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Review
. 2022 Feb 10:2022:9218738.
doi: 10.1155/2022/9218738. eCollection 2022.

Polydatin: A Critical Promising Natural Agent for Liver Protection via Antioxidative Stress

Dandan Tang  1 , Qing Zhang  1 , Huxinyue Duan  1 , Xun Ye  1 , Jia Liu  1 , Wei Peng  1 , Chunjie Wu  1
Affiliations
Review

Polydatin: A Critical Promising Natural Agent for Liver Protection via Antioxidative Stress

Dandan Tang et al. Oxid Med Cell Longev. .

Abstract

Polydatin, one of the natural active small molecules, was commonly applied in protecting and treating liver disorders in preclinical studies. Oxidative stress plays vital roles in liver injury caused by various factors, such as alcohol, viral infections, dietary components, drugs, and other chemical reagents. It is reported that oxidative stress might be one of the main reasons in the progressive development of alcohol liver diseases (ALDs), nonalcoholic liver diseases (NAFLDs), liver injury, fibrosis, hepatic failure (HF), and hepatocellular carcinoma (HCC). In this paper, we comprehensively summarized the pharmacological effects and potential molecular mechanisms of polydatin for protecting and treating liver disorders via regulation of oxidative stress. According to the previous studies, polydatin is a versatile natural compound and exerts significantly protective and curative effects on oxidative stress-associated liver diseases via various molecular mechanisms, including amelioration of liver function and insulin resistance, inhibition of proinflammatory cytokines, lipid accumulation, endoplasmic reticulum stress and autophagy, regulation of PI3K/Akt/mTOR, and activation of hepatic stellate cells (HSCs), as well as increase of antioxidant enzymes (such as catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), superoxide dismutase (SOD), glutathione reductase (GR), and heme oxygenase-1 (HO-1)). In addition, polydatin acts as a free radical scavenger against reactive oxygen species (ROS) by its phenolic and ethylenic bond structure. However, further clinical investigations are still needed to explore the comprehensive molecular mechanisms and confirm the clinical treatment effect of polydatin in liver diseases related to regulation of oxidative stress.

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Conflict of interest statement

The authors declare that there is no conflict of interest regarding the publication of this paper.

Figures

Figure 1
Figure 1
The plant sources of PD.
Figure 2
Figure 2
Cellular and molecular mechanisms of PD in the prevention of oxidative stress induced liver diseases. Bax: BCL-2-associated; Bcl-2: B-cell lymphoma-2; MDA: malondialdehyde; SOD: superoxide dismutase; NOX: nicotinamide adenine dinucleotide phosphate oxidative; CAT: catalase; GSH: glutathione; ROS: reactive oxygen species; 4-HNE: 4-hydroxynonenal; TNF-α: tumor necrosis factor-α; NF-κB: nuclear factor kappa B; IL-1β: interleukin-1β; IL-6: interleukin-6; ALT: alanine aminotransferase; AST: aspartate aminotransferase; TBA: total bile acid; TBIL: total bilirubin; ALP: alkaline phosphatase; ALB: albumin; LDH: lactate dehydrogenase; TG: triglyceride; TC: total cholesterol; FFA: free fatty acid.
Figure 3
Figure 3
Cellular and molecular mechanisms of PD in the prevention of oxidative-associated alcoholic liver disease.
Figure 4
Figure 4
Cellular and molecular mechanisms of PD in the prevention of oxidative-associated nonalcoholic liver diseases.
Figure 5
Figure 5
Cellular and molecular mechanisms of PD in the prevention of oxidative-associated liver fibrosis.
See this image and copyright information in PMC

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