摘要：AbstractObjectives:The present study is to explore the influence of DSS on the proliferation and activation of renal macrophages in the STZ-induced diabetic nephropathy rats.Methods:Seventy rats were grouped according to the random digit table means. 8 rats were randomly selected as the control group. The remaining 62 rats were divided into 5 groups and given a high-fat and high-sugar diet for 4 weeks. Diabetic rats were prepared by intraperitoneal injection of 55 mg/kg STZ. Rats in the DSS groups were given 21 g/kg/day, 14 g/kg/day and 7 g/kg/day DSS separately. The rats in the positive control group were given 6 mg/kg/day TP, while the rats of the model group and control group were received the physiological saline by gastric perfusion directly. Blood glucose, 24 h urine protein, urine urea nitrogen and β2 microglobulin of the rats were measured. And the protein levels of ED-1, MCP-1 and TLR4 in rat kidney were detected by Western Blot. ED-1+/TLR4+, ED-1+/PCNA+ and ED-1+/iNOS+ were detected by immunofluorescence.Results:DSS reduced the levels of blood glucose, 24-h urine protein, urine urea nitrogen and β2 microglobulin and repaired kidney tissue damage of the DN rats. In the WB experiment, DSS clearly decreased the protein expression levels of ED-1, MCP-1, and TLR4 in a dose-dependent manner (p < 0.05). In the immunofluorescence experiment, compared with the model group, the level of ED-1+/TLR4+ in the rats of DSS and TP groups and the level of ED-1+/PCNA+ in the rats of DSS-M group were obviously decreased (p < 0.05). Also, the level of ED-1+/PCNA+ and ED-1+/iNOS+ in the rats of DSS-H and TP groups was decreased evidently (p < 0.01).Conclusion:We inferred that DSS has therapeutic effects on the DN model rats, and its mechanism is likely to be connected with inhibition of macrophage proliferation and activation in rat kidney.
