Division of Nephrology, Department of Medicine, Showa University Fujigaoka Hospital, Yokohama, Japan.
J Nephrol. 2013 Jan-Feb;26(1):199-206. doi: 10.5301/jn.5000125.
The renoprotection of the mineralocorticoid receptor antagonist (MRA) is considered to be mainly via its antifibrotic activity, and the possibility that it may also have antiinflammatory effects has not been studied. We tested the hypothesis that MRA might influence the inflammatory changes that accompany experimental glomerular injury.
Administration of vehicle (control) or a selective MRA, eplerenone (50 mg/kg x 2 times/day) was started 7 days (-7d) before induction of anti-Thy-1.1 glomerulonephritis. Kidney samples were evaluated serially over a 12-day period for the presence of cell proliferation, macrophage infiltration, mesangial cell phenotypic activation and expression of the chemokine monocyte chemoattractant protein-1 (MCP-1).
MRA did not prevent the mesangiolysis associated with anti-Thy-1 antibody. However, MRA significantly inhibited MCP-1 expression, glomerular macrophage infiltration and mesangial phenotypic activation (alpha-smooth muscle actin expression).
MRA alters glomerular inflammation and mesangial cell activation in experimental glomerular injury. MRA may be a novel way to treat acute glomerular diseases.
醛固酮受体拮抗剂（MRA）的肾保护作用被认为主要与其抗纤维化活性有关，而其可能具有抗炎作用的可能性尚未得到研究。我们检验了这样一个假设，即 MRA 可能会影响伴随实验性肾小球损伤的炎症变化。
在抗 Thy-1.1 肾小球肾炎诱导前 7 天（-7d）开始给予载体（对照）或选择性 MRA，依普利酮（50mg/kg x 2 次/天）。在 12 天的时间内，连续评估肾脏样本是否存在细胞增殖、巨噬细胞浸润、系膜细胞表型激活和趋化因子单核细胞趋化蛋白-1（MCP-1）的表达。
MRA 不能预防与抗 Thy-1 抗体相关的系膜溶解。然而，MRA 显著抑制 MCP-1 表达、肾小球巨噬细胞浸润和系膜细胞表型激活（α-平滑肌肌动蛋白表达）。
MRA 改变了实验性肾小球损伤中的肾小球炎症和系膜细胞激活。MRA 可能是治疗急性肾小球疾病的一种新方法。
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