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<p>Pulmonary fibrosis (PF) remains a devastating condition with no fully satisfactory treatment. Bu-Fei-Kang-Xian Decoction (BFKXD), a traditional Chinese medicine decoction,, has shown promise in improving symptoms in patients with PF; however, its underlying molecular mechanism remains elusive. Cell model was constructed using transforming growth factor-β1 (TGFβ1), and the mouse model was established by bleomycin. CCK-8 was used to assay cell viability, and AGE/sRAGE levels were measured by ELISA. Cellular senescence were expressed using γ-H2AX, SA-β-Gal, SASP and senescence-associated protein. The extent of PF lesions in mice was visualized by H&amp;E and Masson staining. The expression levels of SASP and senescence-associated proteins were used as indicators of cellular senescence in mouse models. In addition, WB was used to detect changes in JAK2/STAT3 expression. Our results demonstrated that TGFβ1 inhibited cell viability, elevated AGEs/sRAGE levels, and promoted γ-H2AX expression in MRC-5 cells. TGFβ1 facilitated the elevation of SASP, induced an elevated rate of SA-β-Gal deposition, and promoted the increased abundance of senescence-associated protein expression in cells. And TGFβ1 promoted elevated activation of JAK2/STAT3. BFKXD reversed the aforementioned results. Moreover, BFKXD alleviated bleomycin-induced lung tissue fibrosis and inhibited lung tissue cellular senescence. In conclusion, our results found BFKXD was able to alleviate PF by reducing cellular senescence through inhibition of JAK2/STAT3, providing theoretical support for the clinical application of BFKXD.</p> Graphical abstract <p></p>

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Bu-Fei-Kang-Xian decoction regulates JAK2/STAT3 pathway to inhibit cellular senescence ameliorating pulmonary fibrosis

  • 期刊论文

  • 发表日期：

    2026年1月7日

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  • Yinzhe Gui,
  • Wanchun Zheng,
  • Xiaojing Niu,
  • Weike Li,
  • Ruiyi Chen,
  • Zhiwan Wang

摘要

Pulmonary fibrosis (PF) remains a devastating condition with no fully satisfactory treatment. Bu-Fei-Kang-Xian Decoction (BFKXD), a traditional Chinese medicine decoction,, has shown promise in improving symptoms in patients with PF; however, its underlying molecular mechanism remains elusive. Cell model was constructed using transforming growth factor-β1 (TGFβ1), and the mouse model was established by bleomycin. CCK-8 was used to assay cell viability, and AGE/sRAGE levels were measured by ELISA. Cellular senescence were expressed using γ-H2AX, SA-β-Gal, SASP and senescence-associated protein. The extent of PF lesions in mice was visualized by H&E and Masson staining. The expression levels of SASP and senescence-associated proteins were used as indicators of cellular senescence in mouse models. In addition, WB was used to detect changes in JAK2/STAT3 expression. Our results demonstrated that TGFβ1 inhibited cell viability, elevated AGEs/sRAGE levels, and promoted γ-H2AX expression in MRC-5 cells. TGFβ1 facilitated the elevation of SASP, induced an elevated rate of SA-β-Gal deposition, and promoted the increased abundance of senescence-associated protein expression in cells. And TGFβ1 promoted elevated activation of JAK2/STAT3. BFKXD reversed the aforementioned results. Moreover, BFKXD alleviated bleomycin-induced lung tissue fibrosis and inhibited lung tissue cellular senescence. In conclusion, our results found BFKXD was able to alleviate PF by reducing cellular senescence through inhibition of JAK2/STAT3, providing theoretical support for the clinical application of BFKXD.

Graphical abstract