Abstract：Objective: To investigate the expression of vascular secretory factor Rspondin3 through Wnt/ β- catenin signaling pathway in the molecular mechanism of acute lung injury rat model. Methods: The acute lung injury model of SD rats was established. The rats were divided into control group (n=10), model group (n=10), NC group (n=10) and Rspondin3 high group (n=10). The LPS induced acute lung injury model of rats was established in the model group, NC group and Rspondin3 group. After the NC group and Rspondin3 were established, NC plasmid and Rspondin3 over-expression plasmid were injected through tail vein respectively. The control group and model group were given the same amount of normal saline. After 2 weeks, HE staining was used to detect the level of pathological changes in the lung tissues of rats in each group. ELISA was used to detect the changes of interleukin-1 (interleukin-1, IL-1), interleukin-2 (interleukin-4, IL-2) and interleukin-6 (interleukin-8, IL-6) levels in the lung tissues of rats in each group. Western blot was used to detect Wnt-3a and β- catenin protein expression level. The ultrastructural changes of lung tissue in each group were detected by transmission electron microscopy. Results: Compared with the control group, the model group and NC group showed obvious lung tissue injury, and the degree of lung tissue pathological injury in Rspondin3 group was relatively reduced. ELISA results showed that compared with the control group, the expression levels of inflammatory factors IL-1, IL-2 and IL-6 in the lung tissue of model group, NC group and Rspondin3 group were increased, and compared with the model group and NC group, the expression levels of inflammatory factors IL-1, IL-2 and IL-6 in the lung tissue of Rspondin3 group were decreased. The difference was statistically significant (P<0.01). Western blot results showed that Wnt-3a and β-catenin protein expression levels were reduced in the model group and NC group compared to the control group, and Wnt-3a and β-catenin protein expression was increased and reduced in the lung tissue of the Rspondin3 group compared to the model group and NC group, with statistically significant differences (P<0.01). Transmission electron microscopy showed that compared with the control group, the lung tissue structure of the model group and the NC group was loose, the nucleus disintegrated, cell was incomplete, and the cells were vacuolated, while the ultrastructure of the lung group of the Rspondin3 group showed that the cell structure damage was reduced, the nucleus disintegrated and the cell was relatively complete. Conclusion: Overexpression of Rspondin3 has a protective effect on the lung tissue of rats with acute lung injury, and the mechanism may be related to the activation of the activation of the Wnt-3a/ β-catenin signaling pathway.
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2023, Vol. 29 
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