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Tytuł:
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Hesperidin protects against cadmium-induced pancreatitis by modulating insulin secretion, redox imbalance and iNOS/NF-ĸB signaling in rats.
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Autorzy:
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Aja PM; Department of Biochemistry, Faculty of Science, Ebonyi State University, Abakaliki, Nigeria.
Izekwe FI; Department of Biochemistry, Faculty of Science, Ebonyi State University, Abakaliki, Nigeria.
Famurewa AC; Department of Medical Biochemistry, Faculty of Basic Medical Sciences, College of Medicine, Alex-Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria. Electronic address: .
Ekpono EU; Department of Science Laboratory Technology, Biochemistry Option, Federal Polytechnic Oko, Anambra State, Nigeria.
Nwite FE; Department of Biochemistry, Faculty of Science, Ebonyi State University, Abakaliki, Nigeria.
Igwenyi IO; Department of Biochemistry, Faculty of Science, Ebonyi State University, Abakaliki, Nigeria.
Awoke JN; Department of Biochemistry, Faculty of Science, Ebonyi State University, Abakaliki, Nigeria.
Ani OG; Department of Biochemistry, Faculty of Science, Ebonyi State University, Abakaliki, Nigeria.
Aloke C; Department of Medical Biochemistry, Faculty of Basic Medical Sciences, College of Medicine, Alex-Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria.
Obasi NA; Department of Medical Biochemistry, Faculty of Basic Medical Sciences, College of Medicine, Alex-Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria.
Udeh KU; Department of Science Laboratory Technology, Biochemistry Option, Federal Polytechnic Oko, Anambra State, Nigeria.
Ale BA; Department of Biochemistry, Faculty of Biological Sciences, University of Nigeria, Nsukka, Enugu State, Nigeria.
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Źródło:
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Life sciences [Life Sci] 2020 Oct 15; Vol. 259, pp. 118268. Date of Electronic Publication: 2020 Aug 13.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Publication: <2008->: Amsterdam : Elsevier
Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
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MeSH Terms:
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Hesperidin/*pharmacology
Insulin-Secreting Cells/*drug effects
Pancreatitis/*drug therapy
Animals ; Antioxidants/pharmacology ; Cadmium/toxicity ; Catalase/metabolism ; Glutathione/metabolism ; Hesperidin/metabolism ; Inflammation/metabolism ; Insulin/metabolism ; Insulin Secretion/drug effects ; Insulin Secretion/physiology ; Male ; Malondialdehyde/metabolism ; NF-kappa B/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Oxidation-Reduction/drug effects ; Oxidative Stress/drug effects ; Pancreatitis/metabolism ; Protective Agents ; Rats ; Rats, Wistar ; Signal Transduction/drug effects ; Superoxide Dismutase/metabolism
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Contributed Indexing:
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Keywords: Antioxidant; Cadmium toxicity; Hesperidin; Inflammatory cytokines; Pancreatitis
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Substance Nomenclature:
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0 (Antioxidants)
0 (Insulin)
0 (NF-kappa B)
0 (Protective Agents)
00BH33GNGH (Cadmium)
4Y8F71G49Q (Malondialdehyde)
E750O06Y6O (Hesperidin)
EC 1.11.1.6 (Catalase)
EC 1.14.13.39 (Nitric Oxide Synthase Type II)
EC 1.14.13.39 (Nos2 protein, rat)
EC 1.15.1.1 (Superoxide Dismutase)
GAN16C9B8O (Glutathione)
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Entry Date(s):
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Date Created: 20200818 Date Completed: 20201104 Latest Revision: 20201104
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Update Code:
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20240105
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DOI:
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10.1016/j.lfs.2020.118268
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PMID:
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32800830
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Aim: 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.
Main Methods: Forty (40) rats randomly assigned to 5 groups (n = 8) were administered normal saline or hesperidin (Hsp) followed by Cd intoxication for 28 days.
Key Findings: 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.
Significance: 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.
Competing Interests: Declaration of competing interest The authors declare no conflict of interest.
(Copyright © 2020 Elsevier Inc. All rights reserved.)
