Mogroside-rich extract from Siraitia grosvenorii fruits protects against heat stress-induced intestinal damage by ameliorating oxidative stress and inflammation in mice

氧化应激 超氧化物歧化酶 SOD2 肿瘤坏死因子α 炎症 谷胱甘肽过氧化物酶 过氧化氢酶 化学 封堵器 谷胱甘肽 下调和上调 生物 免疫学 内分泌学 药理学 生物化学 紧密连接 基因
作者
Renhong Lu,Jiahao Hu,Xinxin Liu,Lijiang Yu,Junjie Hu,Huimin Jiang,Shaoyuan Liu,Mengqi Li,Jiakang He,Xiaogan Yang,Xingwei Liang
出处
期刊:Food & Function [Royal Society of Chemistry]
卷期号:14 (2): 1238-1247 被引量:13
标识
DOI:10.1039/d2fo02179j
摘要

Global warming makes humans and animals more vulnerable to heat stress. Heat stress can cause multiorgan dysfunction, especially in the intestine, primarily via oxidative stress and inflammation. Mogroside-rich extract (MGE) is the active ingredient of Siraitia grosvenorii and has significant antioxidant and anti-inflammatory activity. However, whether MGE can alleviate the intestinal damage caused by heat stress has not been explored. In this study, mice were given 600 mg kg-1 MGE followed by exposure to high temperature (40 °C for 2 h per day), and the structures and molecular changes in the ileum were examined. Our findings showed that body weight was decreased by heat stress, while the activity of serum superoxide dismutase (SOD) was increased. We further found that heat stress impaired the intestinal barrier by reducing the number of goblet cells and mRNA levels of the tight junction proteins zona occludens protein 1 (ZO-1), Occludin (OCLD) and recombinant mucin 2 (MUC2 mucin), but it increased the mRNA level of trefoil factor 3 (TFF3). Interestingly, MGE treatment reversed these changes. Furthermore, heat stress increased the activity of SOD in the intestine, downregulated the expression of the oxidative stress-related genes glutathione peroxidase 1 (GPX1), SOD2 and nuclear factor erythroid 2-related factor 2 (NRF2), and upregulated the expression of catalase (CAT). Moreover, heat stress increased tumor necrosis factor-α (TNF-α) levels in the intestine and upregulated the expression of the inflammation-related genes interleukin 10 (IL-10), TNF-α, Interferon-γ (IFN-γ), toll like receptor 4 (TLR4) and nuclear factor-kappa B (NF-kB). However, MGE treatment effectively reduced TNF-α levels and restored the normal activity of SOD and normal mRNA levels for both oxidative stress-related and inflammation-related genes. In summary, our results showed that MGE can protect against heat stress-induced intestinal damage by ameliorating inflammation and oxidative stress.
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