High glucose inhibits the survival of HRMCs and its mechanism

作者：Zhu, Y.; Ruan, C. -X.; Wang, J.; Jiang, F. -F.; Xiong, L. -S.; Sheng, X.; LE, J.; Yu, A. -Q.; Wang, Q.; Liu, Y. -T.; Qin, S. -L.^*

来源：European Review for Medical and Pharmacological Sciences, 2022, 26(16): 5683-5688.

• High glucose
• Survival
• HRMCs

OBJECTIVE: High glucose can pro-mote the apoptosis of glomerular mesangial cells and cause diabetic nephropathy (DN). However, the mechanism remains unclear. In the present study, we investigated the effects of high glucose on the survival of human renal mesangial cells (HRMCs).MATERIALS AND METHODS: Cells were treat-ed with high glucose (30 mM) or normal glucose (5 mM) for 48 hours. Cell proliferation was deter-mined by trypan blue assay. The relative expres-sion of metalloproteinase-3 (TIMP3) and inflamma-tory factors detected by real-time polymerase chain reaction (PCR). Protein expression of Smad2/3, p-Smad2/3 and Smad7 in HRMCs were analyzed by Western blot.RESULTS: Compared with normal glucose, we found that high glucose significantly inhibited cell survival, accompanied by the decrease of tissue metalloproteinase-3 (TIMP3) mRNA expression. Western blot results showed that the expression of p-Smad2/3 was significantly up-regulated, the expression of Smad7 was significantly downreg-ulated, and inflammatory factors IL-6/IL-8 mRNA expression were increased in the HRMCs cultured with the high glucose. We also found that, com-pared with the normal glucose, the level of MDA was significantly increased (p<0.01), and the lev-el of SOD was significantly lower (p<0.05) in the HRMCs cultured with the high glucose.CONCLUSIONS: These findings suggested that high glucose inhibited the survival of HRMCs and may be associated with the downregulation of TIMP3 expression, Smad signaling pathway, inflam-mation and oxidative stress.

• 单位
  南方医科大学; 5; 南昌大学