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. Bifidobacterium longum, a recognized probiotic, has targeted effects on IIR injury, but its mechanisms of action are not yet understood. To investigate the mechanism of Bifidobacterium longum intervention in IIR injury, we conducted a study using a rat IIR injury model. The results showed that Bifidobacterium longum could alleviate inflammation and oxidative stress induced by IIR injury by suppressing the NF-κB inflammatory pathway and activating the Keap1/Nrf2 signaling pathway. Bifidobacterium longum GL001 also increased the abundance of the gut microbiota such as Oscillospira, Ouminococcus, Corynebacterium, Lactobacillus, and Akkermansia, while decreasing the abundance of Allobaculum, [Prevotella], Bacteroidaceae, Bacteroides, Shigella, and Helicobacter. In addition, Bifidobacterium longum 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 Lactobacillus and negatively correlated with Shigella, while DL-proline was positively correlated with Akkermansia. Moreover, bile acids, cholic acid and lithocholic acid, were negatively correlated with Lactobacillus and positively correlated with Shigella. Therefore, Bifidobacterium longum GL001 may alleviate IIR injury by regulating the gut microbiota to modulate intestinal lipid peroxidation and bile acid metabolism.

中文翻译：

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长双歧杆菌GL001通过调节肠道菌群组成和肠道组织代谢减轻大鼠肠道缺血再灌注损伤

肠道缺血再灌注（IIR）损伤会导致炎症和氧化应激，从而导致肠道屏障损伤。益生菌由于其抗炎和抗氧化特性，被认为是 IIR 损伤期间保护肠道屏障的潜在干预措施。长双歧杆菌是一种公认​​的益生菌，对 IIR 损伤具有靶向作用，但其作用机制尚不清楚。为了探讨长双歧杆菌干预 IIR 损伤的机制，我们使用大鼠 IIR 损伤模型进行了研究。结果表明，长双歧杆菌可以通过抑制NF-κB炎症通路、激活Keap1/Nrf2信号通路来减轻IIR损伤引起的炎症和氧化应激。长双歧杆菌GL001 还增加了肠道微生物群的丰度，如颤旋菌属、奇异球菌属、棒状杆菌属、乳杆菌属和阿克曼氏菌属，同时降低了异杆菌属、普氏菌属、拟杆菌科、拟杆菌属、志贺氏菌属和螺杆菌属的丰度。此外，长双歧杆菌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记物DL-半胱氨酸的水平。Spearman相关分析显示，L-胱氨酸与乳酸菌呈正相关，与志贺氏菌呈负相关，DL-脯氨酸与阿克曼氏菌呈正相关。此外，胆汁酸、胆酸和石胆酸与乳酸菌呈负相关，与志贺氏菌呈正相关。因此，长双歧杆菌GL001可能通过调节肠道微生物群调节肠道脂质过氧化和胆汁酸代谢来减轻IIR损伤。