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Rosmarinic acid modulates the antioxidant status and protects pancreatic tissues from glucolipotoxicity mediated oxidative stress in high-fat diet: streptozotocin-induced diabetic rats.
Mol Cell Biochem. 2015 Jun; 404(1-2):143-59.MC

Abstract

Persistent hyperglycemia and elevated levels of free fatty acids (FFA) contribute to oxidative stress, a proximate cause for the onset and progression of diabetes and its complications. The present study was hypothesized to evaluate the anti-diabetic potential of Rosmarinic acid (RA) during high-fat diet (HFD)-streptozotocin (STZ)-induced type 2 Diabetes (T2D) in wistar albino rats. Oral administration of RA (100 mg/kg b.w) significantly (p < 0.05) increased the insulin sensitivity index (ISI0,120), while the levels of blood glucose, HbA1c, advanced glycation end products (AGE), TNF-α, IL-1β, IL 6, NO, p-JNK, P38 MAPK and NF-κB were significantly reduced, with a concomitant elevation in the plasma insulin levels in diabetic rats. Furthermore, RA treatment significantly (p < 0.05) reduced the levels of triglycerides, FFA and cholesterol in serum, and reduced the levels of lipid peroxides, AOPP's and protein carbonyls in the plasma and pancreas of diabetic rats. The diminished activities of pancreatic superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) and the decreased levels of plasma ceruloplasmin, vitamin C, vitamin E and reduced glutathione (GSH) in diabetic rats were also significantly (p < 0.05) recovered upon RA treatment denoting its antioxidant potential which was confirmed by Nrf-2, hemeoxyenase (HO-1) levels. Histological, ultrastructural and immunohistochemical data demonstrate that oral administration of RA protects pancreatic β-cells from oxidative niche in HFD-STZ-induced experimental diabetes. Our findings suggest that the oral treatment with RA alleviates pancreatic β-cell dysfunction and glucolipotoxicity-mediated oxidative stress during HFD-STZ-induced T2DM, perhaps through its antioxidant potential.

Authors+Show Affiliations

Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600 025, Tamilnadu, India.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25735949

Citation

Govindaraj, Jayanthy, and Subramanian Sorimuthu Pillai. "Rosmarinic Acid Modulates the Antioxidant Status and Protects Pancreatic Tissues From Glucolipotoxicity Mediated Oxidative Stress in High-fat Diet: Streptozotocin-induced Diabetic Rats." Molecular and Cellular Biochemistry, vol. 404, no. 1-2, 2015, pp. 143-59.
Govindaraj J, Sorimuthu Pillai S. Rosmarinic acid modulates the antioxidant status and protects pancreatic tissues from glucolipotoxicity mediated oxidative stress in high-fat diet: streptozotocin-induced diabetic rats. Mol Cell Biochem. 2015;404(1-2):143-59.
Govindaraj, J., & Sorimuthu Pillai, S. (2015). Rosmarinic acid modulates the antioxidant status and protects pancreatic tissues from glucolipotoxicity mediated oxidative stress in high-fat diet: streptozotocin-induced diabetic rats. Molecular and Cellular Biochemistry, 404(1-2), 143-59. https://doi.org/10.1007/s11010-015-2374-6
Govindaraj J, Sorimuthu Pillai S. Rosmarinic Acid Modulates the Antioxidant Status and Protects Pancreatic Tissues From Glucolipotoxicity Mediated Oxidative Stress in High-fat Diet: Streptozotocin-induced Diabetic Rats. Mol Cell Biochem. 2015;404(1-2):143-59. PubMed PMID: 25735949.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rosmarinic acid modulates the antioxidant status and protects pancreatic tissues from glucolipotoxicity mediated oxidative stress in high-fat diet: streptozotocin-induced diabetic rats. AU - Govindaraj,Jayanthy, AU - Sorimuthu Pillai,Subramanian, Y1 - 2015/03/04/ PY - 2014/11/26/received PY - 2015/02/23/accepted PY - 2015/3/5/entrez PY - 2015/3/5/pubmed PY - 2016/1/26/medline SP - 143 EP - 59 JF - Molecular and cellular biochemistry JO - Mol Cell Biochem VL - 404 IS - 1-2 N2 - Persistent hyperglycemia and elevated levels of free fatty acids (FFA) contribute to oxidative stress, a proximate cause for the onset and progression of diabetes and its complications. The present study was hypothesized to evaluate the anti-diabetic potential of Rosmarinic acid (RA) during high-fat diet (HFD)-streptozotocin (STZ)-induced type 2 Diabetes (T2D) in wistar albino rats. Oral administration of RA (100 mg/kg b.w) significantly (p < 0.05) increased the insulin sensitivity index (ISI0,120), while the levels of blood glucose, HbA1c, advanced glycation end products (AGE), TNF-α, IL-1β, IL 6, NO, p-JNK, P38 MAPK and NF-κB were significantly reduced, with a concomitant elevation in the plasma insulin levels in diabetic rats. Furthermore, RA treatment significantly (p < 0.05) reduced the levels of triglycerides, FFA and cholesterol in serum, and reduced the levels of lipid peroxides, AOPP's and protein carbonyls in the plasma and pancreas of diabetic rats. The diminished activities of pancreatic superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) and the decreased levels of plasma ceruloplasmin, vitamin C, vitamin E and reduced glutathione (GSH) in diabetic rats were also significantly (p < 0.05) recovered upon RA treatment denoting its antioxidant potential which was confirmed by Nrf-2, hemeoxyenase (HO-1) levels. Histological, ultrastructural and immunohistochemical data demonstrate that oral administration of RA protects pancreatic β-cells from oxidative niche in HFD-STZ-induced experimental diabetes. Our findings suggest that the oral treatment with RA alleviates pancreatic β-cell dysfunction and glucolipotoxicity-mediated oxidative stress during HFD-STZ-induced T2DM, perhaps through its antioxidant potential. SN - 1573-4919 UR - https://www.unboundmedicine.com/medline/citation/25735949/Rosmarinic_acid_modulates_the_antioxidant_status_and_protects_pancreatic_tissues_from_glucolipotoxicity_mediated_oxidative_stress_in_high_fat_diet:_streptozotocin_induced_diabetic_rats_ L2 - https://doi.org/10.1007/s11010-015-2374-6 DB - PRIME DP - Unbound Medicine ER -