The aim of this study was to explore the inhibitory effects of Ficus carica leaves (FCL) extract on AMPK/JNK/caspase3 signaling pathway and antioxidation in pancreatic β-cells. H&E staining, insulin immunohistochemistry, and TUNEL methods were used to investigate the effects of FCL on pancreatic histopathology in type 1 diabetic mice. The expression levels of caspase-3, AMPK, and JNK protein in the pancreatic tissue and MIN6 cells [induced by palmitic acid (PA) and hydrogen peroxide] were determined. Flow cytometry was used to detect the effects of FCL on apoptosis and ROS production of MIN6 cells. FCL (2 g/kg, continuous gavage for 6 weeks) significantly improved the pancreatic tissue injury in type 1 diabetic mice and reduced the expression levels of apoptosis-related proteins such as FasL, caspase8, Bax/Bcl-2, Cyt-C, caspase-3, p-AMPK, and p-JNK. FCL inhibited cell apoptosis induced by PA and the protein expression levels of caspase-3, p-AMPK, and p-JNK. The AMPK agonist AICAR could reverse the protective effects of FCL on MIN6 cells. The AMPK inhibitor compound C had a similar effect on MIN6 cells as that of FCL. FCL could inhibit cell apoptosis induced by hydrogen peroxide and reduced the production of ROS. In conclusion, FCL could inhibit pancreatic β-cell apoptosis by inhibiting the AMPK/JNK/caspase-3 signaling pathway and by antioxidation properties.
Keywords: AMPK; Apoptosis; FCL; JNK; Pancreatic β-cells; ROS.
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