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盐酸戊乙奎醚对大鼠创伤性急性肺损伤时TIPE2-TLR4-MyD88信号通路的影响 被引量:3

Effect of penehyelidine hydrochloride on TIPE2-TLR4-MyD88 signaling pathway in a rat model of traumatic acute lung injury
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摘要 目的评价盐酸戊乙奎醚对大鼠创伤性急性肺损伤时肿瘤坏死因子α诱导蛋白8样分子2(TIPE2)-Toll样受体4(TLR4)-髓样分化因子88(MyD88)信号通路的影响。方法SPF级健康雄性SD大鼠30只,8周龄,体重190~210 g,采用随机数字表法分为3组(n=10):假手术组(Sham组)、创伤性急性肺损伤组(ALI组)和盐酸戊乙奎醚组(PHCD组)。Sham组只麻醉不撞击;ALI组和PHCD组制备胸部撞击致大鼠创伤性急性肺损伤模型;PHCD组大鼠于胸部撞击后即刻腹腔注射盐酸戊乙奎醚2 mg/kg。于模型制备成功后8 h后处死大鼠取肺,光镜下观察肺组织病理学结果,电镜下观察肺组织超微结构,确定肺组织湿干重(W/D)比值,采用Western blot法检测肺组织TLR4和MyD88表达。结果与Sham组比较,ALI组和PHCD组肺组织W/D比值升高,TIPE2表达下调,TLR4和MyD88表达上调(P<0.05);与ALI组比较,PHCD组肺组织W/D比值降低,TIPE2表达上调,TLR4和MyD88表达下调(P<0.05)。PHCD组肺组织病理学损伤和超微结构损伤较ALI组减轻。结论盐酸戊乙奎醚减轻大鼠创伤性急性肺损伤的机制与激活TIPE2-TLR4-MyD88信号通路有关。 Objective To evaluate the effect of penehyelidine hydrochloride(PHCD)on tumor necrosis factorα-induced protein 8-like-2(TIPE2)-Toll-like receptor 4(TLR4)-myeloid differentiation factor 88(MyD88)signaling pathway in a rat model of traumatic acute lung injury(ALI).Methods Thirty SPF healthy male Sprague-Dawley rats,aged 8 weeks,weighing 190-210 g,were divided into 3 groups(n=15 each)by a random number table method:sham operation group(group Sham),traumatic ALI group(group ALI)and group PHCD.ALI was induced by blunt chest trauma in ALI and PHCD groups.PHCD 2 mg/kg was intraperitoneally injected immediately after blunt chest trauma in group PHCD.The rats were sacrificed and lung tissues were removed at 8 h after the model was successfully established for examination of the pathological changes and ultrastructure of lung tissues(with a light microscope or an electron microscope)and for determination of the wet to dry weight ratio(W/D ratio)and expression of TLR4 and MyD88 in lung tissues.Results Compared with group Sham,the W/D ratio was significantly increased,TIPE2 expression was down-regulated,and the expression of TLR4 and MyD88 was up-regulated in ALI and PHCD groups(P<0.05).Compared with group ALI,the W/D ratio was significantly decreased,TIPE2 expression was up-regulated,and the expression of TLR4 and MyD88 was down-regulated(P<0.05),and the pathological changes of lung tissues and ultrastructure were significantly attenuated in group PHCD.Conclusion The mechanism by which PHCD reduces traumatic AIL is related to activating TIPE2-TLR4-MyD88 signaling pathway in rats.
作者 段薇娜 袁敏 孔倩 冷燕 邱珍 黄琴 吴晓静 Duan Weina;Yuan Min;Kong Qian;Leng Yan;Qiu Zhen;Huang Qin;Wu Xiaojing(Department of Anesthesiology,Renmin Hospital,Wuhan University,Wuhan 430060,China)
出处 《中华麻醉学杂志》 CAS CSCD 北大核心 2019年第10期1237-1239,共3页 Chinese Journal of Anesthesiology
基金 湖北省自然科学基金(2016CFB251)。
关键词 胆碱能拮抗剂 急性肺损伤 泛素特异性蛋白酶类 TOLL样受体4 髓样分化因子88 Cholinergic antagonists Acute lung injury Ubiquitin-specific proteases Toll-like receptor 4 Myeloid differentiation factor 88
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