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目的 探讨细胞凋亡与急性肺损伤 (ALI)发生、发展的关系以及地塞米松在全身炎症反应及急性肺损伤中的作用机制及意义。方法 通过复制内毒素性大鼠ALI模型 ,采用TUNEL法、原位杂交、SqRT PCR以及免疫组化等技术观察ALI肺组织细胞凋亡变化、Fas基因与Fas基因配体 (Fas/FasL)系统mRNA和蛋白质表达的改变以及地塞米松对细胞凋亡及Fas、FasL表达的影响。结果 ALI早期肺组织细胞凋亡明显增加 (P <0 0 1) ;Fas、FasLmRNA和蛋白质表达明显上调 (P <0 0 1) ,地塞米松可明显抑制大鼠ALI血清TNF α释放、抑制肺部炎症反应 ;明显抑制LPS诱导的肺组织细胞凋亡 (P<0 0 1) ,并明显下调Fas、FasLmRNA和蛋白质的表达 (P <0 0 1)。结论 肺组织细胞凋亡及Fas/FasL系统表达上调 ,可能参与大鼠ALI早期的发病 ;地塞米松可通过抑制炎症介质释放 ,抑制Fas/FasL系统的活化 ,阻断、调控肺组织靶细胞凋亡 ,而减轻肺组织损伤。
Objective To investigate the relationship between apoptosis and the occurrence and development of acute lung injury (ALI) and the mechanism and significance of dexamethasone in systemic inflammatory response and acute lung injury. Methods Apoptosis of ALI lung tissue was observed by TUNEL method, in situ hybridization, SqRT PCR and immunohistochemistry. The expressions of Fas and Fas ligand (Fas / FasL) mRNA And protein expression changes and dexamethasone on apoptosis and Fas, FasL expression. Results The apoptosis of lung tissue was significantly increased in the early stage of ALI (P <0.01), and the expressions of Fas and FasL mRNA and protein were significantly increased (P <0.01). Dexamethasone could significantly inhibit the release of TNFα from the serum of ALI rats, (P <0.01), and significantly decreased the expression of Fas, FasL mRNA and protein (P <0.01). Conclusion The apoptosis of lung tissue and the up-regulation of Fas / FasL system may be involved in the early stage of ALI in rats. Dexamethasone can inhibit the activation of Fas / FasL system by inhibiting the release of inflammatory mediators, Death, while reducing lung tissue damage.