title: [6]-Gingerol isolated from ginger attenuates sodium arsenite induced oxidative stress and plays a corrective role in improving insulin signaling in mice.
abstract: Arsenic toxicity induces type 2 diabetes via stress mediated pathway. In this study, we attempt to reveal how sodium arsenite (iAs) could induce stress mediated impaired insulin signaling in mice and if an isolated active fraction of ginger, [6]-gingerol could attenuate the iAs intoxicated hyperglycemic condition of mice and bring about improvement in their impaired insulin signaling. [6]-Gingerol treatment reduced elevated blood glucose level and oxidative stress by enhancing activity of super oxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and GSH. [6]-Gingerol also helped in increasing plasma insulin level, brought down after iAs exposure. iAs treatment to primary cell culture of β-cells and hepatocytes in vitro produced cyto-degenerative effect and accumulated reactive oxygen species (ROS) in pancreatic β-cells and hepatocytes of mice. [6]-Gingerol appeared to inhibit/intervene iAs induced cyto-degeneration of pancreatic β-cells and hepatocytes, helped in scavenging the free radicals. The over-expression of TNFα and IL6 in iAs intoxicated mice was down-regulated by [6]-gingerol treatment. iAs intoxication reduced expression levels of GLUT4, IRS-1, IRS-2, PI3K, AKT, PPARγ signaling molecules; [6]-gingerol mediated its action through enhancing the expressions of these signaling molecules, both at protein and mRNA levels. Thus, our results suggest that [6]-gingerol possesses an anti-hyperglycemic property and can improve impaired insulin signaling in arsenic intoxicated mice.
authors.affiliation: Department of Zoology, University of Kalyani, Kalyani, West Bengal, India.
authors.forename: Debrup
authors.initials: D
authors.lastname: Chakraborty
authors.forename: Avinaba
authors.initials: A
authors.lastname: Mukherjee
authors.forename: Sourav
authors.initials: S
authors.lastname: Sikdar
authors.forename: Avijit
authors.initials: A
authors.lastname: Paul
authors.forename: Samrat
authors.initials: S
authors.lastname: Ghosh
authors.forename: Anisur Rahman
authors.initials: AR
authors.lastname: Khuda-Bukhsh
mesh_terms: D000818:Animals; D018053:Arsenites / Q000009:adverse effects* / Q000037:antagonists & inhibitors; D001786:Blood Glucose / Q000032:analysis; D002374:Catalase / Q000187:drug effects / Q000378:metabolism; D002396:Catechols / Q000494:pharmacology*; D005233:Fatty Alcohols / Q000494:pharmacology*; D005979:Glutathione Peroxidase / Q000187:drug effects / Q000378:metabolism; D022781:Hepatocytes / Q000737:chemistry / Q000187:drug effects; D007328:Insulin / Q000819:agonists* / Q000097:blood / Q000502:physiology; D050417:Insulin-Secreting Cells / Q000737:chemistry / Q000187:drug effects; D051379:Mice; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000032:analysis; D015398:Signal Transduction / Q000187:drug effects; D017670:Sodium Compounds / Q000009:adverse effects* / Q000037:antagonists & inhibitors; D013482:Superoxide Dismutase / Q000187:drug effects / Q000378:metabolism
chemical_list: D018053:Arsenites; D001786:Blood Glucose; D002396:Catechols; D005233:Fatty Alcohols; D007328:Insulin; D017382:Reactive Oxygen Species; D017670:Sodium Compounds; C017947:sodium arsenite; C007845:gingerol; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase