ArticleInternational journal of molecular epidemiology and genetics2020
Chrysophanol protects human bronchial epithelial cells from cigarette smoke extract (CSE)-induced apoptosis.
Article in International journal of molecular epidemiology and genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- The Bufei Nashen Pill Alleviates COPD by Targeting Endoplasmic Reticulum Stress Through the PERK/eIF2α Signaling Pathway.Immunity, inflammation and disease · 2026Article
- USP8 inhibits cigarette smoke extract combined with LPS-induced inflammatory response and ER stress by regulating the ABCB1-mediated MAPK signaling pathway in human bronchial epithelial cells.Journal of inflammation (London, England) · 2025Article
- Identification of Genes Related to Endoplasmic Reticulum Stress (ERS) in Chronic Obstructive Pulmonary Disease (COPD) and Clinical Validation.International journal of chronic obstructive pulmonary disease · 2023Article
- Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives.Biomolecules · 2022Review
- Cellular and Molecular Signatures of Oxidative Stress in Bronchial Epithelial Cell Models Injured by Cigarette Smoke Extract.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveChronic obstructive pulmonary disease (COPD) is a common respiratory disease characterized by the persistent airflow obstruction. Chrysophanol, an anthraquinone derivative isolated from the rhizomes of
methodsCCK8 cell viability assay was conducted to evaluate the protective effect of chrysophanol on 16HBECs after CSE induction. Western blot analysis, Annexin V/PI staining and TUNEL assay were conducted to test the effect of chrysophanol on 16HBECs apoptosis induced by CSE. Then the western blot assay measured associated molecular pathways to dissect the mechanisms underlying protective effect of chrysophanol on 16HBECs.
resultsChrysophanol protects 16HBECs against CSE-induced apoptosis in a dose dependent manner. Specifically, pre-treatment of 16HBECs with 20 mmol/l of chrysophanol, reduced CSE-induced apoptosis by almost 10%. Mechanistically, chrysophanol manifested high potency to attenuate CSE-induced expression of apoptotic markers, Bax and cleaved caspase 3. In particular, chrysophanol not only represses CSE-induced oxidative stress by inhibiting CYP1A1 expression, but also suppresses CSE-induced ER stress by inhibiting pPERK, ATF4 and ATF6 expression.
conclusionChrysophanol showed protective effect on CSE-induced epithelial injuries in cell line 16HBECs. And our data support that chrysophanol could be employed to reduce the toxicity of cigarette smoke in bronchial epithelial cells, which may have the potential to decrease the risk for developing COPD in smoking subjects.
Indexed as
Identifiers
33488953PMC7811954W3122069372What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.