State Key Laboratory of Animal Nutrition, China Agricultural University, Beijing 100193, China.
J Agric Food Chem. 2023 Apr 12;71(14):5438-5449. doi: 10.1021/acs.jafc.3c00798. Epub 2023 Apr 3.
Heat stress (HS) occurs when the sensible temperature of animals exceeds their thermoregulatory capacity, a condition that exerts a detrimental impact on health and growth. The intestinal tract, as a highly sensitive organ, has been shown to respond to HS by exhibiting mucosal injury, intestinal leakage, and disturbances in the gut microbiota. Oxidative stress and endoplasmic reticulum stress (ERS) are both potential outcomes of long-term exposure to high temperatures and have been linked to apoptosis, autophagy, and ferroptosis. In addition, HS alters the composition of the gut microbiota accompanied by changed levels of bacterial components and metabolites, rendering the gut more vulnerable to stress-related injury. In this review, we present recent advances in mechanisms of oxidative stress-associated ERS in response to HS, which is destructive to intestinal barrier integrity. The involvement of autophagy and ferroptosis in ERS was highlighted. Further, we summarize the relevant findings regarding the engagement of gut microbiota-derived components and metabolites in modulation of intestinal mucosal injury induced by HS.
热应激（HS）是指动物的体感温度超过其体温调节能力时发生的情况，这种情况对健康和生长有不利影响。肠道作为一个高度敏感的器官，已经被证明会对 HS 做出反应，表现为黏膜损伤、肠道渗漏和肠道微生物群紊乱。氧化应激和内质网应激（ERS）都是长期暴露于高温下的潜在结果，与细胞凋亡、自噬和铁死亡有关。此外，HS 改变了肠道微生物群的组成，同时改变了细菌成分和代谢物的水平，使肠道更容易受到与应激相关的损伤。在这篇综述中，我们介绍了氧化应激相关 ERS 机制的最新进展，这些机制对肠道屏障完整性具有破坏性。强调了自噬和铁死亡在 ERS 中的参与。此外，我们总结了关于肠道微生物群衍生成分和代谢物在调节 HS 诱导的肠道黏膜损伤中的相关发现。
