The global burden of non-alcoholic steatohepatitis (NASH) is on the rise. Researchers recognize inhibiting ferroptosis, a form of cell death leading to iron-dependent oxidative damage, as a promising therapy for treating NASH. Lycopene, a natural antioxidant compound, exhibits various pharmacological properties. However, the anti-NASH efficacy of the dietary recommended concentration of lycopene and the role of lycopene in combating ferroptosis in NASH have remained unclear. Our study investigated lycopene’s impact on ferroptosis in various diet-induced mouse NASH models and corresponding cellular models, unveiling its anti-inflammatory and anti-fibrotic effects. Our findings demonstrated that lycopene notably reduced ferroptosis in methionine- and choline-deficient (MCD) diet-fed mice and a normal mouse hepatocyte cell line (NCTC1469) by restoring balanced ferrous iron levels, lipid reactive oxygen species, and normal mitochondrial morphology. These effects were linked to the regulation of ferroptosis markers glutathione peroxidase 4 (GPX4) and prostaglandin G/H synthase 2. Additionally, lycopene’s anti-ferroptosis action was validated in mice fed a high-fat, high-cholesterol diet and HepG2 cells treated with free fatty acid. Our transcriptomic analysis highlighted peroxisome proliferator-activated receptor α (PPARα) as a primary target of lycopene, crucial for activating the glutathione system because GW6471, a PPARα antagonist, blocked lycopene-induced GPX4 activation. Furthermore, nuclear factor erythroid 2-related factor 2 (Nrf2) played a crucial role in lycopene’s impact on iron metabolism-related proteins ferritin heavy chain 1 and transferrin receptor 1. Notably, when inhibiting PPARα or Nrf2 in MCD diet-fed mice by GW6471 or ML385, lycopene’s protective effects against ferroptosis and NASH progression diminished. These findings underscore the crucial role of PPARα-mediated glutathione system activation and Nrf2-mediated iron metabolism modulation in lycopene’s anti-ferroptosis effects.

Neurodegenerative diseases (NDs), mainly including Alzheimer's disease, Parkinson's disease, and multiple sclerosis, represent a major public health challenge with the steady increase of aging population worldwide. Emerging evidence has revealed the key role of the microbiota-gut-brain axis in the pathogenesis of NDs. Diet is one of the most important environmental factors shaping the structure and function of gut microbiota. Manipulating the gut microbiota through specific diet patterns may represent a promising approach for NDs prevention. In this review, we highlight gut microbiota variations in NDs, outline several crucial signaling pathways of the gut-brain communication, and discuss the interplay of nutrients-microbes and biological effect of diet-derived microbial metabolites on neural physiology. In particular, we summarized the current knowledge about the application of dietary patterns in NDs to prevent disease progression via the modulation of the gut microbiota. Our study provides novel insights on the diet-microbiota-gut-brain axis in neurodegenerative disorders and highlights the potential of developing microbiome-targeted personalized dietary intervention for NDs management.

Acrylamide is a ubiquitous toxicant in various heat-processed foods. Coffee is one of the most important dietary sources of acrylamide. This paper explains the liver toxicity, neurotoxicity and reproductive toxicity of acrylamide in animals and cells, and it analyzes the major pathway for acrylamide formation during coffee roasting. During the selection and roasting of raw coffee beans and coffee extraction and brewing, the factors influencing acrylamide formation include the types of coffee beans, roasting temperature, roasting time and storage conditions. Different coffee processing methods can also cause differences in acrylamide content. Furthermore, this review summarizes the efficient measures to prevent the formation of acrylamide during coffee roasting, with the aim of providing a theoretical reference for the control of acrylamide formation in the food industry.

Colorectal cancer is a heterogeneous disease of the intestinal epithelium characterized by the accumulation of genetic mutations and the dysregulation of immune responses. The occurrence of colorectal cancer is the result of a combination of environmental, genetic and other factors. Among environmental factors, dietary factors are closely related to the occurrence of colorectal cancer. Dietary factors play an important role in regulating the intestinal microbiota. In addition, the composition and metabolism of the intestinal microbiome are important contributors to the development of colorectal cancer. Specific intestinal microorganisms such as Fusobacterium nucleatum have been shown to be closely correlated with the occurrence of colorectal cancer. Regulating gut microbiota has emerged as a potential means of preventing and treating colorectal cancer. In order to provide a theoretical reference for the clinical treatment of colorectal cancer, this article reviews the intervening effects of probiotics, next-generation probiotics and their metabolites on colorectal cancer, with a focus on the current status of research on the biological effects of various metabolic secretion products of probiotics, including cell-free supernatants, extracellular polysaccharides, short-chain fatty acids, bacteriocins, bacterial enzymes, bile acids and tryptophan metabolites on colorectal cancer.