La Russa Daniele, Marrone Alessandro, Mandalà Maurizio, Macirella Rachele, Pellegrino Daniela
Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy.
LARSO (Analysis and Research on Oxidative Stress Laboratory), University of Calabria, 87036 Rende, Italy.
Biomedicines. 2020 Nov 25;8(12):532. doi: 10.3390/biomedicines8120532.
Caloric restriction (CR) represents a powerful intervention for extending healthspan and lifespan in several animal models, from yeast to primates. Additionally, in humans, CR has been found to induce cardiometabolic adaptations associated with improved health. In this study, we evaluated in an aged and obese rat model the effect of long-term (6 months) caloric restriction (-40%) on the oxidative/inflammatory balance in order to investigate the underlining mechanisms. In plasma, we analyzed the oxidative balance by photometric tests and the adiponectin/tumor necrosis factor-α-induced gene/protein 6 (TSG-6) levels by Western blot analysis. In the white adipose tissue, we examined the protein levels of AdipoR1, pAMPK, NFκB, NRF-2, and glutathione S-tranferase P1 by Western blot analysis. Our results clearly showed that caloric restriction significantly improves the plasmatic oxidative/inflammatory balance in parallel with a major increase in circulating adiponectin levels. Additionally, at the level of adipose tissue, we found a positive modulation of both anti-inflammatory and antioxidant pathways. These adaptations, induced by caloric restriction, with the achievement of normal weight, suggest that inflammatory and redox imbalance in obese aged rats appear to be more linked to obesity than to aging.
热量限制(CR)是一种强有力的干预措施,在从酵母到灵长类动物的多种动物模型中,它都能延长健康寿命和寿命。此外,在人类中,已发现热量限制能诱导与健康改善相关的心脏代谢适应性变化。在本研究中,我们在老年肥胖大鼠模型中评估了长期(6个月)热量限制(-40%)对氧化/炎症平衡的影响,以探究其潜在机制。在血浆中,我们通过光度测试分析氧化平衡,并通过蛋白质印迹分析检测脂联素/肿瘤坏死因子-α诱导基因/蛋白6(TSG-6)水平。在白色脂肪组织中,我们通过蛋白质印迹分析检测AdipoR1、磷酸化腺苷酸活化蛋白激酶(pAMPK)、核因子κB(NFκB)、核因子E2相关因子2(NRF-2)和谷胱甘肽S-转移酶P1的蛋白水平。我们的结果清楚地表明,热量限制显著改善了血浆氧化/炎症平衡,同时循环脂联素水平大幅增加。此外,在脂肪组织水平,我们发现抗炎和抗氧化途径均有正向调节。热量限制诱导的这些适应性变化以及体重恢复正常表明,肥胖老年大鼠的炎症和氧化还原失衡似乎与肥胖的关系比与衰老的关系更大。