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作 者:张颖[1] 张海峰[1] 任青爱[1] 谢晓华[1]
出 处:《解放军医学杂志》2015年第7期564-567,共4页Medical Journal of Chinese People's Liberation Army
基 金:军队"十二五"重点科研课题(BWS12J051)~~
摘 要:目的探讨螺内酯对截肢后大鼠肾脏的保护作用及其可能机制。方法健康成年雄性Wistar大鼠42只,随机分为正常对照组,手术后6、24、48、72h组及螺内酯干预组,每组7只。测定血浆尿素氮(Ur)、肌酐(Cr)、髓过氧化物酶(MPO)、丙二醛(MDA)、白介素6(IL-6)、一氧化氮(NO)、血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD)浓度及肾组织MPO、MDA、ALD含量和钙调神经磷酸酶(Ca N)m RNA表达水平,光镜观察肾组织的形态学变化。结果截肢后6h大鼠肾组织出现损伤性变化;血浆Cr、AngⅡ、MDA、MPO、IL-6浓度及肾组织MDA、MPO含量升高,血浆及肾组织ALD水平在截肢后6h降低,随后升高;肾组织中Ca N m RNA表达水平在截肢后明显升高。螺内酯干预后肾组织损伤有所减轻,血浆MPO、IL-6、AngⅡ浓度及肾组织MPO、ALD含量和Ca N m RNA表达水平显著降低,血浆NO浓度显著升高,但血浆Cr、Ur、MDA、ALD浓度及肾组织MDA含量无明显变化。结论螺内酯对截肢后大鼠肾损伤具有保护作用,其机制可能与抑制醛固酮分泌、降低Ca N m RNA的表达及活化,从而减少炎症因子的释放有关。Objective To explore the protective effect and its possible mechanism of spirolactone against kidney injury in rats after amputation. Methods Forty-two male Wistar rats were randomly divided into 6 groups: normal control, 6 hours, 24 hours, 48 hours, 72 hours after the operation and spirolactone intervention groups(n=7, each). Plasma angiotensin Ⅱ(Ang Ⅱ), aldosterone(ALD), myeloperoxidase(MPO), malondialdehyde(MDA), interleukin-6(IL-6), nitric oxide(NO), urea nitrogen(Ur), creatinine(Cr) concentration and renal tissue ALD, MPO, MDA and calcineurin(Ca N) m RNA levels were determined. Renal pathological changes were observed by light microscopy. Results At 6h after amputation, traumatic changes in rat kidney tissue were seen, and the levels of Cr, AngⅡ, MDA, MPO, IL-6 and Ca N-m RNA were significantly elevated, while NO concentration was significantly lowered. Spirolactone intervention reduced the damage of kidney tissue, and the levels of MPO, IL-6, Ang Ⅱ in plasman, contents of MPO and ALD and expression level of Ca N m RNA in kidney tissue were significantly lowered, but the levels of Cr, Ur, MDA and ALD in plasma and content of MDA in kidney tissue showed no significant change. Conclusion Spirolactone can provide protective effect against renal damage in rats after amputation, and it may be related to the mechanism that spirolactone inhibits secretion of ALD and lowers the expression and activation of Ca N m RNA, thus reducing the release of pro-inflammatory factors.
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