Naringenin and Vanillin Mitigate Cadmium-Induced Pancreatic Injury in Rats via Inhibition of JNK and p38 MAPK Pathways

Abstract

Chemicals NGN, VLN and CdCl 2 were purchased from Sigma-Aldrich, USA. VLN and CdCl 2 were ABSTRACT Background: Cadmium can induce pancreatic injury via oxidative stress, inflammation and apoptosis. Naringenin (NGN) and vanillin (VLN) exert antioxidant, anti-inflammatory, and antiapoptotic effects. Objective: The likely ameliorative effects of NGN, VLN and their combination were studied in rats exposed to cadmium-induced pancreatic injury. Materials and Methods: Rats received NGN (50 mg/kg/day, p.o.), VLN (100 mg/ kg/day, p.o.), or NGN + VLN for 7 days and one injection of CdCl 2 (2 mg/kg, i.p.) on the 6 th day. Results: Cadmium significantly lowered serum amylase and insulin levels. Cadmium also caused significant increments of malondialdehyde, tumor necrosis factor-α, interleukin-1β, nuclear factor-κB p65, Bax/Bcl-2 ratio and phosphorylated c-Jun N-terminal kinase (p-JNK) and p38 mitogen-activated protein kinases (MAPKs) and significant decrements of reduced glutathione and catalase in the pancreas of rats received CdCl 2. Additionally, CdCl 2 caused marked histopathological necrosis and significantly increased caspase-3 expression in pancreatic tissue. The cadmium-induced biochemical, histopathological and immunohistochemical changes were significantly ameliorated by NGN, VLN and NGN + VLN. However, NGN + VLN caused more significant ameliorative effects than did NGN and VLN alone. Conclusion: NGN, VLN and NGN + VLN afforded significant protection of pancreas in rats exposed to cadmium insult through modulation of JNK and p38 MAPK pathways and inhibition of oxidative stress, inflammation and apoptosis.

Anti‐inflammatory activity of β‐glucans from different sources before and after fermentation by fecal bacteria in vitro

“…Vanillin significantly decreased the production of NO and pro‐inflammatory cytokines in LPS‐induced microglia and inhibited the phosphorylation of MAPKs and NF‐ κ B 26 . It also had the ability to inhibit the JNK and p38 MAPK pathways 27 . The treatment of caffeic acid alleviated colitis by inhibiting the NF‐kB signaling pathway 28 .…”

“…26 It also had the ability to inhibit the JNK and p38 MAPK pathways. 27 The treatment of caffeic acid alleviated colitis by inhibiting the NF-kB signaling pathway. 28 It may also attenuate LPS-induced NO production by inhibiting the phosphorylation of p38 MAPK and JNK1/2.…”