title: Olive leaf down-regulates the oxidative stress and immune dysregulation in streptozotocin-induced diabetic mice.
abstract: Type 1 diabetes is an endocrinologic disorder characterized by uncontrolled glucose regulation and oxidative stress. Olive leaves have been studied extensively for their antioxidant activity and capacity to improve immune function. We hypothesized that olive leaf powder supplementation will be effective in inhibiting the oxidative stress and immune dysregulation in streptozotocin (STZ)-induced diabetic mice. Mice were assigned to 1 of 5 groups: control (C), STZ-induced diabetes (D), and STZ-induced diabetes supplemented with very low dose (VLOL), low dose (LOL), or high dose of olive leaf powder (HOL). Blood glucose in the VLOL and LOL groups was lower than that in the D group (P < .05). Insulin levels were increased in all experimental groups in comparison with that in the D group, (P < .05). Superoxide dismutase, glutathione peroxidase, and catalase activities were shown to decrease in the D group, whereas these were increased in the VLOL and LOL groups. Nitric oxide levels decreased in the VLOL and LOL groups, as compared with the D group. The messenger RNA expression levels of inducible nitric oxide synthase were significantly decreased in the VLOL and HOL groups, and interferon-γ levels were significantly decreased in the liver of the VLOL, LOL, and HOL groups compared with the levels in the D group. Interleukin-17 levels were significantly decreased in the VLOL and HOL groups. Th1 and Th17 cytokine levels were increased in the D group but decreased in all the experimental groups. Th2 cytokine levels were increased in all olive leaf-supplemented groups compared with those in the D group. These results indicate a reduction in the levels of proinflammatory cytokines, suggesting that olive leaves have the potential to provide therapeutic inhibition of diabetic complications.
authors.affiliation: Division of Biological Science, College of Science, Sookmyung Women's University, Seoul, Korea.
authors.forename: Jung-Hyun
authors.initials: JH
authors.lastname: Park
authors.forename: Ji-Hye
authors.initials: JH
authors.lastname: Jung
authors.forename: Jin-Young
authors.initials: JY
authors.lastname: Yang
authors.forename: Hyun-Sook
authors.initials: HS
authors.lastname: Kim
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use; D016207:Cytokines / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D019587:Dietary Supplements; D015536:Down-Regulation; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009569:Nitric Oxide / Q000097:blood; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D031658:Olea; D018384:Oxidative Stress / Q000187:drug effects*; D008517:Phytotherapy; D018515:Plant Leaves; D028321:Plant Preparations / Q000494:pharmacology / Q000627:therapeutic use; D012333:RNA, Messenger / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D016207:Cytokines; D018836:Inflammation Mediators; D028321:Plant Preparations; D012333:RNA, Messenger; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II
keywords: CAT; GPx; IFN; IL; Inducible nitric oxide synthase; Mice; NO; Olive leaf powder; ROS; RT-PCR; SOD; STZ; T1D; TNF; Th1Th2Th17 cytokines; Type 1 diabetes; catalase; glutathione peroxidase; iNOS; inducible nitric oxide synthase; interferon; interleukin; mRNA; messenger RNA; nitric oxide; reactive oxygen species; reverse transcription polymerase chain reaction; streptozotocin; superoxide dismutase; tumor necrosis factors; type 1 diabetes