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
Received:26 September 2025,
Revised:2025-12-30,
Accepted:31 December 2025,
Published:30 January 2026
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冯立,彭博文,彭斌,等.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[J].中国药房,2026,37(02):174-179.
FENG Li,PENG Bowen,PENG Bin,et al.Effects of Yishen paidu formula on renal fibrosis in rats with chronic renal failure by regulating the ROS/TXNIP/NLRP3 pathway[J].ZHONGGUO YAOFANG,2026,37(02):174-179.
冯立,彭博文,彭斌,等.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[J].中国药房,2026,37(02):174-179. DOI: 10.6039/j.issn.1001-0408.2026.02.07.
FENG Li,PENG Bowen,PENG Bin,et al.Effects of Yishen paidu formula on renal fibrosis in rats with chronic renal failure by regulating the ROS/TXNIP/NLRP3 pathway[J].ZHONGGUO YAOFANG,2026,37(02):174-179. DOI: 10.6039/j.issn.1001-0408.2026.02.07.
目的
2
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
2
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β
1
(TGF-β
1
)、TXNIP、NLRP3蛋白表达情况。
结果
2
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-β
1
、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
2
益肾排毒方可通过抑制ROS/TXNIP/NLRP3通路延缓CRF大鼠肾纤维化。
OBJECTIVE
2
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
2
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-β
1
(TGF-β
1
), TXNIP and NLRP3 in renal tissue were detected.
RESULTS
2
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-β
1
, 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
2
Yishen paidu formula can inhibit renal fibrosis in CRF rats by suppressing the ROS/TXNIP/NLRP3 pathway.
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