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目的了解锌指蛋白A20突变体(A20△)转基因小鼠脓毒症肺损伤的特点,探讨A20△对小鼠脓毒症肺损伤的影响。方法以A20△转基因脓毒症小鼠为动物模型(A20△转基因组),采用流式细胞仪测定肺组织单核巨噬细胞浸润,ELISA测定肺组织A20△、TNF-α、IL-1β水平,结合肺体指数和病理检查对炎症及其损伤程度进行鉴定。实验同时设LPS对照组(LPS组)和生理盐水对照组(对照组)。结果给予LPS后6、12、24h,A20△转基因组小鼠肺体指数较LPS组明显下降(P<0.01,P<0.05);A20△转基因组小鼠肺组织浸润单核/巨噬细胞数较LPS组明显下降(P<0.01)。给予LPS后3、6h,A20△转基因组小鼠肺组织炎症细胞因子TNF-α水平较LPS组明显下降(P<0.01);IL-1β水平也较LPS组明显下降(P<0.05,P<0.01);给予LPS后12、24h,TNF-α和IL-1β水平差异无统计学意义(P>0.05)。病理学观察表明A20△转基因组小鼠肺组织充血程度、肺泡积液及肺间质增厚程度均较LPS组轻。结论A20△转基因小鼠在一定程度上具有抵御LPS诱导性肺损伤的能力,其机制可能是通过抑制单核细胞向肺组织浸润和降低肺内炎症细胞因子水平实现的。
Objective To investigate the characteristics of lung injury in sepsis mice induced by A20 △ transgenic mice and explore the effect of A20 △ on lung injury induced by sepsis in mice. Methods A20 △ transgenic sepsis mice were used as animal models (A20 △ transgenic). The infiltration of monocytes was measured by flow cytometry. The levels of A20 △, TNF-α and IL-1β , Combined with lung index and pathological examination of inflammation and the degree of damage identified. At the same time, LPS control group (LPS group) and saline control group (control group) were set up. Results The lung index of A20 △ transgenic mice decreased significantly (P <0.01, P <0.05) at 6, 12 and 24 hours after LPS administration. The number of infiltrating monocytes / macrophages in A20 △ transgenic mice Compared with LPS group decreased significantly (P <0.01). At 3h and 6h after LPS administration, the levels of TNF-α in lung tissue of A20 △ transgenic mice were significantly decreased compared with LPS group (P <0.01), and the levels of IL-1β in lung tissue of A20 △ transgenic mice were significantly decreased compared with LPS group (P <0.05, P < 0.01). There was no significant difference in the levels of TNF-α and IL-1β between 12 and 24 hours after LPS administration (P> 0.05). Pathological observation showed that lung tissue hyperemia, alveolar effusion and pulmonary interstitial thickening in A20 △ transgenic mice were lighter than those in LPS group. Conclusion A20 △ transgenic mice have the ability to resist LPS-induced lung injury to a certain extent. The mechanism may be through inhibiting the mononuclear cells infiltrating into the lung tissue and reducing the levels of inflammatory cytokines in the lung.