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Cadmium (Cd) toxicity poses a significant threat to human health and the environment due to its widespread occurrence and persistence. In recent years, considerable attention has been directed towards exploring natural compounds with potential protective effects against Cd-induced toxicity. Among these compounds, resveratrol (RV) has emerged as a promising candidate, demonstrating a range of beneficial effects attributed to its antioxidant and anti-inflammatory properties. This literature review systematically evaluates the protective role of RV against Cd toxicity, considering the various mechanisms of action involved. A comprehensive analysis of both in vitro and in vivo studies is conducted to provide a comprehensive understanding of RV efficacy in mitigating Cd-induced damage. Additionally, this review highlights the importance of phytoremediation strategies in addressing Cd contamination, emphasizing the potential of RV in enhancing the efficiency of such remediation techniques. Through the integration of diverse research findings, this review underscores the therapeutic potential of RV in combating Cd toxicity and underscores the need for further investigation to elucidate its precise mechanisms of action and optimize its application in environmental and clinical settings.

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease; however, no specific pharmacological therapy has yet been approved for this condition. Plant-derived extracts can be an important source for the development of new drugs. The aim of this study was to investigate the effects of (E)-β-caryophyllene (BCP), a phytocannabinoid recently found to be beneficial against metabolic diseases, on HepG2 steatotic hepatocytes. Using a fluorescence-based lipid quantification assay and GC-MS analysis, we show that BCP is able to decrease lipid accumulation in steatotic conditions and to change the typical steatotic lipid profile by primarily reducing saturated fatty acids. By employing specific antagonists, we demonstrate that BCP action is mediated by multiple receptors: CB2 cannabinoid receptor, peroxisome proliferator-activated receptor α (PPARα) and γ (PPARγ). Interestingly, BCP was able to counteract the increase in CB2 and the reduction in PPARα receptor expression observed in steatotic conditions. Moreover, through immunofluorescence and confocal microscopy, we demonstrate that CB2 receptors are mainly intracellularly localized and that BCP is internalized in HepG2 cells with a maximum peak at 2 h, suggesting a direct interaction with intracellular receptors. The results obtained with BCP in normal and steatotic hepatocytes encourage future applications in the treatment of NAFLD.