Oxidative stress plays an important role in the development of aging-related diseases by accelerating the lipid peroxidation of polyunsaturated fatty acids in the cell membrane, resulting in the production of aldehydes, such as malondialdehyde and 4-hydroxy-2-nonenal (4-HNE) and other toxic substances. The compound 4-HNE forms adducts with DNA or proteins, disrupting many cell signaling pathways including the regulation of apoptosis signal transduction pathways. The binding of proteins to 4-HNE (4-HNE-protein) acts as an important marker of lipid peroxidation, and its increasing concentration in brain tissues and fluids because of aging, ultimately gives rise to some hallmark disorders, such as neurodegenerative diseases (Alzheimer’s and Parkinson’s diseases), ophthalmic diseases (dry eye, macular degeneration), hearing loss, and cancer. This review aims to describe the physiological origin of 4-HNE, elucidate its toxicity in aging-related diseases, and discuss the detoxifying effect of aldehyde dehydrogenase and glutathione in 4-HNE-driven aging-related diseases.

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Neuroinflammatory response is the immune response mechanism of the innate immune system of the central nervous system. Both primary and secondary injury can activate neuroinflammatory response. Among them, the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome plays a key role in the inflammatory response of the central system. Inflammasome is a type of pattern recognition receptor, a cytoplasmic polyprotein complex composed of members of the Nod-like receptor (NLR) family and members of the pyrin and HIN domain (PYHIN) family, which can be affected by a variety of pathogen-related molecular patterns or damage-related molecular patterns are activated. As one of the research hotspots in the field of medical research in recent years, there are increasing researches on immune function abnormalities in the onset of neurological diseases such as depression, AD, ischemic brain injury and cerebral infarction, the NLRP3 inflammasome causes the activated caspase-1 to cleave pre-interleukin-1β and pre-interleukin-18 into mature interleukin-1β and interleukin-18, in turn, a large number of inflammatory factors are produced, which participate in the occurrence and development of the above-mentioned diseases. Targeted inhibition of the activation of inflammasomes can reduce the inflammatory response, promote the survival of nerve cells, and achieve neuroprotective effects. This article reviews NLRP3 inflammasome’s role in neurological diseases and related regulatory mechanisms, which providing references for future research in this field.

Stroke is a leading cause of death and disability world-widely. The incidence rate of stroke has been increasing due to the aging population and lifestyle changes. At present, the only drug approved by the US Food and Drug Administration (FDA) for the treatment of ischemic stroke is tissue plasminogen activator (t-PA), but its clinical application is greatly limited because of its narrow time window and bleeding risk. Natural products have a long history of being used in traditional medicine with good safety, making them an important resource for the development of new drugs. Indeed, some natural products can target a variety of pathophysiological processes related to stroke, including oxidative stress, in lammation and neuronal apoptosis. Therefore, the development of high-e ficiency, lowtoxicity, safe and cheap active substances from natural products is of great significance for improving the treatment alternatives of patients with stroke. This article reviews the neuroprotective e fects of 33 natural compounds by searching recent related literature. Among them, puerarin, pinocembrin, quercetin, epigallocatechin-3-gallate (EGCG), and resveratrol have great potential in the clinical treatment of ischemic stroke. This review will provide a powerful reference for screening natural compounds with potential clinical application value in ischemic stroke or synthesizing new neuroprotective agents with natural compounds as lead compounds.

Modern agriculture contributes significantly to greenhouse gas emissions. How to reduce such emissions without sacrificing agricultural development is a common issue concerning most developing countries. In China, a rural revitalization strategy proposed in 2018 aims to achieve agricultural modernization by 2050, while reaching a carbon emission peak by 2030 and neutrality by 2060. However, China’s progress towards these goals is largely unknown. This study evaluates the coupling coordination and spatiotemporal dynamic evolution between agricultural carbon emissions and agricultural modernization in China from 2010 to 2020 through a joint employment of spatial autocorrelation and coupling coordination degree modeling. The results show that from 2010 to 2020, the agricultural modernization level increased from 0.155 to 0.272, and the agricultural carbon emission intensity decreased from 4.9 tons per CYN million to 2.43 tons. Agricultural carbon emissions and the agricultural modernization level manifest significant spatially agglomerative patterns with noticeable discrepancies across different regions. Moreover, the coupling coordination degree between agricultural carbon emissions and agricultural modernization has increased every year, but disparities among provinces continued to widen. Specifically, coupling coordination in northern China is significantly higher than that in the south, and its spatial distribution exhibits a positive correlation and increasing levels of clustering. These results point to the continued need for sustainable agricultural development efforts, such as strengthening rural infrastructure and diffusing green technologies in achieving China’s dual carbon emission and agricultural modernization goals. This study also examines the sustainable agricultural development issue from a new perspective, and the findings can provide policy references for sustainable agricultural development policies in China.