ORIGINAL ARTICLE The antioxidant effect of the Malaysian Gelam honey on pancreatic hamster cells cultured under hyperglycemic conditions Kalaivani Batumalaie • Rajes Qvist • Kamaruddin Mohd Yusof • Ikram Shah Ismail • Shamala Devi Sekaran Received: 29 October 2012 / Accepted: 24 March 2013 Ó Springer-Verlag Italia 2013 Abstract Type 2 diabetes consists of progressive hyper- glycemia, insulin resistance, and pancreatic b-cell failure which could result from glucose toxicity, inflammatory cytokines, and oxidative stress. In the present study, we investigate the effect of pretreatment with Gelam honey (Melaleuca spp.) and the individual flavonoid components chrysin, luteolin, and quercetin, on the production of reactive oxygen species (ROS), cell viability, lipid perox- idation, and insulin content in hamster pancreatic cells (HIT-T15 cells), cultured under normal and hyperglycemic conditions. Phenolic extracts from a local Malaysian spe- cies of Gelam honey (Melaleuca spp.) were prepared using the standard extraction methods. HIT-T15 cells were cul- tured in 5 % CO 2 and then preincubated with Gelam honey extracts (20, 40, 60, and 80 lg/ml) as well as some of its flavonoid components chrysin, luteolin, and quercetin (20, 40, 60, and 80 lM), prior to stimulation by 20 and 50 mM of glucose. The antioxidative effects were measured in these cultured cells at different concentrations and time point by DCFH-DA assay. Pretreatment of cells with Ge- lam honey extract or the flavonoid components prior to culturing in 20 or 50 mM glucose showed a significant decrease in the production of ROS, glucose-induced lipid peroxidation, and a significant increase in insulin content and the viability of cells cultured under hyperglycemic condition. Our results show the in vitro antioxidative property of the Gelam honey and the flavonoids on the b-cells from hamsters and its cytoprotective effect against hyperglycemia. Keywords Type 2 diabetes Á Oxidative stress Á Antioxidant Á Flavonoids Á Gelam honey Introduction Diabetes is one of the most common non-communicable diseases affecting millions of the people globally [1]. Type 2 diabetes consists of progressive hyperglycemia, insulin resistance, and pancreatic b-cell failure. b-cell dysfunction can result from glucose toxicity, inflammatory cytokines, oxidative stress (OS), and/or lipotoxicity in the presence of excess glucose. Oxidative stress through the production of reactive oxygen species (ROS) has been proposed as the root cause underlying the development of insulin resis- tance, b-cell dysfunction, impaired glucose tolerance, and type 2 diabetes mellitus [2]. There is a clear link between diabetic hyperglycemia and the development of secondary complications, indicating that OS may play an important role in the etiology of diabetic complications [3]. Oxidative stress induced by reactive oxygen and nitrogen species is critically involved in the impairment of b-cell dysfunction, possibly due to low levels of antioxidant enzyme expres- sions in the b-cells [4]. Free radicals are formed in type 2 diabetes by glucose oxidation, non-enzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins [5]. K. Batumalaie (&) Á R. Qvist Á I. S. Ismail Department of Medicine, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia e-mail: kalaivanibatumalaie@gmail.com K. M. Yusof Department of Molecular Biology and Genetics, Faculty of Arts and Science, Canik Basari University, Samsun, Turkey e-mail: mykamar77@gmail.com S. D. Sekaran Department of Microbiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia e-mail: shamala@um.edu.my 123 Clin Exp Med DOI 10.1007/s10238-013-0236-7