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首页|期刊导航|中国药房|肾福康胶囊通过STAT3/YAP通路调控细胞串扰改善肾间质纤维化的机制

肾福康胶囊通过STAT3/YAP通路调控细胞串扰改善肾间质纤维化的机制

杜炜 杨玉芳 廖燕红 邹小琴 梁志伟 冯祥乾 钟小斌

中国药房2026,Vol.37Issue(12):1547-1552,6.
中国药房2026,Vol.37Issue(12):1547-1552,6.DOI:10.6039/j.issn.1001-0408.2026.12.05

肾福康胶囊通过STAT3/YAP通路调控细胞串扰改善肾间质纤维化的机制

Mechanism of Shenfukang capsule in ameliorating renal interstitial fibrosis by regulating cellular crosstalk via the STAT3/YAP pathway

杜炜 1杨玉芳 2廖燕红 1邹小琴 3梁志伟 1冯祥乾 1钟小斌4

作者信息

  • 1. 广西医科大学药学院,南宁 530021
  • 2. 广西医科大学第一附属医院药学部,南宁 530021
  • 3. 广西医科大学第一附属医院科研部,南宁 530021
  • 4. 广西医科大学药学院,南宁 530021||广西医科大学附属肿瘤医院临床药学部,南宁 530012
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摘要

Abstract

OBJECTIVE To investigate the mechanism by which Shenfukang capsule(SFK)ameliorates renal interstitial fibrosis(RIF)by regulating macrophage-fibroblast crosstalk via the signal transducer and activator of transcription 3(STAT3)/Yes-associated protein(YAP)pathway.METHODS RAW264.7 macrophages were induced to polarize with transforming growth factor-β1(TGF-β1).Subsequently,a non-contact co-culture system of macrophages with renal fibroblasts NRK-49F,as well as a non-contact co-culture system of macrophages with YAP-knockdown renal fibroblasts,were established.Cells were treated with low,medium,and high concentrations(4,8,16 μg/mL)of SFK,as well as a STAT3 inhibitor(STAT3-I,1.64 μg/mL)and losartan potassium tablets(positive control,0.28 μg/mL),for 48 h.After intervention,the protein and mRNA expression levels of CD86,CD163,and STAT3 in macrophages,as well as CD86,F4/80,and STAT3 mRNA,were detected.In co-cultured renal fibroblasts,the protein and mRNA expression levels of α-smooth muscle actin(α-SMA),Vimentin,collagen type Ⅰ(Col-Ⅰ),matrix metalloproteinase-1(MMP-1),and YAP were detected.In co-cultured YAP-knockdown renal fibroblasts,the protein and mRNA expression levels of α-SMA,Vimentin,and MMP-1 were also detected.RESULTS Following TGF-β1 induction,the protein expression levels of CD86,CD163,and STAT3,as well as the mRNA expression levels of CD86,F4/80,and STAT3 in macrophages were significantly increased(P<0.05).The conditioned medium from polarized macrophages activated renal fibroblasts,as evidenced by significantly increased protein and mRNA expression levels of α-SMA,Vimentin,Col-Ⅰ,and YAP,and significantly decreased protein and mRNA expression levels of MMP-1 in renal fibroblasts(P<0.05).Treatment with SFK and STAT3-I reversed the changes in the above indicators,with the medium concentration SFK group showing stronger effects on some indicators than the low and high concentration groups.In the non-contact co-culture experiment of macrophages and YAP-knockdown renal fibroblasts,there were no statistically significant differences in the protein and mRNA expression of α-SMA,Vimentin,and MMP-1 among the groups.CONCLUSIONS SFK can inhibit macrophage-renal fibroblast crosstalk by blocking the STAT3/YAP pathway,thereby delaying the progression of RIF.

关键词

肾福康胶囊/肾间质纤维化/巨噬细胞/成纤维细胞/细胞串扰/STAT3/YAP通路

Key words

Shenfukang capsule/renal interstitial fibrosis/macrophage/fibroblast/cellular crosstalk/STAT3/YAP pathway

分类

医药卫生

引用本文复制引用

杜炜,杨玉芳,廖燕红,邹小琴,梁志伟,冯祥乾,钟小斌..肾福康胶囊通过STAT3/YAP通路调控细胞串扰改善肾间质纤维化的机制[J].中国药房,2026,37(12):1547-1552,6.

基金项目

国家自然科学基金项目(No.82360811) (No.82360811)

广西自然科学基金区域高发疾病研究联合专项资助(No.2023GXNSFAA026233) (No.2023GXNSFAA026233)

中国药房

1001-0408

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