Dampness syndrome aggravates T helper 17/regulatory T imbalance to promote renal injury in rats with experimental membranous nephropathy.

Abstract

Objective: To examine the T helper 17 (Th17)/regulatory T (Treg) immune balance in passive Heymann nephritis (PHN) rats with dampness syndrome (DS).

Methods: Rats were divided into four groups: normal control (NC), PHN model, PHN + DS model, and DS model. The DS model was created by administering lard, a 60% cold sucrose solution, and Chinese Baijiu viagavage. In contrast, PHN was induced in male Sprague-Dawley rats by injecting anti-Fx1A serum into the tail vein. The general condition of the rats was assessed, while the levels of urine protein, albumin, and serum creatinine were measured using commercially available kits. Pathological renal damage was evaluated using hematoxylin and eosin, periodic acid-schiff, and periodic acid-silver methenamine staining, while podocyte damage was assessed through immunohistochemistry. The proportions of Th17 cells and Treg cells in peripheral blood mononuclear cells were quantified by flow cytometry. Plasma cytokine levels of interleukin 17, transforming growth factor-β1, and interleukin 6 were determined by enzyme-linked immunosorbent assay.

Results: This study demonstrated a significant increase in proteinuria and total cholesterol levels in PHN rats with DS, along with more severe histopathological kidney damage. DS exacerbated podocyte damage in PHN rats. Additionally, the number of Treg cells was significantly reduced, while the ratio of Th17/Treg cells was significantly elevated in PHN rats with DS.

Conclusion: In conclusion, the findings of our study indicate that the presence of DS exacerbates renal injury in PHN, a rat model used to simulate experimental membranous nephropathy. This observation may be closely linked to the exacerbation of the Th17/Treg imbalance and podocyte injury in PHN rats induced by DS.