Exploring Protective Effect of Phellinus linteus Polysaccharides on Liver Injury in Exercise Fatigue Mice Based on Nrf2 Signaling Pathway
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Abstract:
Ultrasound-assisted hot water extraction was utilized to obtain Phellinus linteus polysaccharides (PLPs), and its protective effect on liver injury in exercise-induced fatigue mice was investigated through modulation of the Nrf2 signaling pathway. Results showed a PLP extraction yield of 7.64%, with a purification efficiency of 23%. PLP administration led to a significant reduction in the liver coefficient of mice compared to the exercise-induced fatigue model group. Moreover, it increased swimming endurance times of the low-, medium-and high-dose groups by 15.58%, 34.69% and 53.06%, respectively. Compared to the sedentary control group, the model group exhibited significantly diminished activities of antioxidative enzymes in the liver, including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHPx), alongside increased malondialdehyde (MDA) content; serum inflammatory factors such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6); and alanine transaminase (ALT) and aspartate transaminase (AST) activities. Conversely, the low-, medium-and high-dose groups demonstrated elevated antioxidant enzymes activity in the liver and reduced MDA content in comparison to the model group. Notably, the high-dose group exhibited significant reductions in serum TNF-α, IL-1β, and IL-6 levels by 50.54%, 50.51%, and 46.21%, respectively, alongside ALT and AST activities by 33.30% and 34.57%, respectively. Moreover, mRNA expression levels of Nrf 2, HO-1, and NQO1 were significantly lower in the model group compared to the sedentary group, while Keap1 mRNA expression was significantly higher. Post-PLP supplementation, mRNA expression levels of Nrf 2, HO-1 and NQO1 significantly increased in the low-, medium-and highdose groups, while Keap1 mRNA expression significantly decreased. These findings collectively suggest that PLPs enhance hepatic antioxidant capacity and reduce inflammatory factors in exercise-induced fatigue mice by activating the hepatic Nrf2 signaling pathway, thereby mitigating liver injury.
