The study investigated the role of volunteer exercise and an obesogenic diet (OBD) in mice, focusing on the splenocardiac axis and inflammation-resolution signaling. Male C57BL/6J mice (2 months old) were assigned to control (CON) or OBD groups for ten months, then randomized into sedentary (Sed) or exercise (Exe) groups for two weeks. Leukocytes, heart function, structure, and spleen tissue examined for inflammation-resolution mediators and macrophage-centric gene transcripts. After two weeks of volunteer exercise, cardiac function shows limited changes, but structural changes were notable in the heart and spleen. Exercise induced cardiac nuclear hyperplasia observed in both CON and OBD groups. OBD-Sed mice showed splenic changes and increased neutrophils, whereas increased neutrophils were noted in the CON post exercise. OBD-Sed increased pro-inflammatory lipid mediators in the heart, reduced by exercise in OBD-Exe, while CON-Exe preserved resolution mediators. Chronic OBD-Sed depletes long chain fatty acids (DHA/EPA) in the heart and spleen, while exercise independently regulates lipid metabolism genes in both organs, affecting macrophage-centric lipid and lipoprotein pathways. Chronic obesity amplified cardiac inflammation, countered by exercise that lowered pro-inflammatory bioactive lipid mediators in the heart. OBD sustained inflammation in the heart and spleen, while exercise conserved resolution mediators in CON mice. In summary, these findings emphasize the interplay of diet with exercise and highlight the intricate connection of diet, exercise, inflammation-resolution signaling in splenocardiac axis and immune health.

中文翻译：

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运动可减少促炎脂质并保留调节介质，这些调节介质可校准衰老小鼠肥胖饮食后脾脏和心脏中以巨噬细胞为中心的免疫代谢

该研究调查了志愿者锻炼和致肥饮食（OBD）对小鼠的作用，重点关注脾心轴和炎症消退信号传导。雄性 C57BL/6J 小鼠（2 个月大）被分配到对照组 (CON) 或 OBD 组，为期十个月，然后随机分为久坐组 (Sed) 或运动组 (Exe)，为期两周。检查白细胞、心脏功能、结构和脾组织的炎症消退介质和以巨噬细胞为中心的基因转录物。经过两周的志愿者锻炼，心脏功能变化有限，但心脏和脾脏的结构变化显着。CON 组和 OBD 组均观察到运动诱发的心肌核增生。OBD-Sed 小鼠表现出脾脏变化和中性粒细胞增加，而运动后 CON 中发现中性粒细胞增加。OBD-Sed 增加了心脏中的促炎脂质介质，通过 OBD-Exe 的运动减少，而 CON-Exe 保留了消解介质。慢性 OBD-Sed 会消耗心脏和脾脏中的长链脂肪酸 (DHA/EPA)，而运动则独立调节两个器官中的脂质代谢基因，影响以巨噬细胞为中心的脂质和脂蛋白途径。慢性肥胖会加剧心脏炎症，而运动则可以降低心脏中促炎生物活性脂质介质的水平。OBD 维持了 CON 小鼠心脏和脾脏的炎症，而运动则保留了消退介质。总之，这些发现强调了饮食与运动的相互作用，并强调了饮食、运动、脾心轴炎症消解信号和免疫健康之间的复杂联系。