《中国应用生理学杂志》2015年第1期19-22,共4页Chinese Journal of Applied Physiology
基 金:国家自然基金资助项目(81070892;81171048);江苏省麻醉学重点学科资助项目(XK201140)
摘 要:目的:在大鼠慢性炎性痛模型上,观察大鼠脊髓背角单羧酸转运蛋白-2(MCT-2)表达的变化。方法:健康雄性SD大鼠96只,体重180-220 g,采用随机数字表法将其随机分为2组(n=48):生理盐水组(NS组)和完全性弗氏佐剂组(CFA组)。CFA组左侧后足足底中部皮下注射完全性弗氏佐剂(CFA)100μl;NS组注射等量的生理盐水。在注射前(T0)及注射后3 h(T1)、第1天(T2)、3天(T3)、5天(T4)、7天(T5)、14天(T6)和第21天(T7)测定大鼠机械缩足反应阈值(MWT)和热缩足反应潜伏期(TWL),并于上述各时间点分别随机取4只大鼠,处死后取脊髓背角,采用Western blot法测定MCT-2表达的变化。结果:CFA组大鼠在注射CFA后3 h即出现痛觉过敏,并持续至第14天,其疼痛程度显著大于NS组(P〈0.05);且T1-6时脊髓背角MCT-2与NS组相比显著增加(P〈0.05)。大鼠脊髓背角MCT-2的表达与MWT和TWL相关(P〈0.05,P〈0.01)。结论:慢性炎性痛大鼠脊髓MCT-2表达上调,该变化可能参与慢性炎性痛中枢敏化的形成和维持。Objective: To investigate the changes in the levels of monocarboxylate transporter-2 in spinal cord horn in a rat model of chronic inflammatory pain. Methods: Male SD rats weighting 180 - 220 g were randomly divided into two groups( n = 48) : normal saline group( NS group),complete Freund's adjuvant group( CFA group). Rats were given injections of CFA 100 μl in left hind paw in group CFA,and an equal volume of saline was given injection in group NS. Mechanical withdraw threshold( MWT) and thermal withdraw latency( TWL) were measured at before injection( T0) and 3 h,1 d,3 d,7 d,14 d,and 21 d after injection( T1-7). Four rats were chosen from each group at T0-7and sacrificed,and L4-5 segments of the spinal cord horn were removed for measurement of the expression of monocarboxylate transporter-2 by Western blot analysis. Results: In CFA group,mechanical hyperalgesia and allodynia appeared on the 3 h after CFA injection,then until the day 14. The expression of monocarboxylate transporter-2 in the spinal dorsal horn of rats in CFA group was significantly higher than that in normal control group at T1-6( P 〈0. 05). The protein level of monocarboxylate transporter-2 was apparently correlated with MWT and TWL( P 〈0. 01 and P 〈0. 05) in CFA group. Conclusion: The level of monocarboxylate transporter-2 in spinal dorsal horn is significantly increased in a rat model of chronic inflammatory pain and the change may involve in the formation and maintenance of central sensitization in spinal cord of chronic inflammatory pain.
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