ArticleFrontiers in pharmacology2020
Jianpiyifei II Granules Suppress Apoptosis of Bronchial Epithelial Cells in Chronic Obstructive Pulmonary Disease
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Total Astragalus Saponins Modulate Ferroptosis Pathways in Cigarette Smoke and LPS-Induced Models of COPD: An in vitro and in vivo Investigation.Journal of inflammation research · 2026Article
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- Endoplasmic reticulum stress: a vital process and potential therapeutic target in chronic obstructive pulmonary disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Classical monocyte-derived macrophages as therapeutic targets of umbilical cord mesenchymal stem cells: comparison of intratracheal and intravenous administration in a mouse model of pulmonary fibrosis.Respiratory research · 2023Article
- Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives.Biomolecules · 2022Review
- Liriopesides B induces apoptosis and cell cycle arrest in human non‑small cell lung cancer cells.International journal of molecular medicine · 2020Article
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Authors and funding
10 authors at 1 institution in 1 country.
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Abstract
Jianpiyifei II granules (JPYF II), a herbal formula, are used for the treatment of chronic obstructive pulmonary disease (COPD) in Guangdong Provincial Hospital of Chinese Medicine. The protective effects of JPYF II against bronchial epithelial cell apoptosis in mice exposed to cigarette smoke (CS) and apoptosis of human bronchial epithelial cell lines (BEAS-2B and 16-HBE) stimulated with cigarette smoke extract (CSE) were investigated. Mice were exposed to CS generated from four cigarettes/day for 30 days and administered a dose of JPYF II (0.75, 1.5, and 3 g/kg/d) from the 3rd week of CS exposure. In mice exposed to CS, JPYF II significantly inhibited CS-induced apoptosis and overexpression of endoplasmic reticulum (ER) stress-related markers in bronchial epithelial cells of the lung tissues. In CSE-stimulated BEAS-2B and 16-HBE cells, JPYF II attenuated apoptosis and cell cycle arrest in the G
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