【摘要】：目的:探討大鼠經(jīng)靜脈注射脂多糖(LPS)對急性肺損傷(ALI)及肺組織中水通道蛋白1(AQP1)和水通道蛋白5(AQP5)表達的影響,闡明其作用機制。方法:SPF級2月齡雄性Wistar大鼠48只隨機分為對照組和LPS組(n=24),分別經(jīng)尾靜脈注射生理鹽水和LPS,每組分別于注射后2、6、12和24h時間點采集標本,每個時間點6只。HE染色觀察肺組織病理學變化;測定大鼠肺濕/干質(zhì)量(W/D)比、肺滲透指數(shù);ELISA法檢測血清腫瘤壞死因子α(TNF-α)和巨噬細胞炎性蛋白1α(MIP~(-1)α)水平;采用Western blotting、免疫組織化學和Real-Time PCR方法檢測大鼠肺組織中AQP1和AQP5蛋白及mRNA表達水平。結(jié)果:與對照組比較,LPS組大鼠血清TNF-α和MIP~(-1)α水平在注射LPS后2、6和12h時間點均明顯升高(P0.05),至24h時逐漸恢復(fù)正常。HE染色,注射LPS后2h大鼠肺組織出現(xiàn)水腫和炎性細胞浸潤,以12h時間點最明顯;LPS組各時間點大鼠肺W/D比、肺滲透指數(shù)均較對照組明顯升高(P0.05),12h時間點最明顯。與對照組比較,LPS組各時間點大鼠肺組織中AQP1和AQP5mRNA及蛋白表達水平均明顯下降(P0.01),以12h時間點下降最明顯。結(jié)論:LPS可導(dǎo)致大鼠ALI和肺組織中AQP1及AQP5表達水平下調(diào),并參與了肺水腫的形成。
[Abstract]:Aim: to investigate the effects of intravenously injected lipopolysaccharide (LPS) on the expression of aquaporin-1 (AQP1) and aquaporin-5 (AQP5) in acute lung injury (ALI) and lung tissue, and to elucidate its mechanism. Methods Forty-eight male Wistar rats of 2 months old were randomly divided into two groups: control group and LPS group (n = 24). Each group was injected with normal saline through tail vein and LPS, was injected into each group at 12 and 24 hours after injection, and the specimens were collected at 12 and 24 hours after injection, respectively. The changes of lung histopathology were observed by HE staining at each time point, the lung wet / dry mass ratio (W / D), the serum levels of tumor necrosis factor 偽 (TNF- 偽) and macrophage inflammatory protein 1 偽 (MIP~ (-1) 偽) were measured by Elisa. The expression of AQP1 and AQP5 protein and mRNA in rat lung tissue were detected by Western blotting, immunohistochemistry and Real-Time PCR method. Results: compared with the control group, the levels of serum TNF- 偽 and MIP~ (-1) 偽 were significantly increased at 2h and 12h after LPS injection (P0.05), and gradually returned to normal at 24 h. The pulmonary tissue edema and inflammatory cell infiltration were observed at 2 h after LPS injection. Compared with the control group, the lung permeability index of LPS group was significantly higher than that of control group (P0.05). Compared with the control group, the expression levels of AQP1, AQP5mRNA and protein in lung tissue of rats in lipopolysaccharide group were significantly decreased at each time point (P0.01), especially at 12h. Conclusion the expression of AQP1 and AQP5 in ALI and lung tissue was down-regulated and involved in the formation of pulmonary edema.
【作者單位】： 廈門大學附屬第一醫(yī)院兒科PICU;
【基金】：福建省衛(wèi)計委醫(yī)學創(chuàng)新基金資助課題(2012-CXB-28)
【分類號】：R563

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