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GL001 通过调节肠道微生物群落组成和肠道组织代谢来减轻大鼠肠缺血再灌注损伤。

GL001 alleviates rat intestinal ischemia-reperfusion injury by modulating gut microbiota composition and intestinal tissue metabolism.

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin, Heilongjiang 150030, China.

Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, China.

出版信息

Food Funct. 2024 Apr 2;15(7):3653-3668. doi: 10.1039/d3fo03669c.

Abstract

Intestinal ischemia-reperfusion (IIR) injury leads to inflammation and oxidative stress, resulting in intestinal barrier damage. Probiotics, due to their anti-inflammatory and antioxidant properties, are considered for potential intervention to protect the intestinal barrier during IIR injury. , a recognized probiotic, has targeted effects on IIR injury, but its mechanisms of action are not yet understood. To investigate the mechanism of intervention in IIR injury, we conducted a study using a rat IIR injury model. The results showed that could alleviate inflammation and oxidative stress induced by IIR injury by suppressing the NF-κB inflammatory pathway and activating the Keap1/Nrf2 signaling pathway. GL001 also increased the abundance of the gut microbiota such as , , , , and , while decreasing the abundance of , [], , , , and . In addition, GL001 reversed the changes in amino acids and bile acids induced by IIR injury and reduced the levels of DL-cysteine, an oxidative stress marker, in intestinal tissue. Spearman correlation analysis showed that L-cystine was positively correlated with and negatively correlated with , while DL-proline was positively correlated with . Moreover, bile acids, cholic acid and lithocholic acid, were negatively correlated with and positively correlated with . Therefore, GL001 may alleviate IIR injury by regulating the gut microbiota to modulate intestinal lipid peroxidation and bile acid metabolism.

摘要

肠道缺血再灌注 (IIR) 损伤会导致炎症和氧化应激,从而损害肠道屏障。由于益生菌具有抗炎和抗氧化特性,因此被认为是潜在的干预措施,可以在 IIR 损伤期间保护肠道屏障。 是一种公认的益生菌,对 IIR 损伤具有靶向作用,但作用机制尚不清楚。为了研究 干预 IIR 损伤的机制,我们使用大鼠 IIR 损伤模型进行了一项研究。结果表明, 可以通过抑制 NF-κB 炎症途径和激活 Keap1/Nrf2 信号通路来减轻 IIR 损伤引起的炎症和氧化应激。 GL001 还增加了肠道微生物群的丰度,如 、 、 、 、 ,同时降低了 、 []、 、 、 和 的丰度。此外, GL001 逆转了 IIR 损伤引起的氨基酸和胆汁酸的变化,并降低了肠道组织中氧化应激标志物 DL-半胱氨酸的水平。Spearman 相关性分析表明,L-胱氨酸与 呈正相关,与 呈负相关,而 DL-脯氨酸与 呈正相关。此外,胆汁酸、胆酸和石胆酸与 呈负相关,与 呈正相关。因此, GL001 可能通过调节肠道微生物群来调节肠道脂质过氧化和胆汁酸代谢来缓解 IIR 损伤。

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