發(fā)布時間：2018-05-25 01:03

  本文選題：抗氧化 + N-乙酰半胱氨酸　； 參考：《廣東醫(yī)學》2015年14期

【摘要】：目的探討抗氧化劑N-乙酰半胱氨酸對急性重癥胰腺炎大鼠的療效及JNK信號通路活化的影響。方法選擇清潔級C57BL/6雄性SD大鼠56只,隨機分為空白對照組8只,開腹后僅翻動胰腺,不做任何處理,然后立即關(guān)腹;胰腺炎組24只,采用10%的L-精氨酸腹腔注射法誘導大鼠急性重癥胰腺炎模型;治療組24只,于模型制備前30 min內(nèi)腹腔注射5%的N-乙酰半胱氨酸(200 mg/kg)進行預處理,然后再進行急性重癥胰腺炎大鼠模型制備;胰腺炎組和治療組選取3、6、12 h 3個時間點各8只分為3個小組,觀察各組大鼠血清胰淀粉酶、病理學改變、組織中磷酸化c-jun蛋白水平、丙二醛含量TNF-α、IL-6的變化。結(jié)果胰腺炎組大鼠各時間點的各項指標明顯高于空白對照組;治療組大鼠3、6 h血漿IL-6水平明顯低于胰腺炎組,6、12 h胰腺組織病理學評分均明顯低于胰腺炎組,其余各指標明顯低于胰腺炎組(P0.05)。結(jié)論急性重癥胰腺炎大鼠血清胰淀粉酶、病理學及相關(guān)指標均發(fā)生了明顯的改變,N-乙酰半胱氨酸通過清除氧自由基、減少TNF-α和IL-6的產(chǎn)生等機制對急性重癥胰腺炎大鼠發(fā)揮治療和保護作用,還通過改變組織中磷酸化c-jun蛋白水平來影響JNK信號通路的活化。
[Abstract]:Objective to investigate the effect of antioxidant N-acetylcysteine on acute severe pancreatitis rats and the activation of JNK signaling pathway. Methods Fifty-six C57BL/6 male SD rats of clean grade were randomly divided into control group (n = 8). Acute severe pancreatitis in rats was induced by 10% L-arginine intraperitoneal injection, and 24 rats in the treatment group were pretreated with 5% N-acetylcysteine 200 mg / kg 30 min before the preparation of the model. The rats in the acute severe pancreatitis group and the treatment group were divided into 3 groups at each time point of 6 hours and 12 hours. The serum amylase, pathological changes and phosphorylated c-jun protein levels in the tissues were observed in each group. Changes of malondialdehyde (MDA) content in TNF- 偽 and IL-6. Results the indexes of each time point in the pancreatitis group were significantly higher than those in the blank control group, and the plasma IL-6 level in the treatment group was significantly lower than that in the pancreatitis group at 612 h, and the plasma IL-6 level in the treatment group was significantly lower than that in the pancreatitis group at 612 h. The other indexes were significantly lower than those in the pancreatitis group (P 0.05). Conclusion the changes of serum amylase, histopathology and related indexes in rats with severe acute pancreatitis have been observed by scavenging oxygen free radicals with N-acetylcysteine. The mechanism of decreasing the production of TNF- 偽 and IL-6 plays a therapeutic and protective role in rats with severe acute pancreatitis. It also affects the activation of JNK signaling pathway by changing the level of phosphorylated c-jun protein in the tissue.
【作者單位】： 浙江省立同德醫(yī)院普外科;
【基金】：浙江省醫(yī)藥衛(wèi)生科技計劃項目(編號:2012KYB041)
【分類號】：R576

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本文編號：1931367