College of Life Sciences, Northeast Agricultural University, Harbin, Heilongjiang Province, China.
Neurochem Res. 2021 May;46(5):1058-1067. doi: 10.1007/s11064-020-03220-x. Epub 2021 Mar 24.
Albicanol is a natural terpenoid derived from Dryopteris fragrans. Herein, we assessed the ability of Albicanol to protect against oxidative stress-induced senescence. Using a murine model of D-galactose (D-gal)-induced aging, we determined that Albicanol treatment can reverse D-gal-mediated learning impairments and behavioral changes, while also remediating brain tissue damage in treated mice. We found that serum SOD, CAT, GSH-Px, and T-AOC levels were significantly decreased in aging mice, and that Albicanol treatment significantly increased the serum levels of these antioxidant enzymes. We additionally evaluated the impact of Albicanol treatment on the Keap1/Nrf2/ARE signaling pathway, and found that it was able to decrease Keap1 expression while increasing the expression of Nrf2, thereby activating this signaling pathway, suppressing oxidative damage, and enhancing the expression of downstream target genes including SOD, GSH, GST, HO-1, and NQO1 in this murine aging model system. Albicanol treatment also inhibited the secretion of inflammatory TNF-a and IL-1b. Together, these data indicated that Albicanol can activate Nrf2 pathway-related genes, thereby inhibition of delayed aging by alleviating oxidative stress-induced damage.
阿尔比卡醇是一种天然萜类化合物，来源于鳞毛蕨。在此，我们评估了阿尔比卡醇预防氧化应激诱导衰老的能力。使用 D-半乳糖（D-gal）诱导衰老的小鼠模型，我们确定阿尔比卡醇治疗可以逆转 D-gal 介导的学习障碍和行为变化，同时修复治疗小鼠的脑组织损伤。我们发现，衰老小鼠血清中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）和总抗氧化能力（T-AOC）水平显著降低，而阿尔比卡醇治疗显著增加了这些抗氧化酶的血清水平。我们还评估了阿尔比卡醇治疗对 Keap1/Nrf2/ARE 信号通路的影响，发现它能够降低 Keap1 表达，同时增加 Nrf2 表达，从而激活该信号通路，抑制氧化损伤，并增强下游靶基因包括 SOD、GSH、GST、HO-1 和 NQO1 在该小鼠衰老模型系统中的表达。阿尔比卡醇治疗还抑制了炎症 TNF-a 和 IL-1b 的分泌。综上所述，这些数据表明，阿尔比卡醇可以激活 Nrf2 通路相关基因，从而通过减轻氧化应激诱导的损伤来抑制衰老。
