Hesperidin protects against cadmium-induced pancreatitis by modulating insulin secretion, redox imbalance and iNOS/NF-ĸB signaling in rats

Cadmium is a persistent ubiquitous environmental toxicant that elicits several biological defects on delicate body organs. Growing evidence suggests that cadmium (Cd) may perturb signaling pathways to induce oxidative pancreatitis. Thus, we explored whether hesperidin, a flavonone, could mitigate Cd...

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Bibliographic Details
Published in:Life sciences (1973) 2020-10, Vol.259, p.118268-118268, Article 118268
Main Authors: Aja, Patrick M., Izekwe, Friday I., Famurewa, Ademola C., Ekpono, Ezebuilo U., Nwite, Felix E., Igwenyi, Ikechuku O., Awoke, Joshua N., Ani, Onyedika G., Aloke, Chinyere, Obasi, Nwogo A., Udeh, Kester U., Ale, Boniface A.
Format: Article
Language:English
Subjects:
Amylases
Antioxidant
Antioxidants
Attenuation
Cadmium
Cadmium toxicity
Catalase
Glutathione
Glutathione peroxidase
Hesperidin
Histology
Inflammation
Inflammatory cytokines
Insulin
Insulin secretion
Interleukin 6
Intoxication
Lipase
Malondialdehyde
NF-κB protein
Nitric oxide
Nitric-oxide synthase
Organs
Overexpression
Oxidative stress
Pancreas
Pancreatitis
Peroxidase
Signaling
Superoxide dismutase
Toxicants
Tumor necrosis factor-TNF
Tumor necrosis factor-α
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Summary:Cadmium is a persistent ubiquitous environmental toxicant that elicits several biological defects on delicate body organs. Growing evidence suggests that cadmium (Cd) may perturb signaling pathways to induce oxidative pancreatitis. Thus, we explored whether hesperidin, a flavonone, could mitigate Cd-induced oxidative stress-mediated inflammation and pancreatitis in Wistar rats. Forty (40) rats randomly assigned to 5 groups (n = 8) were administered normal saline or hesperidin (Hsp) followed by Cd intoxication for 28 days. Cadmium accumulated in the pancreas of rats, and markedly decreased insulin, pancreatic superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities and glutathione (GSH) level. Cadmium considerably increased malondialdehyde (MDA), serum lipase and amylase activities. Cadmium induced pancreatic pro-inflammation via over-expression of inducible nitric oxide synthase (iNOS), nuclear factor-ĸB (NF-κB), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), along with histopathological alterations. Hesperidin prominently decreased serum amylase and lipase activities, and markedly increased insulin level, pancreatic antioxidant defense mechanism, whereas iNOS, NF-κB, IL-6 and TNF-α levels significantly decreased. Changes in histology confirmed our biochemical findings. Our findings suggest that Cd induced pancreatitis via pro-inflammation and oxidative stress; Hsp, thus, protects against Cd-induced pancreatitis via attenuation of oxidative stress and proinflammatory responses in pancreas. •Cadmium induced oxidative inflammatory pancreatitis and insulin deficit in rats.•Cadmium provokes deficit in insulin secretion and glucose control.•Hesperidin attenuated cadmium-induced pancreatic oxidative stress.•Hesperidin prevents pancreatic inflammation via enhancing antioxidant mechanism.•Hesperidin improves insulin secretion and inhibits hyperglycemia.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2020.118268