Wenjun Shan, Haowen G U, Haiyu Guan, Ping L I, Yi Wang, Miaoru Han, Houchun Wang, Xiaoyan Huang, Kun Bao
Guangzhou University of Chinese Medicine, Guangzhou 510145, China.
State Key Laboratory of Dampness Syndrome of Chinese Medicine, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510006, China.
J Tradit Chin Med. 2025 Oct;45(5):1028-1039. doi: 10.19852/j.cnki.jtcm.2025.05.009.
To examine the T helper 17 (Th17)/regulatory T (Treg) immune balance in passive Heymann nephritis (PHN) rats with dampness syndrome (DS).
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 gavage. 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.
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.
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.
研究被动型海曼肾炎（PHN）湿证大鼠的辅助性T细胞17（Th17）/调节性T细胞（Treg）免疫平衡。
将大鼠分为四组：正常对照组（NC）、PHN模型组、PHN+湿证模型组和湿证模型组。通过灌胃猪油、60%冷蔗糖溶液和中国白酒建立湿证模型。相反，通过尾静脉注射抗Fx1A血清诱导雄性Sprague-Dawley大鼠发生PHN。评估大鼠的一般状况，同时使用市售试剂盒测量尿蛋白、白蛋白和血清肌酐水平。使用苏木精和伊红、过碘酸-希夫和过碘酸-银甲胺染色评估肾脏病理损伤，通过免疫组织化学评估足细胞损伤。通过流式细胞术定量外周血单个核细胞中Th17细胞和Treg细胞的比例。采用酶联免疫吸附测定法测定血浆中白细胞介素17、转化生长因子-β1和白细胞介素6的细胞因子水平。
本研究表明，伴有湿证的PHN大鼠蛋白尿和总胆固醇水平显著升高，肾脏组织病理学损伤更严重。湿证加重了PHN大鼠的足细胞损伤。此外，伴有湿证的PHN大鼠Treg细胞数量显著减少，而Th17/Treg细胞比例显著升高。
总之，我们的研究结果表明，湿证的存在会加重PHN（一种用于模拟实验性膜性肾病的大鼠模型）的肾损伤。这一观察结果可能与湿证诱导的PHN大鼠Th17/Treg失衡和足细胞损伤的加重密切相关。
