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Background <p>Interstitial lung disease (ILD) is the leading cause of death in systemic sclerosis (SSc), and current treatments present low efficacy or high toxicity. Therefore, it is clinically important to search for drugs with obvious efficacy and low side effects for SSc-ILD.</p> Objective <p>The aim of this study was to investigate the effects and mechanisms of <i>Capparis</i> <i>spinosa</i> (<i>C</i>. <i>spinosa</i>) on SSc-ILD.</p> Methods <p>Mice were injected with bleomycin to establish the SSc-ILD model. After 28 d of modeling, HE and Masson staining were performed to observe the pathological changes of skin and lung tissues, hydroxyproline (HYP) content of skin and lung tissues were measured, immunohistochemistry was performed to detect the expression of TGF-β1 and α-SMA in lung tissues, and ELISA was performed to detect TNF-α, IL-6, and IL-1β content in mouse serum and bronchoalveolar lavage fluid. Transforming growth factor β1 (TGF-β1)-induced mouse fibroblast cell line NIH3T3 to establish a cell model. Cell proliferation was detected by MTT and colony formation assay, cell migration was detected by scratch assay, and α-SMA, Collagen I, fibronectin, and proteins related to MAPK pathway were detected by Western blot.</p> Results <p><i>C</i>. <i>spinosa</i> showed significant dose-dependent amelioration of systemic inflammatory response, skin tissue fibrosis, and lung tissue inflammation and fibrosis in SSc-ILD mice model. In TGF-β1-induced NIH3T3 cells, <i>C</i>. <i>spinosa</i> intervened to effectively inhibit cell hyperproliferation, migration, and fibrosis in a concentration-dependent manner. <i>C</i>. <i>spinosa</i> inhibited the phosphorylation of MAPKs in vivo and in vitro. MAPK pathway inhibitor (SP600125) mimicked while MAPK pathway agonist (Anisomycin) blocked the inhibitory effects of <i>C</i>. <i>spinosa</i> on TGF-β1-induced myofibroblast hyperproliferation, migration, and fibrosis.</p> Conclusion <p><i>C</i>. <i>spinosa</i> inhibits the proliferation and fibrosis of myofibroblasts in SSc-ILD by regulating the MAPK pathway.</p>

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Capparis spinosa inhibits proliferation and fibrosis of myofibroblasts in systemic sclerosis through modulation of MAPK signaling

  • 期刊论文

  • 发表日期：

    2025年4月3日

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  • Xin Xin Qi,
  • Fei Fei Lou,
  • Feng Yan Sun,
  • Ning Zhao,
  • Jia Sun,
  • Ai Juan Shen,
  • Chun Long Liu

摘要

Background

Interstitial lung disease (ILD) is the leading cause of death in systemic sclerosis (SSc), and current treatments present low efficacy or high toxicity. Therefore, it is clinically important to search for drugs with obvious efficacy and low side effects for SSc-ILD.

Objective

The aim of this study was to investigate the effects and mechanisms of Capparis spinosa (C. spinosa) on SSc-ILD.

Methods

Mice were injected with bleomycin to establish the SSc-ILD model. After 28 d of modeling, HE and Masson staining were performed to observe the pathological changes of skin and lung tissues, hydroxyproline (HYP) content of skin and lung tissues were measured, immunohistochemistry was performed to detect the expression of TGF-β1 and α-SMA in lung tissues, and ELISA was performed to detect TNF-α, IL-6, and IL-1β content in mouse serum and bronchoalveolar lavage fluid. Transforming growth factor β1 (TGF-β1)-induced mouse fibroblast cell line NIH3T3 to establish a cell model. Cell proliferation was detected by MTT and colony formation assay, cell migration was detected by scratch assay, and α-SMA, Collagen I, fibronectin, and proteins related to MAPK pathway were detected by Western blot.

Results

C. spinosa showed significant dose-dependent amelioration of systemic inflammatory response, skin tissue fibrosis, and lung tissue inflammation and fibrosis in SSc-ILD mice model. In TGF-β1-induced NIH3T3 cells, C. spinosa intervened to effectively inhibit cell hyperproliferation, migration, and fibrosis in a concentration-dependent manner. C. spinosa inhibited the phosphorylation of MAPKs in vivo and in vitro. MAPK pathway inhibitor (SP600125) mimicked while MAPK pathway agonist (Anisomycin) blocked the inhibitory effects of C. spinosa on TGF-β1-induced myofibroblast hyperproliferation, migration, and fibrosis.

Conclusion

C. spinosa inhibits the proliferation and fibrosis of myofibroblasts in SSc-ILD by regulating the MAPK pathway.