Major depressive disorder (MDD) involves multifaceted pathologies including neurotransmission, neuroplasticity, inflammation, and hypothalamic-pituitary-adrenal (HPA) axis dysfunction. Growing evidence implicates zinc homeostasis imbalance in MDD, yet a systematic framework integrating it into these mechanisms is lacking. This narrative review synthesizes literature (2000-2024) to elucidate the multidimensional associations between zinc homeostasis and MDD pathology, focusing on zinc's roles in neurotransmitter regulation, BDNF signaling, inflammation, oxidative stress, and HPA axis activity. Epidemiological studies indicate an inverse correlation between serum zinc levels and MDD. Mechanistically, zinc imbalance may disrupt neural signaling via glutamate/GABA/5-HT receptors, impair neurotrophy via BDNF, exacerbate neuroinflammation and oxidative stress, and promote HPA axis hyperactivity. Zinc supplementation shows efficacy in mild-to-moderate MDD and augments conventional antidepressants, especially in treatment-resistant cases. Novel targets like GPR39 and zinc transporters, along with brain-targeted formulations, offer promising therapeutic avenues. Zinc homeostasis is critically involved in MDD's heterogeneous pathology, making it a promising target for precision treatment. However, this potential is tempered by inconsistent data and methodological limitations. Future research should prioritize: standardizing assessment methods; investigating brain region-specific zinc dynamics; developing novel targeted formulations; and exploring gene-environment interactions in zinc signaling.

Ant-pathogenic fungi are mainly found in the Ophiocordycipitaceae, rarely in the Cordycipitaceae. During a survey of entomopathogenetic fungi from Southwest China, a new species, Cordyceps yinjiangensis, was isolated from the ponerine. It differs from other Cordyceps species by its ant host, shorter phialides, and smaller septate conidia formed in an imbricate chain. Phylogenetic analyses based on the combined datasets of (LSU+RPB2+TEF) and (ITS+TEF) confirmed that C. yinjiangensis is distinct from other species. The new species is formally described and illustrated, and compared to similar species.

Objective: To investigate the anti-inflammatory effects and underlying mechanisms of LCS2, the active fraction of litchi seed extract, against lipopolysaccharide (LPS)-induced prostatitis. Methods: LCS2 was isolated from litchi seed extract through extraction, purification and anti-inflammatory activity screening, and its chemical components were identified via UPLC-Q-TOF-MS/MS. The anti-inflammatory activity of LCS2 and its regulatory effects on NF-κB/MAPK signaling pathways were evaluated in LPS-stimulated RAW264.7 macrophages and a LPS-induced rat prostatitis model using molecular biological assays. Results: A total of 26 compounds, mainly flavonoids, polyphenols and tannins, were identified in LCS2. In vitro, LCS2 significantly inhibited LPS-induced production of nitric oxide (NO), reactive oxygen species (ROS) and pro-inflammatory cytokines. In vivo, LCS2 ameliorated pathological damage of rat prostate tissue, reduced white blood cell and neutrophil counts, downregulated pro-inflammatory factor levels, and suppressed phosphorylation of key molecules in NF-κB and MAPK pathways as well as nuclear translocation of NF-κB p65. Conclusion: LCS2 exerts significant anti-prostatitis activity both in vitro and in vivo, providing experimental evidence for the medicinal development of litchi seeds and the research of natural anti-prostatitis agents.

Litchi seed is a major by-product of the litchi processing industry, rich in polyphenols and flavonoids with documented anti-inflammatory properties. Prostatic inflammatory injury remains a prevalent male health concern, and dietary intervention with natural bioactive components represents a promising strategy for prostate health maintenance. This study investigated the protective efficacy of LCS2, a bioactive fraction isolated from litchi seed by-product, against lipopolysaccharide (LPS)-induced prostatic inflammatory injury in rats and explored its underlying mechanisms. LCS2 was obtained via extraction, purification, and activity screening, and its chemical profile was characterized by ultra-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry (UPLC-Q-TOF-MS/MS). Its anti-inflammatory activity and pathway regulatory effects were evaluated in LPS-stimulated RAW264.7 macrophages and further verified in a rat model of LPS-induced acute prostatic inflammation. A total of 26 compounds, mainly flavonoids, polyphenols, and tannins, were tentatively identified in LCS2. In vitro, LCS2 pretreatment with LCS2 at concentrations up to 40 μg/mL dose-dependently suppressed LPS-induced overproduction of nitric oxide (NO) and reactive oxygen species (ROS), reduced pro-inflammatory cytokine mRNA levels, and downregulated iNOS and COX-2 protein expression. In vivo, 7-day dietary pretreatment with LCS2 at doses up to 100 mg/kg ameliorated prostate histopathological injury, reduced peripheral inflammatory cell counts, and decreased inflammatory mediator levels in serum and prostate tissue by inhibiting NF-κB and MAPK pathway activation. These findings support the high-value valorization of litchi seed by-product and highlight the potential of LCS2 for further development as a bioactive component for prostate health applications.