ArticleApplied biochemistry and biotechnology2024
Baicalin Relieves Airway Inflammation in COPD by Inhibiting miR-125a.
Article in Applied biochemistry and biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Multi-target Therapeutic Potential of Baicalin in Respiratory Diseases: Mechanisms and Clinical Prospects.Chinese journal of integrative medicine · 2026Review
- Research on the Mechanism of Natural Products Acting on Chronic Obstructive Pulmonary Disease.Food science & nutrition · 2026Review
- Baicalin: bridging traditional medicine and modern science in food and functional applications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Research advances in polyphenols from Chinese herbal medicine for the prevention and treatment of chronic obstructive pulmonary disease: a review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Identification and Experimental Validation of Biomarkers Related to MiR-125a-5p in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2025Article
- NLBK alleviates airway remodeling in COPD by inhibiting RXRA-mediated transcription of PLA2G2A.American journal of translational research · 2025Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
To investigate the effects of Baicalin on the apoptosis of human bronchial epithelial cells (16HBE) induced by cigarette smoke extract (CSE) and the release of inflammatory factors, and to clarify its possible mechanism. CSE was used to treat 16HBE cells and construct COPD cell model. The activity of 16HBE cells was detected by CCK-8 and BrdU. Real-time fluorescence quantitative PCR (RT-QPCR) was used to detect the expression level of miR-125a in each group of 16HBE cells. At the same time, the levels of 16HBE inflammatory cytokines IL-1β, IL-8, IL-6, and TNF-α were detected. The apoptosis rate of 16HBE cells in each group was detected by TUNEL. Compared with the control group, the proliferation of 16HBE cells in CSE group was decreased. Baicalin reversed the effect of 2% CSE on the proliferation of 16HBE cells. Baicalin also reversed the effect of 2% CSE on apoptosis and inflammatory factors in 16HBE cells. miR-125a is highly expressed in COPD, and Baicalin can inhibit the expression of miR-125a. Silencing miR-125a reduces apoptosis and inflammatory response of 16HBE cells in COPD. miR-125a reversed the effects of Baicalin on apoptosis and inflammation of 16HBE cells. Baicalin can reduce CSE-induced apoptosis of human bronchial epithelial cells and release of inflammatory factors, and its mechanism may be related to the inhibition of miR-125a.
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Registered trials
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