Biomedical Research

Objective: Diabetic nephropathy (DN) has become the second common cause for terminal nephropathy. Serum amyloid A (SAA) is a marker for body inflammation. Previous study showed involvement of SAA in DN onset and pathogenesis. This study aimed to investigate the regulation of inflammatory factor TNF-α and extracellular matrix (ECM) FN by SAA, as well as the effects of SAA on renal glomerular cells in DN patients.

Patients and Methods: A total of 188 diabetic patients were divided into pure diabetic, micro-albumin urea and clinical albumin urea groups. ELISA was used to measure the concentration of SAA and TNF- α. Pearson correlation was used to analyze the association of SAA or TNF-α with UAER. RNA interference was used to inhibit SAA expression in glomerular cells, whilst Western blot was performed to measure the SAA and TNF-α expression in cultured cell supernatant after treated with different glucose concentrations. ELISA was then used to evaluate FN expression.

Results: Micro-albumin urea and clinical albumin urea groups had significantly higher serum SAA and TNF-α concentrations (p<0.05 compared with pure diabetic group). Their concentrations were positively correlated with UAER (r=0.463, and 0.278, p<0.05). After transfection of anti-SAA, renal glomerular cells showed lower TNF-α and FN levels (p<0.05 compared with control cells cultured under highglucose medium).

Conclusions: This study indicated positive correlation between SAA concentration and UAER, indicating the possible involvement of SAA in the onset/progression of DN, which might be possibly via mediating the expression levels of TNF-α and FN.

Author(s): Hongchun Shen, Yao Ming, Sha Zhao, Yanwen Xu, Chuanlan Xu, Qiong Zhang
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