Related Experiment Video
Updated: May 12, 2026

A Novel In Vitro Wound Healing Assay to Evaluate Cell Migration
Published on: March 17, 2018
Effect of Sceptridium ternatum extract (STE) on radiation-induced pulmonary fibrosis by inhibiting cell adhesion
Yiwen Zhang1, Yujia Liu2, Xiaoxia Li2
1Clinical Pharmacy Center, Department of Pharmacy, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China; Zhejiang Provincial Clinical Research Center for Malignant Tumor, Hangzhou, 310014, China; Zhejiang Key Laboratory of Precision Medicine Research on Head & Neck Cancer, Hangzhou, 310014, China.
Ethnopharmacological Relevance:
Traditional Chinese medicine Botrychium ternatum (Thunb.) Sw, also known as Sceptridium ternatum (STE) has the efficacy of relieving cough and asthma, resolving phlegm, and clearing heat and toxicity. However, the effects and mechanisms of STE on RIPF have not been reported.
Aim Of The Study:
Radiation-induced pulmonary fibrosis (RIPF) leads to decreased survival and severely affects the quality of life of patients by irreversible destruction of lung tissue, and deterioration of lung function. In RIPF, excessive accumulation of extracellular matrix (ECM) destroys normal lung physiology.
Materials And Methods:
We established IR-induced RIPF model in rats, MRI showed the area of pulmonary fibrosis; we used HE staining and Masson staining to measure the damaged structure of alveoli.
Results:
MRI showed STE significantly reduced the area of pulmonary fibrosis; HE staining and Masson staining also showed STE could improve the damaged structure of alveoli and reduce collagen and matrix deposition, significantly inhibiting RIPF; STE down-regulated the expression of α-SMA and suppress EMT. Cell Adhesion Factor CEACAM1 were significantly upregulated after IR induction and STE significantly reversed it, siRNA-CEACAM1 significantly inhibited EMT. STE and its component phlorizin inhibited IR-induced EMT through regulating EGFR/p38-MAPK/NF-κB/CEACAM1 signaling pathway.
Conclusion:
Our study confirmed the significant therapeutic effect of STE on RIPF through in vivo and vitro experiments, and revealed that STE may exert anti-RIPF effect through regulating EGFR/p38-MAPK/NF-κB/CEACAM1 signaling pathway.
More Related Videos
08:32Analysis of Cancer Cell Invasion and Anti-metastatic Drug Screening Using Hydrogel Micro-chamber Array HMCA-based Plates
Published on: October 25, 2018
10:26Assessment of Mitochondrial Health in Cancer-Associated Fibroblasts Isolated from 3D Multicellular Lung Tumor Spheroids
Published on: October 21, 2022