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| 右美托咪啶预处理对脓毒症肾损伤大鼠炎性因子和氧化应激的影响 | |
| 引用本文： | 陈裕洁,龚楚链,谭芳,周少丽. 右美托咪啶预处理对脓毒症肾损伤大鼠炎性因子和氧化应激的影响[J]. 南方医科大学学报, 2015, 35(10): 1472 |
| 作者姓名： | 陈裕洁 龚楚链 谭芳 周少丽 |
| 摘 要： | 目的探讨右美托咪啶对脓毒血症大鼠AKI（急性肾损伤）的炎性因子和氧化应激的影响。方法将32只雄性SD大鼠随机 均分为以下4组（每组8只大鼠）：假手术组、脂多糖（LPS）组、右美托咪啶（DEX）+LPS组、育亨宾（YOH）+DEX+LPS组；后3组分 别于术前30 min经尾静脉注射LPS（5 mg/kg）；LPS + DEX组LPS前10 min尾静脉注射DEX（10 μg/kg）；YOH+DEX+LPS组于 LPS前40 min经腹腔注射YOH（1 mg/kg），及LPS前10min尾静脉注射DEX 10 μg/kg。4 h后处死大鼠提取标本测定血浆和肾 组织中的白介素-1β（IL-1β）、超氧化物歧化酶（SOD）和丙二醛（MDA）水平，并观察肾组织病理学变化。结果与假手术组相比， LPS组中血浆和肾组织IL-1β、MDA水平明显升高，SOD明显降低（P<0.05），肾脏病理损伤严重；与LPS组相比，DEX +LPS组 中血浆和肾组织IL-1β、MDA水平明显降低，SOD明显增高（P<0.05），肾脏病理学损伤也明显减轻；YOH+DEX+LPS组和DEX +LPS组相比，IL-1β、MDA均上升，SOD下降（P<0.05），肾脏病理学损伤较明显。结论DEX可以减轻脓毒症相关肾损伤的炎症 反应和氧化应激，且这种作用可能是通过α2受体起作用的。 |
Pretreatment with dexmedetomidine ameliorates renal inflammation and oxidative stressin rats with lipopolysaccharide-induced sepsis and acute kidney injury |
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| Abstract: | Objective To investigate the effects of dexmedetomidine on inflammatory reaction, oxidative stress, and renal pathologies in a rat model of lipopolysaccharide (LPS)-induced sepsis. Methods Thirty-two SD rats were randomly divided into 4 groups, including a sham-operated group, LPS group with LPS (5 mg/kg) injection via the caudal vein 30 min before the operation, dexmedetomidine (Dex) +LPS group with additional Dex (10 μg/kg) injection via the caudal vein 10 min before LPS injection, and yohimbine+DEX+LPS group with intraperitoneal yohimbine (1 mg/kg) injection 40 min before and Dex injection 10 min before LPS injection. The levels of IL-1β, SOD and MDA in the plasma and renal tissues were determined, and the renal pathologies were examined. Results Compared with the sham-operated rats, the rats in LPS group showed significantly increased IL-1β and MDA levels and lowered SOD activity in the plasma and renal tissues (P<0.05) with obvious renal pathologies. Dex pretreatment obviously lowered IL-1β and MDA levels and enhanced SOD activity in the plasma and renal tissues in LPS-challenged rats (P<0.05), and significantly lessened LPS-induced renal pathologies. Conclusion Dex can protect the rats against LPS-induced renal injury by alleviating the inflammatory reactions and cytokine oxidative stress, and this effect is mediated possibly by α2 receptors. |
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