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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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          冯 立 ,彭博文 ,彭 斌 ,冯 雪 ,朱双益 ,熊 玮 ,胡 溪 ,孙小慧(1. 武汉市中医医院肾病科,武汉
          430014;2.武汉市中医医院骨科,武汉 430014)
          中图分类号  R965      文献标志码  A      文章编号  1001-0408(2026)02-0174-06
          DOI  10.6039/j.issn.1001-0408.2026.02.07
          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(Collagen Ⅲ)、α-平滑肌肌动蛋白(α-SMA)、转化生长因子β1 (TGF-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Collagen Ⅲ、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。
          关键词  益肾排毒方;慢性肾衰竭;肾纤维化;ROS/TXNIP/NLRP3通路

          Effects of Yishen paidu formula on renal fibrosis in rats with chronic renal failure by regulating the ROS/
          TXNIP/NLRP3 pathway
          FENG Li ,PENG Bowen ,PENG Bin ,FENG Xue ,ZHU Shuangyi ,XIONG Wei ,HU Xi ,SUN Xiaohui
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         (1.  Dept.  of  Nephrology, Wuhan  Hospital  of Traditional  Chinese  Medicine, Wuhan  430014,  China;2.  Dept.  of
          Orthopedics, Wuhan Hospital of Traditional Chinese Medicine, Wuhan 430014, China)
          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,
              Δ 基金项目 武汉市知识创新专项(No.2023020201020556);武汉
                                                              ROS,  MDA,  TNF- α,  IL-6  and  IL-1β,  and  the  protein
          市中医药科研项目(No.WZ22Q51)
                                                              expressions  of  Collagen  Ⅲ ,  α -SMA,  TGF- β1,  TXNIP  and
             *第一作者 主治医师,硕士。研究方向:中医肾脏病学。E-mail:
          w8jefw@163.com                                      NLRP3  were  significantly  decreased,  while  SOD  levels  were


          · 174 ·    China Pharmacy  2026 Vol. 37  No. 2                               中国药房  2026年第37卷第2期
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