Abstract
Objective:
To investigate the protective effects and possible mechanisms of ferulic acid on diabetic nephropathy by observing the effects of ferulic acid on the level of inflammation and autophagy in glomerular mesangial cells induced by high glucose.
Methods:
SV40 MES 13 cells were cultured and randomly divided into the following groups: normal group (Control, 5.6 mmol/L glucose), mannitol group (Man, 30 mmol/L mannitol), high glucose group (HG, 30 mmol/L glucose), ferulic acid group (FA, 30 mmol/L glucose + 12.5, 25, 50, 100, 200 μmol/L ferulic acid), and the proliferation of SV40 MES 13 cells in each group was observed by MTT method. The levels of tumour necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1) and interleukin 1β(IL-1β)in cell supernatant were determined by enzyme-linked immunosorbent assay (ELISA). The expressions of NLRP3, IL-1β, LC3-II/I and p62 proteins in SV40 MES 13 cells were detected by Western blot.
Results:
①The proliferative activity of SV40 MES 13 cells was significantly higher in the HG group compared to the control group (P＜0.01), while the proliferative activity of SV40 MES 13 cells was decreased to different degrees in the FA group compared to the HG group (P＜0.05～0.01). ②Compared to the control group, the levels of TNF-α, MCP-1 and IL-1β were increased significantly in the cell supernatant of HG group (P＜0.01). Compared with the HG group, the levels of TNF-α, MCP-1 and IL-1β were decreased significantly in the FA group (P＜0.01). ③Compared with the control group, LC3-II/Ⅰ protein expression was decreased in the HG group, while the levels of p62, NLRP3 and IL-1β protein were increased significantly (P＜0.01). Compared with the HG group, the expression of LC3-II/Ⅰ protein was elevated significantly (P＜0.05) in the FA group, while the levels of p62, NLRP3 and IL-1β protein in the FA group were decreased significantly (P＜ 0.01).
Conclusion:
FA can inhibit the abnormal proliferation of SV40 MES 13 cells induced by high glucose. FA can protect glomerular mesangial cells by inhibiting inflammation and increasing the level of autophagy.
