Redox imbalance induces oxidative damage and causes age-related pathologies. Mice lacking the antioxidant enzyme SOD1 (Sod1-/-) exhibit various aging-like phenotypes throughout the body and are used as aging model mice. Recent reports suggested that age-related changes in the intestinal environment are involved in various diseases. We investigated cecal microbiota profiles and gastrointestinal metabolites in wild-type (Sod1+/+) and Sod1-/- mice. Firmicutes and Bacteroidetes were dominant in Sod1+/+ mice, and most of the detected bacterial species belong to these two phyla. Meanwhile, the Sod1-/- mice had an altered Firmicutes and Bacteroidetes ratio compared to Sod1+/+ mice. Among the identified genera, Paraprevotella, Prevotella, Ruminococcus, and Bacteroides were significantly increased, but Lactobacillus was significantly decreased in Sod1-/- mice compared to Sod1+/+ mice. The correlation analyses between cecal microbiota and liver metabolites showed that Bacteroides and Prevotella spp. were grouped into the same cluster, and Paraprevotella and Ruminococcus spp. were also grouped as another cluster. These four genera showed a positive and a negative correlation with increased and decreased liver metabolites in Sod1-/- mice, respectively. In contrast, Lactobacillus spp. showed a negative correlation with increased liver metabolites and a positive correlation with decreased liver metabolites in Sod1-/- mice. These results suggest that the redox imbalance induced by Sod1 loss alters gastrointestinal microflora and metabolites.

中文翻译：

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SOD1缺乏症会改变小鼠的胃肠道微生物和代谢产物。

氧化还原失衡会引起氧化损伤并引起与年龄有关的病理。缺乏抗氧化酶SOD1（Sod1-/-）的小鼠在整个身体中表现出各种衰老样表型，并被用作衰老模型小鼠。最近的报告表明，肠道环境中与年龄相关的变化与多种疾病有关。我们调查了盲肠微生物群和野生型（Sod1 + / +）和Sod1-/-小鼠的胃肠道代谢产物。硬毛虫和拟杆菌属在Sod1 + / +小鼠中占主导地位，并且大多数检测到的细菌物种都属于这两个门。同时，与Sod1 + / +小鼠相比，Sod1-/-小鼠的硬毛和拟杆菌比率有所变化。在鉴定出的属中，副球菌，原球菌，鲁米诺球菌和拟杆菌属显着增加，但与Sod1 + / +小鼠相比，Sod1-/-小鼠中的乳酸杆菌明显减少。盲肠微生物群与肝脏代谢产物之间的相关性分析表明，拟杆菌属和普氏杆菌属。被分为同一群，和副球菌和Ruminococcus spp。也被分组为另一个集群。这四个属分别与Sod1-/-小鼠肝脏代谢产物的增加和减少呈正相关和负相关。相反，乳杆菌属。与Sod1-/-小鼠肝脏代谢产物增加呈负相关，与肝脏代谢产物减少呈正相关。这些结果表明，Sod1丢失引起的氧化还原失衡会改变胃肠道菌群和代谢产物。盲肠菌群与肝脏代谢产物之间的相关性分析表明，拟杆菌属和普氏杆菌属。被分为同一群，和副球菌和Ruminococcus spp。也被分组为另一个集群。这四个属分别与Sod1-/-小鼠肝脏代谢产物的增加和减少呈正相关和负相关。相反，乳杆菌属。与Sod1-/-小鼠肝脏代谢产物增加呈负相关，与肝脏代谢产物减少呈正相关。这些结果表明，Sod1丢失引起的氧化还原失衡会改变胃肠道菌群和代谢产物。盲肠微生物群与肝脏代谢产物之间的相关性分析表明，拟杆菌属和普氏杆菌属。被分为同一群，和副球菌和Ruminococcus spp。也被分组为另一个集群。这四个属分别与Sod1-/-小鼠肝脏代谢产物的增加和减少呈正相关和负相关。相反，乳杆菌属。与Sod1-/-小鼠肝脏代谢产物增加呈负相关，与肝脏代谢产物减少呈正相关。这些结果表明，Sod1丢失引起的氧化还原失衡会改变胃肠道菌群和代谢产物。这四个属分别与Sod1-/-小鼠肝脏代谢产物的增加和减少呈正相关和负相关。相反，乳杆菌属。与Sod1-/-小鼠肝脏代谢产物增加呈负相关，与肝脏代谢产物减少呈正相关。这些结果表明，Sod1丢失引起的氧化还原失衡会改变胃肠道菌群和代谢产物。这四个属分别与Sod1-/-小鼠肝脏代谢产物的增加和减少呈正相关和负相关。相反，乳杆菌属。与Sod1-/-小鼠肝脏代谢产物增加呈负相关，与肝脏代谢产物减少呈正相关。这些结果表明，Sod1丢失引起的氧化还原失衡会改变胃肠道菌群和代谢产物。