China has a large variety of edible mushrooms and ranks first in the world in terms of production and variety. Nevertheless, due to their high moisture content and rapid respiration rate, they experience constant quality deterioration, browning of color, loss of moisture, changes in texture, increases in microbial populations, and loss of nutrition and flavor during postharvest storage. Therefore, this paper reviews the effects of essential oils and plant extracts on the preservation of edible mushrooms and summarizes their mechanisms of action to better understand their effects during the storage of mushrooms. The quality degradation process of edible mushrooms is complex and influenced by internal and external factors. Essential oils and plant extracts are considered environmentally friendly preservation methods for better postharvest quality. This review aims to provide a reference for the development of new green and safe preservation and provides research directions for the postharvest processing and product development of edible mushrooms.

The king oyster mushroom (Pleurotus eryngii) is a delicious edible mushroom that is highly prized for its unique flavor and excellent medicinal properties. Its enzymes, phenolic compounds and reactive oxygen species are the keys to its browning and aging and result in its loss of nutrition and flavor. However, there is a lack of reviews on the preservation of Pl. eryngii to summarize and compare different storage and preservation methods. This paper reviews postharvest preservation techniques, including physical and chemical methods, to better understand the mechanisms of browning and the storage effects of different preservation methods, extend the storage life of mushrooms and present future perspectives on technical aspects in the storage and preservation of Pl. eryngii. This will provide important research directions for the processing and product development of this mushroom.

Lipid accumulation causes diseases such as obesity and abnormal lipid metabolism, thus impairing human health. Tea polysaccharide is one of the natural, active substances that can lower lipid levels. In this paper, an oleic-acid-induced HepG2 cell model was established. The lipid-lowering effects of a novel group of Fuzhuan brick tea polysaccharides (FTPs)—obtained from Fuzhuan brick tea—were examined in vitro. The monosaccharide composition of FTP3 was Glc, Gal, Ara, Man, Rha, GalAc, GlcAc, and Xyl with a molar ratio of 23.5:13.2:9.0:5.5:5.4:2.7:1.3:1.0, respectively. A molecular weight of 335.68 kDa was identified for FTP3. HepG2 cells treated with FTP3 achieved a prominent lipid-lowering effect compared with cells treated with oleic acid. Images of the Oil Red O staining treatment showed that FTP3-treated groups had significantly fewer red fat droplets. TC and TG levels were lower in FTP3-treated groups. FTP3 alleviated lipid accumulation in HepG2 cells, activated AMPK, and decreased the SREBP-1C and FAS protein expressions associated with fatty acid synthesis. FTP3 holds promising potential for its lipid-lowering effects.

Acrylamide has been well known for its neurotoxicity, genotoxicity, carcinogenicity, etc. Recently, the immunotoxicity of acrylamide has been reported by different research groups, although the underlying mechanisms of acrylamide endangering immune systems have not been fully elucidated. In this study, mouse monocyte–macrophage cells model was used to clarify the toxic mechanism of acrylamide and the inhibitory effect of Yam polysaccharides (YPS) on acrylamide‐induced damage. We found that acrylamide induced RAW 264.7 cell death in a time‐ and concentration‐dependent manner. After acrylamide (2.0, 3.0, 4.0 mmol/L) treatment for 24 h, cell apoptosis, autophagy, and pyroptosis were observed. However, the levels of autophagy and pyroptosis decreased at a high concentration of acrylamide (4.0 mmol/L). Acrylamide upregulated P2X7 expression, but the P2X7 level was not showing a monotone increasing trend. When the P2X7 antagonist was applied, the effect of acrylamide on autophagy and pyroptosis was weakened. Additionally, acrylamide triggered the occurrence of oxidative stress and a decreased nitric oxide (NO) level. However, reactive oxygen species (ROS) generation, the decrease of heme oxygenase‐1 (HO‐1) expression, and the increase of inducible nitric oxide synthase (iNOS) expression were reversed by the inhibition of P2X7. Yam polysaccharides (50.0 μg/ml) significantly inhibited acrylamide‐induced oxidative stress and cell death (including apoptosis, autophagy, and pyroptosis). Yam polysaccharides also effectively reversed the increase of iNOS expression induced by acrylamide. However, Yam polysaccharides promoted the expression of P2X7 rather than prohibit it. These results indicated that acrylamide caused RAW 264.7 cell death due to pro‐apoptosis as well as excessive autophagy and pyroptosis. Apoptosis might be more predominant than autophagy and pyroptosis under a higher concentration of acrylamide (4.0 mmol/L). P2X7‐stimulated oxidative stress was responsible for acrylamide‐induced programmed cell death (PCD), but P2X7 showed limited regulatory effect on apoptosis. Yam polysaccharides with antioxidant activity inhibited acrylamide‐induced cell death (apoptosis, autophagy, and pyroptosis), but exerted limited effect on the acrylamide‐induced P2X7 expression. These findings would offer an insight into elucidating the immunotoxic mechanism of acrylamide and the potential approaches to control its toxicity.

Acrylamide exposure through environment pollution and diet is very common in daily life. With the deepening of the study on the toxicity of acrylamide, it has attracted widespread attention for the effects of acrylamide on multiple organs through affecting a variety of programmed cell death. Multiple studies have shown that acrylamide could exert its toxic effect by inducing programmed cell death, but its specific molecular mechanism is still unclear. In this review, the research on the main forms of programmed cell death (apoptosis, autophagy, and programmed necrosis) induced by acrylamide and their possible mechanisms are reviewed. This review may provide basic data for further research of acrylamide and prevention of its toxicity.