Role of Antibody Anti-AGE in the Expression of Nephrin and RAGE on Primary Glomerulus Cell Exposed with AGE

Abstract

Nephrin is associated with the initial stage of the loss of the permeability barrier in diabetic nephropathy. Interaction AGE-RAGE increases angiotensin II on Renin Angiotensin-Aldosterone System (RAAS) and activation of protein kinase c (PKC) which induce alterations in nephrin mRNA expression. Alterations of nephrin expression induce transformation of slit membrane structure and the permeability changes at the glomerular filtration barrier. Anti-AGE vaccination once may cause the changes of nephrin and RAGE expression and can prevent progression of diabetic nephropathy. This study used primary glomerulus cell culture obtained from renal of Wistar rat aged 3 months, weighing 200-300 grams and assigned into negative control group that exposed to BSA 100 µg/mL, positive control group that exposed to AGE-BSA 100 µg/mL, treatment group 1 that exposed to polyclonal anti-AGE antibody 5 µg/mL and AGE-BSA 100 µg/mL and treatment group 2 that exposed to monoclonal anti-CML antibody 5 µg/mL and AGE-BSA 100 µg/mL. Paired t-test with a 0.05 level of confidence results showed that there were significantly different v in level of RAGE expression between experimental groups with control groups. Administration of polyclonal anti-AGE antibody decreased RAGE expression compared to negative control (p = 0.188) and positive control (p = 0.000). RAGE expression did not differ significantly in administration of monoclonal anti-CML antibody compared to negative control but significant with positive control. Administration of monoclonal anti-CML antibody inhibited increasing of nephrin expression compared to negative and positive control (p = 0.73; 0.125). In conclusion, this study suggested that administration of polyclonal anti-AGE or monoclonal anti-CML antibody could inhibit increasing of RAGE and nephrin expression in glomerulus primary culture that exposed to AGE which is expected to prevent the progression of diabetic nephropathy.