Effect of Schizandrin B on lung injury in rats with acute pancreatitis through TLR4/NF-κB signaling pathway.

Objective: To investigate the effect of Schizandrin B on lung injury in rats with acute pancreatitis (AP) via Toll-like receptor 4 (TLR4) /nuclear factor-κB (NF-κB) signaling pathway. Methods: SD rats were taken and induced the establishment of AP lung injury model by retrograde injection of 5% sodium taurocholate into the bile duct. According to random number table method, they were divided into model group, schisandrin B group, TLR4 overexpression vector group, TLR4 empty group, schisandrin B+ TLR4 overexpression vector group, 12 rats per group. Twelve SD rats only flipped the intestines without injecting 5% sodium taurocholate, as the sham operation group. After intervening rats in groups with drugs, pulmonary function of rats in each group, the amount of ascites and lung tissue wet weight/dry weight (W/D) of rats in each group were measured; HE staining was used to detect pathological morphology of lung tissue and score; levels of arterial blood gas indexes of rats in each group were detected by fully automatic biochemical analyser; levels of serum amylase and inflammatory cytokines IL-6 and IL-18 were measured by ELISA; Western blotting was used to detect protein expression of TLR4/NF-κB signaling pathway in lung tissue; expression of TLR4 protein in lung tissue of rat in each group was detected by immunohistochemical staining. Results: Compared with sham operation group, lung tissue of rats in model group showed pathological changes, MV, PEF, PaO2 and OI of model group were significantly reduced (P<0.05), while Ri, ascites volume, W/D, PaCO2, Holfbauer score, serum amylase, IL-6 and IL-18 levels, lung tissue proportion of TLR4 positive cells, expressions of TLR4 and MYD88 protein, p-NF-κB p65/NF-κB p65 level were significantly increased (P<0.05) . Compared with model group and schisandrin B+TLR4 overexpression vector group, respectively, pathological changes of lung tissue of rats in schisandrin B group were reduced, MV, PEF, PaO2 and OI were all increased (P<0.05), while Ri, ascites volume, W/D, PaCO2, Holfbauer score, serum amylase, IL-6 and IL-18 levels, lung tissue proportion of TLR4 positive cells, expressions of TLR4 and MYD88 protein, p-NF-κB p65/NF-κB p65 levels were decreased (P<0.05); in TLR4 overexpression vector group, degree of pathological damage in lung tissue of rats was aggravated, MV, PEF, PaO2 and OI were all decreased (P<0.05), while Ri, ascites volume, W/D, PaCO2, Holfbauer score, serum amylase, IL-6 and IL-18 levels, lung tissue proportion of TLR4 positive cells, expressions of TLR4 and MYD88 protein, p-NF-κB p65/NF-κB p65 level were increased (P<0.05) . Compared with model group, rats in TLR4 empty group showed no significant difference (P>0.05). Conclusion: Schizandrin B can down-regulate TLR4/NF-κB signaling pathway to inhibit inflammation, reduce lung injury in AP rats, and repair lung function. [ABSTRACT FROM AUTHOR]