Albicanol Alleviates D-Galactose-Induced Aging and Improves Behavioral Ability Via by Alleviating Oxidative Stress-Induced Damage
Albicanol Alleviates D-Galactose-Induced Aging and Improves Behavioral Ability Via by Alleviating Oxidative Stress-Induced Damage
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DOI：
10.1007/s11064-020-03220-x
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发表时间：
2021-03-24
影响因子：
4.4
通讯作者：
Wang, Wen Fei
中科院分区：
文献类型：
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作者：
Chen, Ling Ling;Zhang, Dong Rui;Wang, Wen Fei
Albicanol是从香鳞毛蕨中提取的一种天然萜类化合物。在此，我们评估了Albicanol对氧化应激诱导的衰老的保护能力。使用D-半乳糖（D-gal）诱导衰老的小鼠模型，我们确定Albicanol治疗可以逆转D-gal介导的学习障碍和行为变化，同时还可以修复治疗小鼠的脑组织损伤。我们发现，血清SOD，CAT，GSH-Px，和T-AOC水平显着下降，在老龄小鼠，和Albicanol治疗显着增加这些抗氧化酶的血清水平。我们还评估了Albicanol治疗对Keap 1/Nrf 2/ARE信号通路的影响，发现它能够降低Keap 1的表达，同时增加Nrf 2的表达，从而激活该信号通路，抑制氧化损伤，并增强该小鼠衰老模型系统中下游靶基因（包括SOD、GSH、GST、HO-1和NQO 1）的表达。Albicanol治疗还抑制炎症性TNF-α和IL-1b的分泌。总之，这些数据表明Albicanol可以激活Nrf 2通路相关基因，从而通过减轻氧化应激诱导的损伤来抑制延迟衰老。
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.