Biomedical subjects

Xiaohong Chen

Publications and source records attributed to Xiaohong Chen.

3 recordsLinked to original sources

PubMed2026

Puerarin Attenuates Binge Ethanol-Induced Cortical Neurotoxicity in Association with AKT/mTOR Signaling and Autophagy-Related Responses.

Puerarin (Pue), a major isoflavone derived from Pueraria lobata, has demonstrated neuroprotective potential in multiple neurological disorders; however, its effects on ethanol (EtOH)-induced cortical injury and the associated molecular responses remain incompletely understood. In the present study, network pharmacology was combined with in vivo and in vitro experiments to investigate molecular responses associated with the effects of Pue on EtOH-induced neurotoxicity. Public databases were used to predict targets of Pue and alcohol-related brain injury, followed by protein-protein interaction analysis, Gene Ontology annotation, and Kyoto Encyclopedia of Genes and Genomes pathway enrichment. A total of 101 overlapping targets were identified, among which TNF, AKT1, EGFR, TP53, and PPARG emerged as major hub targets, and PI3K-Akt signaling pathway was among the pathways that remained significantly enriched after FDR correction. In a 4-day binge EtOH rat model, Pue attenuated EtOH-associated increases in oxidative stress, neuronal degeneration, and apoptotic markers in cortical tissue. This was accompanied by attenuation of the EtOH-associated reductions in the p-AKT/AKT and p-mTOR/mTOR ratios, as well as an attenuation of EtOH-associated changes in LC3, ATG5, and Beclin-1 expression. In primary cortical neurons, Pue partially attenuated the EtOH-associated loss of neuronal viability and preserved neurite morphology. Bafilomycin A1 (BafA1)-based analysis of LC3-II and p62/SQSTM1 showed an overall BafA1-sensitive increase in LC3-II without a significant treatment-dependent difference in the BafA1 response. Collectively, these findings suggest that Pue attenuates binge EtOH-induced cortical neurotoxicity in association with changes in AKT/mTOR phosphorylation and autophagy-related responses.

AKT/mTOR signaling↗

PubMed2026

Multi-omics unveils seasonal remodeling and metabolic crosstalk between testis and abdominal fat body in a non-amplexus stream frog Nanorana taihangnica (Anura: Dicroglossidae).

BACKGROUND: Energy allocation between reproduction and survival represents a fundamental life-history challenge for animals in seasonal environments. Using integrated transcriptomics and metabolomics, we investigated Nanorana taihangnica (Anura: Dicroglossidae), a non-amplexus stream frog endemic to China, to elucidate the seasonal morphological and molecular coordination between the testis and abdominal fat body. RESULTS: Morphological analysis showed that fat body adipocyte cross-sectional area minimized at the end of the breeding season but rapidly recovered thereafter, while testicular volume continued declining post-breeding and only recovered during the non-breeding period. During breeding season, multi-omics analyses revealed that the fat body enhanced fatty acid oxidation, upregulated histidine-carnosine metabolism, activated NAD+ metabolism and FOXO3-mediated antioxidative responses to mitigate metabolic stress, and regulated adipocyte survival and apoptosis via sphingolipid signaling. Seasonal testicular development was centrally regulated by the mTOR signaling pathway, whose activity integrated autophagy levels, NAD+ availability, and aspartate metabolism to coordinate spermatogonial proliferation and spermatogenesis. CONCLUSIONS: This study demonstrates that N. taihangnica optimizes seasonal energy storage, allocation, and reproductive investment through molecular and metabolic crosstalk between the fat body and testis, providing empirical insights into the physiological integration of life-history strategies in animals inhabiting fluctuating environments.

Animals↗

PubMed2025

Strain-Promoted mRNA Transdermal Delivery by Lipoic Lipid Nanoparticles for Therapeutic Skin Genome Editing.

Lipid nanoparticle (LNP)-mRNA formulations have revolutionized the field of nucleic acid therapeutics, yet their broader clinical application is constrained by inflammatory side effects and oxidative stress, particularly in the context of inflammatory diseases. Herein, we report the rational design and synthesis of a lipoic acid-based ionizable lipid library to address these limitations. By leveraging the antioxidant properties and thiol-mediated uptake potential of lipoic acid, we identified LA-A2B2CD3 as an optimal candidate through a structure-activity relationship study and design of experiment (DOE) optimization. LA-A2B2CD3 LNPs exhibited superior reactive oxygen species scavenging, enhanced mRNA translation, and reduced inflammatory cytokine production in vitro and in vivo. Mechanistic studies revealed that the efficient cellular uptake and the transdermal delivery capacity of LA-A2B2CD3 heavily rely on the reducible disulfide ring of lipoic acid. Application of LA-A2B2CD3 LNPs for the localized transdermal delivery of Cas9 mRNA and CD93 sgRNA in a murine model of psoriasis resulted in effective CD93 genome editing and the inhibition of the CD93-p38 MAPK-AKT-SMAD2/3 pathway, leading to significant therapeutic improvement. This work presents a robust, biocompatible LNP platform with minimized immunogenicity and strong potential for genome-editing therapies in inflammatory conditions, offering a transformative approach for the mRNA-based treatment of skin and other inflammation-related disorders.

Animals↗