Abstract
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 H2O2‐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.
Highlights
Aging is a biological process characterized by progressive degeneration of physiological functions that results in an increase in the prevalence of morbidity and mortality
The NF-E2-related factor 2 (Nrf2) pathway regulates the expression of several antioxidant and detoxification enzymes including the catalytic subunits of glutamate–cysteine ligase (GCLC), heme oxygenase-1 (HO-1), and NAD(P)H quinone oxidoreductase 1 (NQO1) by binding to the antioxidant response element (ARE) in their promoter regions (Kubben et al, 2016)
There was a markedly increase in the oxidative stress biomarkers of MDA, advanced glycation end-products (AGEs), and 8-OH-dG levels in the D-gal group (p < .01), while chitosan oligosaccharide (COS) or VE treatment significantly decreased MDA, AGEs, and 8-OH-dG levels compared with D-gal group (p < .05) (Figure 2a–c)
Summary
Aging is a biological process characterized by progressive degeneration of physiological functions that results in an increase in the prevalence of morbidity and mortality. Current studies suggest that chitosan oligosaccharide (COS) activates numerous antioxidant genes and promotes Nrf translocation (Hyung, Ahn, Il Kim, Kim, & Je, 2016; Zhang, Ahmad, et al, 2019). Whether COS can regulate the oxidative and antioxidant balance in aging cells by regulating the expression of Nrf pathway remains unclear. Studies have shown that COS possesses a wide range of biological effects including anti-inflammation, antioxidation, antitumor, anti-Alzheimer's disease, antihypertension, and anti-obesity (Azuma, Osaki, Minami, & Okamoto, 2015; Muanprasat & Chatsudthipong, 2017). Previous studies have already demonstrated that COS possesses hepatoprotective and renoprotective effects in D-galinduced subacute aging mice to realize its anti-aging activity (Kong et al, 2018), the effects of COS on aging-related liver injury triggered by D-gal and its potential molecular mechanism remain to be explored. We investigated the effects of COS on liver injury at two dose levels using a D-gal-induced animal aging model
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