Effect of Gelam Honey on the Oxidative Stress-Induced Signaling Pathways in Pancreatic Hamster Cells

被引:24
作者
Batumalaie, Kalaivani [1 ]
Safi, Sher Zaman [1 ]
Yusof, Kamaruddin Mohd [2 ]
Ismail, Ikram Shah [1 ]
Sekaran, Shamala Devi [3 ]
Qvist, Rajes [1 ]
机构
[1] Univ Malaya, Dept Med, Fac Med, Kuala Lumpur 50603, Malaysia
[2] Canik Basari Univ, Dept Mol Biol & Genet, Fac Arts & Sci, Samsun, Turkey
[3] Univ Malaya, Dept Microbiol, Fac Med, Kuala Lumpur 50603, Malaysia
关键词
ACTIVATED PROTEIN-KINASES; INSULIN-RESISTANCE; KAPPA-B; DIABETES-MELLITUS; GLUCOSE TOXICITY; CHRONIC EXPOSURE; GENE-EXPRESSION; POTENTIAL ROLE; BETA-CELLS; HIT CELLS;
D O I
10.1155/2013/367312
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background. Oxidative stress induced by reactive oxygen and nitrogen species is critically involved in the impairment of.. cell function during the development of diabetes. Methods. HIT-T15 cells were cultured in 5% CO2 and then preincubated with Gelam honey extracts (20, 40, 60, and 80 mu g/mL) as well as quercetin (20, 40, 60, and 80 mu M), prior to stimulation by 20 and 50 mM of glucose. Cell lysate was collected to determine the effect of honey extracts and quercetin on the stress activated NF-kappa B, MAPK pathways, and the Akt (ser473) activated insulin signaling pathway. Results. HIT-T15 cells cultured under hyperglycemic conditions demonstrated insulin resistance with a significant increase in the levels of MAPK, NF-kappa B, and IRS-1 serine phosphorylation (ser307); however, Akt expression and insulin contents are significantly decreased. Pretreatment with quercetin and Gelam honey extract improved insulin resistance and insulin content by reducing the expression of MAPK, NF-kappa B, and IRS-1 serine phosphorylation (ser307) and increasing the expression of Akt significantly. Conclusion. Gelam honey-induced differential expression of MAPK, NF-kappa B, IRS-1 (ser307), and Akt in HIT-T15 cells shows that Gelam honey exerts protective effects against diabetes-and hyperglycemia-induced oxidative stress by improving insulin content and insulin resistance.
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页数:10
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共 44 条
[1]   Mechanisms of disease - Nuclear factor-kappa b - A pivotal transcription factor in chronic inflammatory diseases [J].
Barnes, PJ ;
Larin, M .
NEW ENGLAND JOURNAL OF MEDICINE, 1997, 336 (15) :1066-1071
[2]  
Batumalaie K., 2013, CLIN EXPT MED
[3]   Defective insulin secretion and increased susceptibility to experimental diabetes are induced by reduced Akt activity in pancreatic islet β cells [J].
Bernal-Mizrachi, E ;
Fatrai, S ;
Johnson, JD ;
Ohsugi, M ;
Otani, K ;
Han, ZQ ;
Polonsky, KS ;
Permutt, MA .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (07) :928-936
[4]   Enhanced basal activation of mitogen-activated protein kinases in adipocytes from type 2 diabetes - Potential role of p38 in the downregulation of GLUT4 expression [J].
Carlson, CJ ;
Koterski, S ;
Sciotti, RJ ;
Poccard, GB ;
Rondinone, CM .
DIABETES, 2003, 52 (03) :634-641
[5]   Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKBβ) [J].
Cho, H ;
Mu, J ;
Kim, JK ;
Thorvaldsen, JL ;
Chu, QW ;
Crenshaw, EB ;
Kaestner, KH ;
Bartolomei, MS ;
Shulman, GI ;
Birnbaum, MJ .
SCIENCE, 2001, 292 (5522) :1728-1731
[6]   Mechanisms of pancreatic β-cell death in type 1 and type 2 diabetes -: Many differences, few similarities [J].
Cnop, M ;
Welsh, N ;
Jonas, JC ;
Jörns, A ;
Lenzen, S ;
Eizirik, DL .
DIABETES, 2005, 54 :S97-S107
[7]  
Cordero H. I., 2013, MOL NUTR FOOD RES
[8]   Quercetin, a flavonoid antioxidant, prevents and protects streptozotocin-induced oxidative stress and β-cell damage in rat pancreas [J].
Coskun, O ;
Kanter, M ;
Korkmaz, A ;
Oter, S .
PHARMACOLOGICAL RESEARCH, 2005, 51 (02) :117-123
[9]   Tumor necrosis factor α produces insulin resistance in skeletal muscle by activation of inhibitor κB kinase in a p38 MAPK-dependent manner [J].
de Alvaro, C ;
Teruel, T ;
Hernandez, R ;
Lorenzo, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (17) :17070-17078
[10]   PATHOGENESIS OF NIDDM - A BALANCED OVERVIEW [J].
DEFRONZO, RA ;
BONADONNA, RC ;
FERRANNINI, E .
DIABETES CARE, 1992, 15 (03) :318-368