Wang Yueming, Xiong Yanlei, Zhang Aiping, Zhao Nannan, Zhang Jiashen, Zhao Dongmei, Yu Zhenhai, Xu Ning, Yin Yancun, Luan Xiying, Xiong Yanlian
Department of Anatomy School of Basic Medicine Binzhou Medical University Yantai China.
Department of Pathology Xuanwu Hospital Capital Medical University Beijing China.
Food Sci Nutr. 2020 Jun 5;8(7):3872-3881. doi: 10.1002/fsn3.1681. eCollection 2020 Jul.
Chitosan oligosaccharide (COS) is the depolymerized product of chitosan possessing various biological activities and protective effects against inflammation and oxidative injury. The aim of the present study was to investigate the antioxidant effects of COS supplements on aging-related liver dysfunction. We found that COS treatment significantly attenuated elevated liver function biomarkers and oxidative stress biomarkers and decreased antioxidative enzyme activities in liver tissues in D-galactose (D-gal)-treated mice. Furthermore, COS treatment significantly upregulated the expression of Nrf2 and its downstream target genes HO-1, NQO1, and CAT. Moreover, in vitro experiments showed that COS treatment played a vital role in protecting HO-exposed L02 cells against oxidative stress by activating Nrf2 antioxidant signaling. These data indicate that COS could protect against D-gal-induced hepatic aging by activating Nrf2 antioxidant signaling, which may provide novel applications for the prevention and treatment of aging-related hepatic dysfunction.
壳寡糖(COS)是壳聚糖的解聚产物,具有多种生物活性以及对炎症和氧化损伤的保护作用。本研究的目的是探讨补充COS对衰老相关肝功能障碍的抗氧化作用。我们发现,在D-半乳糖(D-gal)处理的小鼠中,COS治疗显著降低了肝功能生物标志物和氧化应激生物标志物的升高,并降低了肝组织中的抗氧化酶活性。此外,COS治疗显著上调了Nrf2及其下游靶基因HO-1、NQO1和CAT的表达。此外,体外实验表明,COS治疗通过激活Nrf2抗氧化信号通路,在保护HO暴露的L02细胞免受氧化应激方面发挥了至关重要的作用。这些数据表明,COS可以通过激活Nrf2抗氧化信号通路来预防D-gal诱导的肝脏衰老,这可能为衰老相关肝功能障碍的预防和治疗提供新的应用。
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