Mechanism of biochanin A alleviating PM 2.5 -induced oxidative damage based on an XRCC1 knockout BEAS-2B cell model.
Yue YuAng LiShihao LiBowen ZhengJuan MaYazhou LiuXiaohong KouZhaohui XuePublished in: Food & function (2022)
PM 2.5 induces oxidative/antioxidant system imbalance and excessive release of reactive oxygen species (ROS) and produces toxic effects and irreversible damage to the genetic material including chromosomes and DNA. Biochanin A (BCA), an isoflavone with strong antioxidant activity, effectively intervenes against PM 2.5 -induced oxidative damage. The X-ray repair cross-complementary protein 1 (XRCC1)/BER pathway involves DNA damage repair caused by oxidative stress. This paper aims to explore the mechanism of BCA alleviating oxidative DNA damage caused by PM 2.5 by establishing the in vitro cell model based on CRISPR/Cas9 technology and combining it with mechanism pathway research. The results showed that PM 2.5 exposure inhibited the expression of BER and NER pathway proteins and induced the overexpression of ERCC1. BCA showed an effective intervention in the toxicity of PM 2.5 in normal cells, rather than XRCC1 knock-out cells. This laid a foundation for further exploring the key role of XRCC1 in PM 2.5 -caused oxidative damage and the BER/DNA damage repair pathway.
Keyphrases
- dna damage
- oxidative stress
- dna repair
- particulate matter
- diabetic rats
- air pollution
- induced apoptosis
- polycyclic aromatic hydrocarbons
- heavy metals
- crispr cas
- water soluble
- reactive oxygen species
- high glucose
- randomized controlled trial
- ischemia reperfusion injury
- poor prognosis
- genome wide
- magnetic resonance
- single cell
- drug induced
- genome editing
- gene expression
- endoplasmic reticulum stress
- high resolution
- bone marrow
- risk assessment
- endothelial cells
- physical activity
- cell therapy
- transcription factor
- copy number
- heat shock
- mesenchymal stem cells
- weight gain
- circulating tumor cells