Abstract
Excessive alcohol consumption leads to serious liver injury, associating with oxidative stress and inflammatory response. Previous study has demonstrated that polydatin (PD) exerted antioxidant and anti-inflammatory effects and attenuated ethanol-induced liver damage, but the research remained insufficient. Hence, this experiment aimed to evaluate the hepatoprotective effect and potential mechanisms of PD on ethanol-induced hepatotoxicity. Our results showed that PD pretreatment dramatically decreased the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) in the serum, suppressed the malonaldehyde (MDA) and triglyceride (TG) content and the production of reactive oxygen species (ROS), and enhanced the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), andalcohol dehydrogenase (ADH), and aldehyde dehydrogenase (ALDH), paralleled by an improvement of histopathology alterations. The protective effect of PD against oxidative stress was probably associated with downregulation of cytochrome P450 2E1 (CYP2E1) and upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its target gene haem oxygenase-1 (HO-1). Moreover, PD inhibited the release of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) via downregulating toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB) p65. To conclude, PD pretreatment protects against ethanol-induced liver injury via suppressing oxidative stress and inflammation.
Highlights
Long-term excessive consumption of alcohol is harmful to the liver and inevitably induces alcoholic liver disease (ALD) [1]
Alcohol is converted to acetaldehyde mainly by alcohol dehydrogenase (ADH), cytochrome P450 2E1 (CYP2E1), and catalase and is further oxidized to acetate by aldehyde dehydrogenase (ALDH) and is converted to carbon dioxide via the citric acid cycle [4]
Accumulating evidence has shown that chronic excessive alcohol intake increases the level of inflammatory cytokines, such as TNF-α, IL-1β, and IL6 [13]. The release of these cytokines is mainly associated with the activation of toll-like receptor 4 (TLR4) and its downstream nuclear factor kappa B (NF-κB), which remains the key inflammatory pathway playing a vital role in alcoholinduced ALD model [14]
Summary
Long-term excessive consumption of alcohol is harmful to the liver and inevitably induces alcoholic liver disease (ALD) [1]. Accumulating evidence has shown that chronic excessive alcohol intake increases the level of inflammatory cytokines, such as TNF-α, IL-1β, and IL6 [13] The release of these cytokines is mainly associated with the activation of toll-like receptor 4 (TLR4) and its downstream nuclear factor kappa B (NF-κB), which remains the key inflammatory pathway playing a vital role in alcoholinduced ALD model [14]. What is more, emerging evidence has demonstrated that resveratrol mitigates ethanol-induced oxidative stress in the liver of rats [20]. All these findings imply that PD is protective to the liver and might be a
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