The apple was found to be involved in antidepressant properties. Thus, this study aimed to explore the effects of apple extract (AE) on depression and to elucidate the underlying mechanisms. Our network pharmacology analysis indicated that AE may exert its antidepressant effects through the regulation of inflammatory responses and the cAMP signaling pathway. Behavioral tests showed that AE significantly improved spatial learning, exploratory behavior, anhedonia, and despair in CUMS mice. Biochemical analyses revealed that AE increased synaptic density in the hippocampus, enhanced brain levels of 5‐hydroxytryptamine (5‐HT) and gamma‐aminobutyric acid (GABA), and reduced the expression of pro‐inflammatory cytokines TNF‐α, IL‐1β, and IL‐6 in both serum and brain tissue. In vitro, AE demonstrated significant neuroprotective effects against CORT‐induced cytotoxicity. Furthermore, AE treatment upregulated the levels of cAMP, phosphorylated PKA (pPKA), and phosphorylated CREB (pCREB) while downregulating PTGS2 expression, suggesting that the cAMP/PKA/CREB/PTGS2 signaling pathway is a key mechanism underlying the antidepressant effects of AE. Therefore, our study indicated that AE can improve cognitive dysfunction and alleviate depressive‐like behavior by targeting the cAMP/PKA/CREB/PTGS2 signaling pathway in CUMS mice. This study paved the way for the clinical application of AE as a novel treatment for depression and provided new targeted therapeutic strategies.

This study investigates the anti‐aging properties of Gastrodia elata ‐derived Parishin extracts (GEPE) by exploring its regulatory effects on oxidative stress, inflammatory responses, apoptosis, and metabolism. Network pharmacology identified 27 active components with parishins as core and 250 anti‐aging intersection targets of Gastrodia elata . Molecular docking confirmed strong binding activity of parishins to key targets such as EGFR, AKT1, and ALB. In vitro experiments showed that the GEPE concentration dependently reduced the activity of senescence marker SA‐β‐gal in D‐galactose‐induced senescent mouse microglial cell (BV2). In vivo experiments showed that GEPE improved cognitive and muscle functions, elevated organ indices of liver, thymus, and spleen, alleviated hepatic lipid accumulation and neuronal damage, reduced oxidative stress, inhibited inflammatory responses and cell apoptosis, and corrected metabolic disorders in D‐galactose‐induced aging mice. These findings demonstrate that GEPE is associated with attenuated aging, potentially through coordinated modulation of oxidative stress, inflammation, apoptosis, and metabolic homeostasis, highlighting its potential as a candidate for anti‐aging interventions.

Apple ring rot, caused by Botryosphaeria dothidea ( B. dothidea ) and Botryosphaeria kuwatsukai ( B. kuwatsukai ), is an economically important fungal disease of apple that primarily damages apple branches and fruits. This article comprehensively reviews the research progress on apple ring rot, covering its disease symptoms (on branches, fruits and leaves), pathogenesis (etiology and occurrence regularity), host resistance mechanisms (basal resistance and induced resistance), and integrated control strategies (agricultural, physical, chemical and biological control). Meanwhile, it analyzes the key problems existing in current research and prospects future research directions. This review aims to provide a systematic theoretical basis and technical implications for the effective prevention and control of apple ring rot, and ultimately promote the sustainable and healthy development of the apple industry.

Aging is a natural, progressive physiological process accompanied by systemic multi‐organ dysfunction, for which effective intervention strategies remain limited. Gastrodia elata is a well‐known food and medicine homologous resource with extensive bioactive properties. Gastrodia elata polysaccharide (GEP), a bioactive macromolecule isolated from G. elata , is a promising candidate for the development of anti‐aging functional products. In this study, we first verified the preliminary anti‐aging effects of GEP in vitro and in Caenorhabditis elegans , and further administered GEP to natural aging mice to explore its anti‐aging effects and underlying mechanisms. The results showed that GEP significantly alleviated d ‐galactose ( d ‐gal)‐induced senescence of BV2 microglia, prolonged the lifespan of nematodes, and in aging mice, it markedly ameliorated cognitive impairment, muscle dysfunction, and hippocampal neuronal damage, while upregulating the expression of neuroprotective BDNF. Moreover, GEP reduced the level of malondialdehyde (MDA) and increased the activities of superoxide dismutase (SOD) and catalase (CAT), and activated the Nrf2/Keap1 signaling pathway by downregulating Keap1 and upregulating HO‐1 and NQO1, suggesting that GEP may ameliorate aging by reversing oxidative stress imbalance. GEP also significantly decreased the levels of pro‐inflammatory factors tumor necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), and interleukin‐6 (IL‐6) in both serum and brain tissue, which may be the result of the alleviation of chronic inflammation by the inactivation of the TLR4/NF‐κB pathway. Furthermore, our results revealed a significant association between GEP‐mediated gut microbial remodeling and its neuroprotective phenotypes. GEP normalized aging‐induced gut dysbiosis, recovered microbial diversity, restored the abundance of beneficial genera including Akkermansia and Lactobacillus , and elevated intestinal tight junction proteins ZO‐1 and occludin. Such intestinal improvements may partially contribute to GEP's anti‐aging capacity through the gut–brain axis, though definitive causal evidence such as fecal microbiota transplantation is lacking in the present study. Collectively, these findings provide a theoretical foundation for the development and application of GEP‐based functional products targeting aging intervention.

Gastrodia elata is not only a traditional Chinese medicine but also a food raw material. Gastrodia is very perishable, and its effective constituents decrease significantly. N ‐Acetyl‐5‐methoxytryptamine (melatonin) is widely used in the preservation of various fruits and vegetables after harvest. In this study, the optimal melatonin treatment concentration and duration (0.2 mM MT immersed for 3 min) were determined to effectively delay the weight loss rate, decay rate, and disease severity index of Gastrodia . Immersion of Gastrodia tubers with 0.2 mM MT for 3 min could delay the degradation of gastrodin (GAS), 4‐hydroxybenzyl alcohol (4‐HBA), balisside A (PA), balisside B (PB), balisside C (PC), and Gastrodia polysaccharide (GEF) during storage. This method can inhibit hydrogen peroxide (H ₂ O ₂ ), superoxide anion (O ₂ • ^- ), and malondialdehyde (MDA); improve the radical clearance of (O ₂ • ^- , OH•, and DPPH) during storage; and enhance the activities of key enzymes in the ascorbic acid–glutathione (AsA‐GSH) cycle, leading to improved regeneration of ascorbic acid (AsA) and glutathione (GSH). Melatonin treatment also increased the activities of antioxidant enzymes, such as catalase (CAT) and superoxide dismutase (SOD); decreased the activity of peroxidase (POD); and enhanced the scavenging ability of reactive oxygen species (ROS). In addition, exogenous melatonin treatment increased endogenous melatonin content, thereby regulating the aging process of Gastrodia .