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益肾排毒方调控ROS/TXNIP/NLRP3通路对慢性肾衰竭大鼠肾纤维化的影响
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| 篇名： | 益肾排毒方调控ROS/TXNIP/NLRP3通路对慢性肾衰竭大鼠肾纤维化的影响 |
| TITLE： | Effects of Yishen paidu formula on renal fibrosis in rats with chronic renal failure by regulating the ROS/TXNIP/NLRP3 pathway |
| 摘要： | 目的 通过活性氧（ROS）/硫氧还蛋白相互作用蛋白（TXNIP）/NOD样受体热蛋白结构域相关蛋白3（NLRP3）通路，探讨益肾排毒方对慢性肾衰竭（CRF）大鼠肾纤维化的作用及机制。方法将大鼠随机分为对照组、模型组、益肾排毒方低剂量（益肾排毒方-L）组、益肾排毒方高剂量（益肾排毒方-H）组、益肾排毒方-H+携带阴性对照序列的pcDNA载体（pcDNA-NC）组、益肾排毒方-H+携带TXNIP基因的pcDNA载体（pcDNA-TXNIP）组，每组10只。除对照组外，其余大鼠均通过喂养含0.5%腺嘌呤的饲料构建CRF模型，并灌胃或尾静脉注射相应药物或生理盐水，每日1次，连续8周。末次给药后，检测各组大鼠血肌酐（Scr）、尿素氮（BUN）、活性氧（ROS）、超氧化物歧化酶（SOD）、丙二醛（MDA）、肿瘤坏死因子α（TNF-α）、白细胞介素（IL）-6、IL-1β水平；观察肾组织病理变化；检测肾组织中胶原蛋白Ⅲ（CollagenⅢ）、α-平滑肌肌动蛋白（α-SMA）、转化生长因子β（1TGF-β1）、TXNIP、NLRP3蛋白表达情况。结果与模型组比较，益肾排毒方-L组和益肾排毒方-H组大鼠肾组织病理损伤和纤维化均明显缓解，Scr、BUN、ROS、MDA、TNF-α、IL-6、IL-1β水平和CollagenⅢ、α-SMA、TGF-β1、TXNIP、NLRP3蛋白表达水平均明显/显著降低，SOD水平均显著升高（P＜0.05），且益肾排毒方-H组变化更显著（P＜0.05）；与益肾排毒方-H+pcDNA-NC组比较，益肾排毒方-H+pcDNA-TXNIP组大鼠上述指标水平均显著逆转（P＜0.05）。结论益肾排毒方可通过抑制ROS/TXNIP/NLRP3通路延缓CRF大鼠肾纤维化。 |
| ABSTRACT： | OBJECTIVE To investigate the effects and mechanism of the Yishen paidu formula on renal fibrosis in rats with chronic renal failure （CRF） through the reactive oxygen species （ROS）/thioredoxin-interacting protein （TXNIP）/NOD-like receptor thermal protein domain associated protein 3 （NLRP3） pathway. METHODS Rats were randomly divided into control group， model group， Yishen paidu formula low-dose （Yishen paidu formula-L） group， Yishen paidu formula high-dose （Yishen paidu formula- H） group， Yishen paidu formula-H+pcDNA-NC group， and Yishen paidu formula-H+ pcDNA-TXNIP group， with 10 rats in each group. Except for control group， all other rats were fed a diet containing 0.5% adenine to establish a CRF model； the rats were then administered corresponding drugs or normal saline intragastrically or via tail vein， once daily， for 8 consecutive weeks. After the last administration， the levels of serum creatinine （Scr）， blood urea nitrogen （BUN）， ROS， superoxide dismutase （SOD）， malondialdehyde （MDA）， tumor necrosis factor-α （TNF-α）， interleukin （IL）-6， and IL-1β were measured in each group. Pathological changes in renal tissue were observed， and the protein expression levels of Collagen Ⅲ， α-smooth muscle actin （α-SMA）， transforming growth factor-β1 （TGF-β1）， TXNIP and NLRP3 in renal tissue were detected. RESULTS Compared with model group， the renal histopathological damage and fibrosis of rats in Yishen paidu formula-L group and Yishen paidu formula-H group were significantly alleviated. The levels of Scr， BUN， ROS， MDA， TNF- α， IL-6 and IL-1β， and the protein expressions of Collagen Ⅲ， α-SMA， TGF-β1， TXNIP and NLRP3 were significantly decreased， while SOD levels were significantly increased （P＜0.05）. Moreover， the changes were more pronounced in the Yishen paidu formula-H group （P＜0.05）. Compared with Yishen paidu formula-H+pcDNA-NC group， above indexes of rats in Yishen paidu formula-H+pcDNA-TXNIP group were reversed significantly （P＜0.05）. CONCLUSIONS Yishen paidu formula can inhibit renal fibrosis in CRF rats by suppressing the ROS/TXNIP/NLRP3 pathway. |
| 期刊： | 2026年第37卷第02期 |
| 作者： | 冯立；彭博文；彭斌；冯雪；朱双益；熊玮；胡溪；孙小慧 |
| AUTHORS： | FENG Li，PENG Bowen，PENG Bin，FENG Xue，ZHU Shuangyi，XIONG Wei，HU Xi，SUN Xiaohui |
| 关键字： | 益肾排毒方；慢性肾衰竭；肾纤维化；ROS/TXNIP/NLRP3通路 |
| KEYWORDS： | Yishen paidu formula； chronic renal failure； renal fibrosis； ROS/TXNIP/NLRP3 pathway |
| 阅读数： | 3 次 |
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