简介：痛风性肾病（GN）是由于嘌呤摄入过多、代谢紊乱或合成异常，血液中尿酸过饱和，导致肾组织中尿酸盐结晶沉积所致。戴痛消（DTX）是中国傣族人使用的一种药物。它具有降低尿酸水平的功效，并具有抗炎和保护肾脏的特性。方法：采用腺嘌呤和氧酸钾诱导GN大鼠模型。 DTX 给药后，评估尿液、血清和肾组织的各种参数。蛋白质印迹分析评估 TLR4/MyD88/NF-κB 信号蛋白，而免疫荧光检查 NF-κB 核表达。结果：DTX治疗改善了GN大鼠的肾脏形态，增加了体重和肾脏指数，并提高了尿素氮（Bun）、24小时尿蛋白、尿酸（UA）和尿囊素的水平，降低了UA、Bun、血清分析中的肌酐 (Cre)、半胱氨酸蛋白酶抑制剂 C (CysC)、血清淀粉样蛋白 A (SAA)、α1-微球蛋白 (MG) 和 β2-MG。肾组织评估显示黄嘌呤氧化酶 (XOD)、羟脯氨酸 (Hyp)、α-平滑肌肌动蛋白 (α-SMA) 和 IV 型胶原蛋白 (COL-IV) 降低。肾脏损伤的严重程度显着降低。 DTX 降低大鼠血清炎症因子，如白细胞介素 (IL) -18、肿瘤坏死因子-α (TNF-α)、C 反应蛋白 (CRP)、转化生长因子-β1 (TGF-β1) 和 IL-1β血清中，减少趋化因子单核细胞趋化蛋白-1（MCP-1）和粘附因子血管细胞粘附分子-1（VCAM-1）。 Western blotting显示TLR4/MyD88/NF-κB通路蛋白下调，免疫荧光显示肾组织中NF-κB表达减少。讨论：DTX 通过调节 TLR4/MyD88/ NF-κB 通路蛋白表达、减少炎症因子释放、抑制 GN 进展而表现出显着的抗肾小球肾炎作用。版权所有 © 2024 刘白万罗张张吴陈尹、谢和郭。

Introduction: Gouty nephropathy (GN) arises from factors like excessive purine intake, metabolic disorders or abnormal synthesis, and uric acid hypersaturation in the blood, leading to urate crystal deposition in kidney tissue. DaiTongXiao (DTX) is a remedy used by the Dai people of China. It shows efficacy in lowering uric acid levels and exhibits anti-inflammatory and kidney-protective properties. Methods: A GN rat model was induced using adenine and potassium oxonate. Following DTX administration, various parameters were assessed in urine, serum, and kidney tissue. Western blot analysis evaluated TLR4/MyD88/NF-κB signaling proteins, while immunofluorescence examined NF-κB nuclear expression. Results: DTX treatment improved kidney morphology, increased body weight, and kidney index and enhanced urinary levels of blood urea nitrogen (Bun), 24-h urinary protein, uric acid (UA), and allantoin in GN rats, reducing UA, Bun, creatinine (Cre), cystatin C (CysC), serum amyloid A (SAA), α1-microglobulin (MG), and β2-MG in serum analysis. Renal tissue assessments showed decreased xanthine oxidase (XOD), hydroxyproline (Hyp), α-smooth muscle actin (α-SMA), and collage type Ⅳ (COL-Ⅳ). Kidney damage severity was notably reduced. DTX lowered serum inflammatory factors like interleukin (IL) -18, tumor necrosis factor-α (TNF-α), C-reactive protein (CRP), transforming growth factor-β1 (TGF-β1), and IL-1β in the rat serum, reducing chemokine monocyte chemoattractant protein-1 (MCP-1) and adhesion factor vascular cell adhesion molecule-1(VCAM-1). Western blotting demonstrated the downregulation of TLR4/MyD88/NF-κB pathway proteins, and immunofluorescence revealed reduced NF-κB expression in renal tissue. Discussion: DTX exhibits significant anti-GN effects by modulating TLR4/MyD88/ NF-κB pathway protein expression, reducing inflammatory factor release, and inhibiting GN progression.Copyright © 2024 Liu, Bai, Wan, Luo, Zhang, Wu, Chen, Yin, Xie and Guo.