TY - JOUR T1 - Niacin Regulates Glucose Reactive Protein (GRP78), Protein Carbonyl Content (PCC) and Malondialdehyde (MDA) in the Hyperglycemic Human Lens Epithelial Cells JF - Pharmacognosy Journal Y1 - 2019 A1 - Nina Handayani A1 - Hidayat Sujuti A1 - Nur Permatasari A1 - Achmad Rudijanto KW - Diabetic cataract KW - Glucose KW - GRP78 KW - MDA KW - Niacin KW - Oxidative stress KW - PCC AB -

Introduction: Niacin is part of the chemical structure of coenzymes nicotinamide adenine nucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). Previous studies suggested that a high niacin intake could decrease the prevalence of cataracts, which may delay the onset of diabetic cataract. Aim: The aim of this study was to evaluate the effect of niacin on the hyperglycemia-induced osmotic stress and oxidative stress in human lens epithelial cells. Materials and Methods: Human lens epithelial cells were cultured in a high glucose condition. Oxidative stress markers, including malondialdehyde (MDA), protein carbonyl content (PCC) and glucose reactive protein (GRP), were measured using TBARS analysis (MDA) and ELISA (PCC and GRP) after 72 h incubation. Results: The MDA levels increased after high glucose administration relative to that in the control group (p <0.05). Further, the groups that were co-treated with niacin showed decrease in the MDA levels for all doses of niacin and the lowest mean MDA level was obtained with 100 μM niacin. There was a decrease in the PCC levels for all doses, whereas the lowest mean PCC level was observed at a 100 μM niacin dose. The GRP levels increased after high glucose administration as compared with the control group. Also, the groups that were co-treated with niacin exhibited statistically significant reduction. Conclusion: These results suggest that niacin can inhibit the osmotic stress and oxidative stress which may lead to the progression of a diabetic cataract. Also, it may maintain lens transparency by acting as a precursor for glutathione biosynthesis and an antioxidant.

VL - 11 IS - 1 ER -