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作 者:尹家乐[1] 张爱香[2] 王毓炜[3] 张洪泉[3]
机构地区:[1]徐州医学院,江苏徐州221002 [2]新疆医科大学第六附属医院,乌鲁木齐830002 [3]扬州大学医药研究所,江苏扬州225001
出 处:《中药新药与临床药理》2010年第1期18-21,共4页Traditional Chinese Drug Research and Clinical Pharmacology
摘 要:目的研究大黄酸精氨酸预防大鼠实验性肠粘连的作用并探讨其抗炎机制。方法取雄性SD大鼠60只,随机分为6组:正常对照组、模型组、地塞米松组和大黄酸精氨酸低、中、高剂量组。除正常对照组外,其余各组大鼠均制备肠粘连模型。正常对照组和模型组腹腔注射生理盐水,地塞米松组腹腔注射地塞米松磷酸钠(10mg·kg-1),大黄酸精氨酸低、中、高剂量组腹腔注射大黄酸精氨酸(7.5,15,30mg·kg-1),连续给药1周。各组于术后第8天取血,ELISA法测定血清IL-1β、IL-4及TNF-α含量,肉眼观察肠粘连的程度并分级;同时取盲肠与腹壁切口组织测定羟脯氨酸(hydroxyproline,Hyp)含量,并做病理观察。结果大黄酸精氨酸能显著减轻肠粘连大鼠肠粘连的程度,明显降低肠粘连大鼠IL-1β和TNF-α的表达水平,抑制纤维结缔组织的增生,但对IL-4的表达水平几乎没有影响。结论大黄酸精氨酸可通过抑制炎症因子的过度表达,减轻炎症反应而有效预防术后肠粘连的形成。Objective To observe the protective effect of rhein - arginine (RhA) on rats ankylenteron and to explore the anti- inflammatory mechanism. Methods Sixty male SD rats were randomly divided into 6 groups: normal control group, model group, dexamethasone group (in the dose of 10 mg·kg^-1) and low - , medium- and high -dose RhA groups (in the dose of 7.5 mg·kg^-1, 15 mg·kg^-1, 30 mg·kg^-1 respectively). Except that the normal control group, the rats in other groups were induced ankylenteron. Intraperitoneal injection of saline was administered to the rats in the normal control group and the model group, and dexamethasone group and RhA groups were given the corresponding drugs according to the experimental design. The treatment lasted 7 days. On the 8th day after surgery the blood samples of each group were collected. The levels of interleukin - 1β(IL - 1β), interleukin -4(IL -4)and tumor necrosis factor- α(TNF- α)were determined by enzyme linked immunosorbent assay. Grades of intestinal adhesion were ranked by macroscopic observation. The adhesive tissues between cecum and abdominal wall were taken for pathological observation and the determination of hydroxyproline (Hyp) content. Results RhA significantly relieved the experimental intestinal adhesion, Obviously decreased the levels of IL - 1β and TNF - α, and inhibited the hyperplasia of fibrous connective tissue. However, there was no significant impact on the level of IL- 4. Conclusion RhA can effectively prevent the information of postoperative ankylenteron by inhibiting the expression of inflammatory cytokines and reducing the inflammatory response.
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