1.25(OH)2D3 decreases PCNA and mTOR expression and alleviates renal injury in Thy-1 nephritis rat model.

Objective: This study investigated the role and mechanisms of 1.25(OH)₂D₃ in proliferative glomerulonephritis and its effect on the regulation of mesangial cells. Methods: Sixty male SD rats were randomly divided into four groups: control (CG), nephritis (NG), nephritis + 1.25(OH)₂D₃(NVG), and nephritis + 1.25(OH)₂D₃+ rapamycin (NVRG) (n = 15 per group). Three rats from each group were sacrificed on days 1, 3, 7, 14, and 21 after intervention. Urine samples were collected over 24 hours on day 0 to measure urinary protein excretion. Renal tissue samples were stained with HE and PAS to evaluate the extent of renal injury, while immunohistochemistry was employed to quantify PCNA and mTOR expression in the renal tissues. Results: Compared to the NG, mesangial cell proliferation in the renal tissues was significantly reduced in the NVG and NVRG at all time points (all p<0.05). PCNA expressionwas significantly higher in the NG compared to the CG (p < 0.05) and significantly lower in the NVG and NVRG (p < 0.05). mTOR expression was also significantly increased in the NG compared to the CG, with a significant reduction observed in the NVG and NVRG compared to the NG. Conclusion: Our findings demonstrate that 1.25(OH)₂D₃significantly inhibits the proliferation of glomerular mesangial cells in rats. Additionally, mTOR protein is involved in the regulation of glomerular mesangial cells by 1.25(OH)₂D₃. These results further elucidate the molecular mechanism by which 1.25(OH)₂D₃alleviates renal injury in glomerulonephritis. [ABSTRACT FROM AUTHOR]