Tang Yongyan, Zheng Wenya, Chen Jingfang, Xie Yan, Yang Jinxin, Wang Zhipeng, Qin Hong
Xiangya School of Public Health, Central South University, Changsha, China.
Tropical Disease and Chronic Disease Prevention and Control Institute, Hainan Provincial Center for Disease Control and Prevention, Haikou, China.
Plant Foods Hum Nutr. 2024 Dec 16;80(1):11. doi: 10.1007/s11130-024-01249-9.
Adipocyte senescence is one of the major common features correlated with aging, which can also lead to obesity, and aggravated oxidative stress contributes to cell senescence. Sesamol, a lignan from plants found in sesame, has been proven to alleviate obesity. However, the effects and mechanisms of sesamol on adipose tissue senescence remain unclear. In the current research, we used an aged model of obesity by feeding old mice high-fat diet (HFD), and a senescent cell model by treating 3T3-L1 mature adipocytes with repeated exposure to hydrogen peroxide (HO). Both HFD induced aged obesity mice and HO treated cells presented features associated with senescence. Additionally, obesity in aged mice accelerated the expression of adipose tissue senescence-associated markers. Notably, the presence of sesamol showed marked activation of Nrf2 and inhibition of p-p38MAPK, along with the suppression of oxidative stress (ROS, MDA, SOD), inflammatory factors (IL-6, TNFα) and cell cycle inhibitors (p53, p21, p16). A pretreatment of ML385, an inhibitor of Nrf2, reversed the effects induced by sesamol treatment. In conclusion, our results demonstrated that obesity contributed to deteriorated adipose tissue senescence during aging. Furthermore, sesamol, acted as an activator of Nrf2 and exerted negative impacts on the activation of p38MAPK, which were associated with amelioration of adipose senescence, thereby indicating it could be a potential nutritional intervention for preventing and treating aging-related disorders.
脂肪细胞衰老与衰老相关的主要共同特征之一，它也会导致肥胖，而氧化应激加剧会导致细胞衰老。芝麻酚是一种存在于芝麻中的植物木脂素，已被证明可减轻肥胖。然而，芝麻酚对脂肪组织衰老的影响和机制仍不清楚。在当前研究中，我们通过给老年小鼠喂食高脂饮食（HFD）建立了衰老肥胖模型，并通过用过氧化氢（HO）反复处理3T3-L1成熟脂肪细胞建立了衰老细胞模型。高脂饮食诱导的衰老肥胖小鼠和过氧化氢处理的细胞均呈现出与衰老相关的特征。此外，老年小鼠的肥胖加速了脂肪组织衰老相关标志物的表达。值得注意的是，芝麻酚的存在显著激活了Nrf2并抑制了p-p38MAPK，同时抑制了氧化应激（ROS、MDA、SOD）、炎症因子（IL-6、TNFα）和细胞周期抑制剂（p53、p21、p16）。Nrf2抑制剂ML385的预处理逆转了芝麻酚处理诱导的效应。总之，我们的结果表明肥胖导致衰老过程中脂肪组织衰老恶化。此外，芝麻酚作为Nrf2的激活剂，对p38MAPK的激活产生负面影响，这与改善脂肪衰老有关，从而表明它可能是预防和治疗衰老相关疾病的潜在营养干预措施。
