探討大黃素對犬自體腎移植缺血再灌注損傷的影響及機制。方法 將18只健康雜種犬隨機分為假手術(shù)組、大黃素組和生理鹽水組，每組各6只。假手術(shù)組僅進(jìn)行腎手術(shù)切除；大黃素組在術(shù)前2 h按10 mg/kg ip大黃素，生理鹽水組同法使用相同體積的生理鹽水。再灌注1 h后檢測MDA、MPO、SOD、iNOS、eNOS的水平；術(shù)后24 h檢測血清肌酐（Cr）、尿素氮（BUN）水平以及TNF-α、IL-6、IL-8、IL-10炎性因子的水平；光鏡下觀察腎組織病理學(xué)改變。結(jié)果 生理鹽水組的MDA、iNOS水平顯著高于假手術(shù)組，但MPO、SOD、eNOS水平低于假手術(shù)組（P＜0.05）；大黃素組的MDA、iNOS水平顯著低于生理鹽水組，但MPO、SOD、eNOS水平高于假手術(shù)組（P＜0.05）。生理鹽水組的BUN、Cr、TNF-α、IL-6、IL-8水平顯著高于假手術(shù)組，但I(xiàn)L-10水平低于假手術(shù)組（P＜0.05）；大黃素組的BUN、Cr、TNF-α、IL-6、IL-8水平顯著低于生理鹽水組，但I(xiàn)L-10水平高于生理鹽水組（P＜0.05），腎損傷明顯減輕。結(jié)論 大黃素能減輕腎移植缺血再灌注損傷，其機制可能與減輕腎脂質(zhì)過氧化反應(yīng)以及抑制炎性因子有關(guān)。

Objective To study the mechanism of emodin on ischemia and reperfusion injury in canine autologous renal transplantation. Methods 18 Healthy mongrel dogs were randomly divided into sham group, emodin group, and normal saline group with 6 dogs in each group. Sham group received kidney operation resection. Dogs in emodin group were injected dosage of 10 mg/kg emodin at 2 h before surgery by intraperitoneal injection, and normal saline group with the method using the same volume. MDA, MPO, SOD, iNOS, and eNOS activity were detected after reperfusion after 1 h, and postoperative serum creatinine (Cr) and blood urea nitrogen (BUN) concentration and the level of TNF- α, IL-6, IL-8, and IL-10 inflammatory factor after 24 h were determined. Renal tissues were observed under light microscope pathological changes. Results The content of MDA, iNOS, BUN, Cr, TNF-α, IL-6, and IL-8 in normal saline group was significantly higher than that in sham group, while the content of MPO, SOD, eNOS, and IL-10 on the contrary (P<0.05). The content of MDA, iNOS, BUN, Cr, TNF-α, IL-6, and IL-8 in emodin group was significantly lower than that in normal saline group, while the contents of MPO, SOD, eNOS, and IL-10 on the contrary (P<0.05). Renal injury in emodin group were significantly reduced. Conclusion Emodin can alleviate the ischemia reperfusion injury in renal transplantation, and the mechanism may be related to reduce renal lipid peroxidation and inhibition of inflammatory factor.

黑龍江省青年科學(xué)基金資助項目（QC2012C106）