Regulatory Effects and Mechanisms of Curcumin on Pulmonary Fibrosis in Diabetic Mice
Objective To investigate the improving effect of curcumin(Cur)on pulmonary fibrosis in diabetic(DM)mice and its mechanism.Methods 50 male SPF grade C57BL/6 mice were randomly divided into a normal group(Con group,n=10),a curcumin group(Cur group,n=10),a diabetic model group(DMgroup,n=12)and a diabetic curcumin treatment group(DM+Cur group,n=14).The mice in DMgroup and DM+Cur group were first fed with a high-sugar and high-fat diet for 4 weeks,and then a small dose of streptozotocin[STZ,50mg/(kg·d)]was intraperitoneally injected to establish a diabetic mouse model,once a day for 5 consecutive days.The successful modeling standard was 16.7mmol/L.After successful modeling,the Cur group and the DM+Cur group were gavaged with Cur at200mg/(kg·d).After 16 consecutive weeks,the mice were killed and the lung tissues were obtained.HE staining,Masson staining and Sirius Red staining were used to observe the pathological changes,inflam-matory cell infiltration and collagen deposition in the lung tissues of various groups of mice.Western blot was used to detect the ex-pressions ofTGF-1,p-Smad3、p-P38MAPK and Collagen Ⅲ in the lung tissues of various groups of mice.Results Compared with the Con group,the lung tissue of DM group showed significant fibrosis changes,and the expression of TGF-1,p-Smad3,p-P38MAPK and Collagen Ⅲ proteins in the lung tissue was significantly increased(P＜0.01).After Cur treatment,the pulmonary fibrosis of DMmice was significantly improved,and the protein expression of TGF-1,p-Smad3,p-P38MAPKand CollagenⅢin the lung tissue was decreased(P＜0.05).Conclusion Cur can significantly improve pulmonary fibrosis in STZ-induced DMmice by reducing the expression of fibrosis-related protein CollagenⅢ,which may be related to the inhibition of TGF-b1/Smad/P38MAPK signaling pathway.
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