ArticlePloS one2024
1.25(OH)2D3 decreases PCNA and mTOR expression and alleviates renal injury in Thy-1 nephritis rat model.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThis study investigated the role and mechanisms of 1.25(OH)2D3 in proliferative glomerulonephritis and its effect on the regulation of mesangial cells.
methodsSixty 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.
resultsCompared 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.
conclusionOur 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.
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