Green tea polyphenols alleviate TBBPA-induced gastric inflammation and apoptosis by modulating the ROS-PERK/IRE-1/ATF6 pathway in mouse models.
Jie YangYuan GengBing ZhaoTianjing LiuJi-Long LuoXue-Jiao GaoPublished in: Food & function (2024)
Green tea polyphenols (GTP), an important phytochemical in the daily human diet, bind to various cellular receptors and exert anti-inflammatory and antioxidant benefits. The environmental contaminant tetrabromobisphenol A (TBBPA) enters the digestive system through multiple pathways, resulting in oxidative stress (OS), gastroenteritis, and mucosal injury. The aim of this study was to explore the molecular mechanisms of TBBPA-induced gastritis in mice treated with GTP in vivo and in an in vitro model. The results showed that exposure to TBBPA increased reactive oxygen species (ROS) levels, activated oxidative stress (OS) induced endoplasmic reticulum stress (ERS), and the expression of endoplasmic reticulum stress-related factors ( e.g. , GRP78, PERK, IRE-1, ATF-6, etc .) increased. The inflammatory pathway NF-κB was activated, and the pro-inflammatory factors TNF-α, IL-1β, and IL-6 increased, while triggering a cascade reaction mediated by caspase-3. However, the addition of GTP could inhibit OS, restore the balance of endoplasmic reticulum homeostasis, and improve the inflammatory infiltration and apoptosis of gastric mucosal epithelial cells. Therefore, GTP alleviated ERS, reduced inflammation and apoptosis, and restored the gastric mucosal barrier by alleviating TBBPA-induced OS in mouse gastric tissues and GES-1 cells. This provides basic information for exploring the antioxidant mechanism of GTP and further investigating the toxic effects of TBBPA on mouse gastric mucosa.
Keyphrases
- endoplasmic reticulum stress
- induced apoptosis
- oxidative stress
- diabetic rats
- reactive oxygen species
- high glucose
- dna damage
- anti inflammatory
- ischemia reperfusion injury
- cell death
- drug induced
- endothelial cells
- signaling pathway
- physical activity
- gene expression
- poor prognosis
- immune response
- rheumatoid arthritis
- inflammatory response
- helicobacter pylori
- metabolic syndrome
- binding protein
- mouse model
- health information
- induced pluripotent stem cells
- climate change
- lps induced
- nuclear factor
- cell cycle arrest
- skeletal muscle