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.

Cinnamomi Ramulus (CR) has been extensively used as a remedy for inflammatory diseases in China. This study adopted an integrative approach of experimental research, phytochemistry, and network pharmacology to investigate its alleviative effects on rheumatoid arthritis (RA) and the underlying potential mechanisms. CR extract (50, 100, and 200 mg/kg) and methotrexate (MTX) significantly ameliorated RA symptoms in the collagen-induced arthritis (CIA) rat model. They also reduced paw volume, arthritis index, proinflammatory cytokines (TNF- α , IL-17A, IL-6, and IL-1 β ), and oxidative damage. Sixty-three compounds were systematically identified as the basic components of CR. Fifty-five common genes obtained from compounds and GEO databases were employed to construct the protein-protein interaction (PPI) network. Among them, 20 hub genes were identified via the cytoHubba. Enrichment analysis of the common genes indicated that the TNF signaling pathway and IL-17 signaling pathway might be the potential key pathways. Moreover, molecular docking methods confirmed the high affinity between the top 10 bioactive components of CR and the top 10 targets. In addition, in vitro results showed that CR extract (0.2, 0.4, and 0.8 mg/mL) inhibited inflammation and oxidative damage in MH7A cells stimulated by lipopolysaccharide (LPS). In summary, this study adopted multiple approaches to elucidate the protective effect and potential mechanisms of CR on RA, indicating that CR might be a promising herbal candidate for further investigation of RA treatment.