Mitochondrial response to inflammation is crucial in the metabolic adaptation to infection. This study aimed to explore the mitochondrial response under inflammatory and anti-inflammatory environments, with a focus on the tricarboxylic acid (TCA) cycle. Expression levels of key TCA cycle enzymes and the autophagy-related protein light chain 3b (LC3b) were determined in raw 264.7 cells treated with lipopolysaccharide (LPS) and metformin (Met). Additionally, reactive oxygen species (ROS) levels and mitochondrial membrane potential were assessed using flow cytometry. Moreover, 8-week-old C57BL/6J mice were intraperitoneally injected with LPS and Met to assess the mitochondrial response in vivo. Upon LPS stimulation, the expression of key TCA enzymes, including citrate synthase, α-ketoglutarate dehydrogenase, and isocitrate dehydrogenase 2, and the mitochondrial membrane potential decreased, whereas the levels of LC3b and ROS increased. However, treatment with Met inhibited the reduction of LPS-induced enzyme levels as well as the elevation of LC3b and ROS levels. In conclusion, the mitochondrial TCA cycle is affected by the inflammatory environment, and the LPS-induced effects can be reversed by Met treatment.

线粒体对炎症的反应在代谢适应感染中至关重要。这项研究旨在探讨在炎性和抗炎环境下的线粒体反应，重点是三羧酸（TCA）循环。测定了用脂多糖（LPS）和二甲双胍（Met）处理的原始264.7细胞中关键TCA循环酶和自噬相关蛋白轻链3b（LC3b）的表达水平。此外，使用流式细胞仪评估了活性氧（ROS）水平和线粒体膜电位。此外，向8周大的C57BL / 6J小鼠腹膜内注射LPS和Met，以评估体内的线粒体反应。LPS刺激后，关键TCA酶的表达包括柠檬酸合酶，α-酮戊二酸脱氢酶和异柠檬酸脱氢酶2，线粒体膜电位降低，而LC3b和ROS水平升高。然而，用Met处理抑制了LPS诱导的酶水平的降低以及LC3b和ROS水平的升高。总之，线粒体TCA周期受炎性环境影响，LPS诱导的作用可通过Met治疗逆转。