Neurodegenerative diseases are often characterized by progressive dysfunction and loss of neuronal structure and function, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease. Mitochondria, the center of energy metabolism in the body, are often damaged and accumulated in neurodegenerative diseases. As an efficient way of removing these damaged mitochondria, mitophagy usually shows an abnormal state in the development of these diseases, which aggravates the cognitive and motor dysfunction of the body, and finally speeds up the process of related diseases. In recent years, it has been found that food-derived natural products, such as quercetin, curcumin, resveratrol and silymarin, play significant roles in regulating mitophagy to improve neurodegenerative diseases, which have unique advantages, such as lower toxicity than chemical synthetic drugs and cost-effectiveness. Here, we summarize recent studies on the regulation of mitophagy by food-derived natural products to slow down neurodegenerative disorders in order to provide new ideas for researchers to develop and utilize food-derived natural products.

Acrylamide (ACR) is a common toxic substance in foods, which can cause serious damage to human organs and systems, especially the nervous system. At present, there are no appropriate measures to prevent and treat ACR neurotoxicity. In recent years, it has been reported that some natural plant products with high safety for consumption, strong antioxidant activity and low cost can intervene in ACR-induced neurotoxicity. This paper mainly introduces the neurotoxicity of ACR, natural plant products that can intervene in ACR neurotoxicity, and the underlying mechanism of action in order to provide a theoretical reference and research ideas for the treatment of ACR neurotoxicity in multiple ways and though multiple targets, as well as the development and application of natural products against ACR neurotoxicity.

In this study, we evaluated the inhibitory effect of spinosin (SP) on the glycation of β-lactoglobulin (β-Lg) using fluorescence spectroscopy, ultraviolet visible (UV-Vis) spectroscopy, Fourier transform infrared spectroscopy (FTIR), thioflavin T (ThT) staining, and sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE). Fluorescence spectroscopic results showed that SP effectively inhibited the formation of advanced glycosylation end products (AGEs), stabilized the conformational structure of glycated β-Lg, and altered the microenvironment near Trp and Tyr residues. UV-Vis spectroscopy showed that glycation changed the structure of β-Lg, and SP inhibited the production of AGEs by slowing down the late stage of the Maillard reaction. FTIR spectral analysis showed the involvement of hydrogen bonding in the formation of SP-β-Lg complex. The results of ThT staining showed that SP reduced β-amyloid deposition by attenuating protein misfolding. SDS-PAGE analysis showed inhibition of SP-induced cross-linking of glycated β-Lg. These results demonstrate that SP holds promise as an anti-glycation agent in food systems, with the potential to reduce the formation of harmful glycation products.