炎症体
上睑下垂
多不饱和脂肪酸
化学
氧化应激
丙二醛
吡喃结构域
超氧化物歧化酶
炎症
生物化学
受体
脂肪酸
药理学
内科学
生物
医学
作者
Yue-Hang Chen,Ying Jiang,Jingjing Wei,Xiaodong Li,Peihong Zhang,Ting‐Ting Lian,Ze Zhuang
标识
DOI:10.1016/j.foodres.2022.111943
摘要
Our previous study showed that n-3 PUFAs inhibited inflammation in rats with esophagitis. This study aimed to observe the protective effect of n-3 PUFAs against acid damage to esophageal epithelial cells (Het-1A cells) and to explore its mechanism. The level of malondialdehyde (MDA) was increased by acid exposure, while that of superoxide dismutase (SOD) was decreased. In groups with different ratios of n-6/n-3 PUFAs, the expression levels of nuclear factor E2 related factor 2 (Nrf2) and SOD were increased with increasing proportions of n-3 PUFAs and were highest in the 1:1 group. Compared with those in the 9:1 group, the expression of NOD like receptor pyrin domain-containing protein 3 (NLRP3) and caspase-1 and the pyroptosis rate in the 1:1 group were decreased. Intervention with an Nrf2 agonist increased the expression of Nrf2 and decreased the expression of NLRP3 and caspase-1 and the pyroptosis rate. However, inhibiting Nrf2 expression led to the opposite result. In conclusion, n-3 PUFAs protected esophageal epithelial cells from acid damage by upregulating Nrf2 expression, which disrupted oxidative stress and NLRP3 inflammasome activation and inhibited pyroptosis.
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