Abstract: Objective　To explore the characteristics and molecular mechanisms of dynamic changes in ovarian function during natural aging in mice. Methods　Eighteen female ICR mice of 2, 6, 10 and 14 months of age (referred to as 2M, 6M, 10M, and 14M) were included. The estrous cycle, ovarian index, pregnancy rate and embryo number were detected. The number of follicles was observed using HE staining. Serum anti-Müllerian hormone (AMH) levels were measured using ELISA. Protein and mRNA expression of P16, P21, proliferator-activated receptor-γ coactivator-1α (PGC-1α), and mitochondrial transcription factor A (TFAM) were detected through IHC and qPCR, respectively, and the protein expression of PGC-1α and TFAM was detected by Western blot. Relationships between indicators were evaluated based on Spearman’s rank correlation coefficients and logistic regression analyses. Results　Compared with estimates in the 2M group, the percentage of estrous cycle disorders (P<0.05 in 10M group, P<0.01 in 14M group), ovarian index (P<0.05 in 10M group, P<0.01 in 14M group), serum AMH level (P<0.01 in 10M group, P<0.01 in 14M group), number of embryos (P<0.01 in the 10M group, P<0.01 in 14M group), and pregnancy rate (P<0.01 in 14M group) were significantly lower; the number of follicles at all levels and total number of follicles were lower (all P<0.01), and the number of atretic follicles (all P<0.01) was higher. Furthermore, P16 and P21 mRNA (P16: P<0.01 in 10M and 14M groups; P21: P<0.05 in 10M group, P<0.01 in 14M group) and protein levels (P16: P<0.01 in each group; P21: P<0.01 in 10M and 14 M groups) were elevated. Spearman’s correlation analyses showed that the age in months was negatively correlated with the ovarian index, serum AMH level, primordial follicle number, number of embryos, and expression of PGC-1α and TFAM and positively correlated with the expression of atretic follicle, P16 and P21 (all P<0.01). Logistic regression analysis revealed a significant negative correlation between the age in months and pregnancy rate (P<0.01). PGC-1α mRNA was significantly decreased (all P<0.01), and TFAM mRNA was significantly decreased in 10M and 14M groups (P<0.01). PGC-1α levels were significantly decreased in the 10M group (IHC: P<0.05; Western blot: P<0.01) and 14M group (all P<0.01); TFAM levels were significantly lower in 6M, 10M, and 14 M groups than in the 2M group (IHC: P<0.01; Western blot: P<0.01). Compared with the 2M group, expression levels of PGC-1α and TFAM were positively correlated with the ovarian index and serum AMH level and negatively correlated with P16 and P21 expression (all P<0.01). Conclusions　Ovarian function in mice declines progressively with age in months, as reflected by reductions in follicles and fertility and the up-regulation of aging markers, which may be associated with the decreased expression of the mitochondrial biogenesis factors PGC-1α and TFAM.

Abstract: Objective　To investigate the effect of leucine carboxyl methyltransferase 1 (LCMT1) knockout on fructose-induced lipid deposition in primary mouse hepatocytes. Methods　Primary hepatocytes were isolated from wild-type (WT) and hepatocyte-specific LCMT1 knockout (KO) mice via a two-step hepatic portal vein perfusion method. The cells were divided into four groups: WT-control group, WT-fructose group, KO-control group, and KOfructose group. Cell viability was determined through Alamar-Blue assays. Hepatocyte injury was evaluated based on alanine aminotransferase and aspartate aminotransferase levels. Lipid deposition was visualized via Oil Red O staining and lipid droplet green fluorescence staining, and the cellular triglyceride content was quantified via a GPO-POD assay. The mRNA expression of lipid metabolism-related genes was detected via quantitative real-time PCR, and the protein expression of LCMT1 and PP2Ac was detected via Western blot. Results　Fructose treatment did not alter cell viability significantly in any group, and no significant cell damage was observed (P>0.05). The WT-fructose group exhibited greater accumulation of lipid droplets in hepatocytes than that in the WT-control group (P<0.001), with significantly elevated triglyceride contents (P<0.05). The mRNA levels of the de novo lipid synthesis genes ChREBP, SREBP-1c, and ACC1 were increased significantly (P<0.05, P<0.001, P<0.001), whereas FAS expression did not differ significantly between groups (P>0.05). The mRNA levels of the lipid uptake genes FABP1 and FATP2 also increased significantly (both P<0.05). In contrast, the KO-fructose group presented a reduced number of lipid droplets (P<0.01, P<0.001), decreased triglyceride content (P<0.05), and decreased mRNA levels of ChREBP, SREBP-1c, ACC1, FABP1, and FATP2 (P<0.01, P<0.001, P<0.001, P<0.001, P<0.05); CPT1 mRNA levels were markedly increased (P<0.01). Total PP2Ac expression was significantly higher (P<0.05) and PP2Ac demethylation was significantly lower (P<0.01) in the WT-fructose group than in the WT-control group. In the KO-control group, total PP2Ac expression remained unchanged (P>0.05), whereas PP2Ac demethylation was markedly elevated (P<0.001). Compared with levels in the WT-fructose group, the KO-fructose group presented markedly lower total PP2Ac expression and significantly higher PP2Ac demethylation levels (P<0.05, P<0.01, respectively). Conclusions　LCMT1 knockout alleviates fructose-induced lipid deposition in primary hepatocytes by inhibiting lipid uptake, increasing fatty acid oxidation, and downregulating de novo lipid synthesis. These effects are medicated by the LCMT1 knockout-mediated upregulation of PP2Ac demethylation, thereby modulating PP2A activity.

Abstract: Objective　To investigate the effects and underlying mechanisms of Shexiang Baoxin pill (SBP) on wire injury-induced valvular dysfunction in rats. Methods　A rat model of aortic valve injury was established using a standardized wire injury method. Animals were randomly divided into control, sham, model, and SBP low-, medium-, and high-dose (SBP-L, SBP-M, SBP-H) intervention groups. Aortic valve function was evaluated using echocardiography. Histopathological changes were assessed using hematoxylin-eosin (HE) and Masson’s staining. Serum levels of lipid peroxides (LPO), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and total iron were measured using biochemical assays. Expression levels of ferroptosis-related proteins (ACSL4, SLC7A11, and GPX4) and osteogenic markers (RUNX2 and BMP2) in valve tissues were detected through Western blot and RT-qPCR. Results　The SBP-M and SBP-H groups showed significantly higher aortic valve orifice areas ((3.70±0.04) mm² and (3.90±0.11) mm² vs (2.25±0.37) mm², P<0.0001), lower transvalvular pressure gradients ((0.52±0.09) mmHg and (0.49±0.13) mmHg vs (0.90±0.17) mmHg, P<0.01), and lower aortic valve peak flow velocities ((68.83±4.98) cm/s and (63.61±11.43) cm/s vs (87.14±11.22) cm/s, P<0.05, P<0.01) than those in the model group. HE and Masson’s staining result demonstrated that SBP alleviates valve thickening and fibrosis (fibrotic area: (35.98±5.2)5% vs (53.01±2.44)%, P<0.01). Biochemical tests showed that SBP reduces serum levels of lipid peroxidation products (LPO and MDA) and total iron ions while increasing SOD and GSH levels (P<0.001, P<0.0001). SBP downregulated the ferroptosis-related protein ACSL4 (P<0.01), upregulated the anti-ferroptosis proteins SLC7A11 and GPX4 (P<0.05, P<0.01), and inhibited the expression of the osteogenic molecules RUNX2 and BMP2 (P<0.05, P<0.01, P<0.0001). Conclusions　SBP may alleviate mechanical injury-induced valve dysfunction in rats through the modulation of oxidative stress and restoration of iron homeostasis. These findings provide experimental evidence for the role of SBP in the early intervention of valvular disease. The precise active components, molecular targets, and clinical translation of SBP require further investigation.

Abstract: Objective　To evaluate pulmonary vascular remodeling, right ventricular function, intestinal barrier integrity, and inflammatory factor expression in rat models of pulmonary hypertension (PH) induced by normobaric hypoxia (NH) and hypobaric hypoxia (HH). We also aimed to compare modeling method and establish an experimental basis for understanding the pathogenesis of PH and for developing appropriate treatment strategies. Methods　From June 2024 to December 2024, eighteen 6-week-old male SPF Sprague-Dawley rats were assigned randomly to three groups: normobaric normoxia (Control), NH, and HH groups. Mean pulmonary artery pressure (mPAP) was measured by right heart catheterization. Right ventricular function was assessed using echocardiography and right ventricular hypertrophy index (RVHI). Pulmonary vascular remodeling and intestinal mucosal barrier damage were evaluated via hematoxylin/eosin staining. Colon permeability was quantified by colon ligation followed by fluorescein isothiocyanate-dextran injection. Expression levels of inflammatory factors in lung and colon tissues were analyzed by enzyme-linked immunosorbent assays. Results　Right heart function assessment revealed that mPAP was significantly increased (P<0.05), pulmonary artery acceleration time (PAAT) was shortened, and RVHI and right ventricular free wall thickness (RVFW) were significantly elevated (P<0.05) in rats in NH and HH groups compared with Control group. Rats in NH group demonstrated a prolonged pulmonary ejection time (PET) and reduced PAAT/PET ratio compared with HH group, indicating more pronounced right heart dysfunction. Pulmonary vascular morphology demonstrated that percentage of medial area percentage (MA%) and percentage of wall thickness percentage (WT%) of pulmonary vessels were significantly higher in NH and HH groups compared with Control group (P<0.05). Moreover, MA% was markedly increased in the NH group relative to the HH group (P<0.05), suggesting more severe pulmonary vascular remodeling in NH group. Regarding intestinal injury, rats in NH and HH groups exhibited shorter colon length, increased mucosal damage, and significantly increased permeability compared with Control group (P<0.05), while rats in HH group showed more prominent inflammatory cell infiltration compared with NH group, confirming intestinal mucosal barrier damage in both groups. In terms of inflammation, expression levels of interleukin (IL)6, IL1β, and IL17a were significantly elevated in lung and colon tissues from rats in NH and HH groups compared with Control group (P<0.05). Notably, expression levels of IL6 and IL1β in lung tissue and IL17a in colon tissue were significantly higher in NH group compared with HH group (P<0.05), while IL6 expression in colon tissue was relatively lower (P<0.05), indicating local inflammation in lung and colon tissues in both groups. Conclusions There are phenotypic differences between PH rat models induced by NH and HH, with respect to pulmonary vascular remodeling, right heart function, intestinal mucosal barrier injury, and the expression of inflammatory factors in lung and intestinal tissues. These result demonstrate that air pressure contributes to the pathogenesis and progression of PH. Different air pressures may affect the development of PH via distinct mechanisms, thereby offering critical insights into the pathological changes of PH, potential therapeutic strategies to mitigate disease progression, and the elucidation of inflammatory mechanisms underlying PH based on the lungintestine axis.

Abstract: Objective　To analyze the role and mechanism of PD-L1 in oral cancer metastasis based on TCGA and GEO databases. Methods　The expression characteristics and clinical significance of the PD-L1 in oral cancer were analyzed using the TCGA database. PD-L1 mRNA levels were detected by quantitative reverse transcription-polymerase chain reaction (RT-qPCR)in various oral cancer cell lines.CCK-8, scrath test, Transwell migration, and matrigel-invasion assays were employed to assess the effects of PD-L1 on proliferation, migration, and invasion of oral cancer cells. The interaction network between PD-L1 and functional genes in patients with oral cancer was constructed using STRING software and the GEO database, and key pathways were screened by Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis.The regulatory relationship between PD-L1 and key genes was validated by RT-qPCR. Results　TCGA data revealed that PD-L1 was highly expressed in patients with oral cancer and was correlated with lymph node metastasis (P<0.01). PD-L1 was also highly expressed in oral cancer cell lines and its inhibition significantly inhibited the proliferation, migration, and invasion of Cal27 and SCC25 cells (P<0.05). KEGG analysis indicated that PD-L1 activated the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway by upregulating C-X-C motif chemokine ligand (CXCL) 9 and CXCL10, thereby promoting STAT1 expression to regulate oral cancer metastasis. Inhibition of the JAK/STAT pathway further suppressed the proliferation, migration, invasion, and expression of STAT1, CXCL9, and CXCL10 in Cal27 and SCC25 cells (P<0. 05). Conclusions　PD-L1 may promote oral cancer cell proliferation, migration, and invasion by upregulating CXCL9 and CXCL10 to regulate the JAK/STAT pathway and enhance STAT1 expression, ultimately driving oral cancer growth and metastasis.

Abstract: Objective　This study aimed to investigate how β-glucosidase (GBA) knockdown affects malignant progression in cisplatin (DDP)-resistant ovarian cancer (OC) cells and the role of the EGFR signaling pathway. Methods　The A2780/DDP cells were categorized into four groups, with one of them serving as blank control (Con) group, si-NC group (transfected with negative control si-NC), si-GBA group (transfected with si GBA), and NSC 228155 group (transfected with si-GBA and treated with 2 μmol/L NSC 228155). The protein expression levels of GBA, E-cadherin, N-cadherin, Vimentin, EGFR, p38 mitogen-activated protein kinase (p38 MAPK), phospho (p)-p38 MAPK, extracellular regulated protein kinase (ERK) and p-ERK were detected through Western blot. The relative expression of GBA was evaluated through reverse transcription quantitative polymerase chain reaction. The proliferation activity, migration, and invasion potential were evaluated using cell counting kit-8 (CCK-8), plate clone formation, cell scratch healing, and Transwell migration assays. Thirty-six nude mice were divided into six groups (six mice per group): blank control (injected with normal saline), blank control + DDP (treated with DDP), negative control (injected with A2780/DDP cell suspension transfected with si-NC), negative control + DDP (injected with A2780/DDP cell suspension transfected with si-NC and treated with DDP), knockdown (injected with A2780/DDP cell suspension transfected with si-GBA), and knockdown + DDP groups (injected with A2780/DDP cell suspension transfected with si-GBA and treated with DDP). The tumor volume and weight of nude mice were evaluated. Results　The relative protein and mRNA expression levels of GBA were significantly higher in the A2780/DDP group than in the A2780 group (P<0.05). Compared with estimates in the Con and si-NC groups, the proliferation activity, number of cloned cells, scratch repair rate, and number of transmembrane cells in the si GBA group were significantly lower (P<0.05). The abundance of E-cadherin expression exhibited a notable elevation (P<0.05), and expression levels of Vimentin, N-cadherin, and EGFR as well as the p-p38 MAPK/p38 MAPK and p-ERK/ERK ratios were significantly decreased (P<0.05). The proliferation activity, number of cloned cells, scratch repair rate, and the count of transmembrane cells and the expression level of E-cadherin in the NSC 228155 group were markedly higher and lower, respectively, than those in the si-GBA group (P<0.05), and the expression levels of Vimentin, N-cadherin, and EGFR as well as the ratios of p-p38 MAPK/p38 MAPK and p-ERK/ERK were significantly increased (P<0.05). In the nude mouse xenograft study, the tumor size and mass in the blank control + DDP group were notably smaller and lighter, respectively, compared to those in the blank control group (P<0.05). The tumor volume and weight were significantly lower in the negative control + DDP group than in the negative control group (P<0.05), significantly lower in the knockdown + DDP group than in the knockdown group (P<0.05), moreover, they were markedly reduced in the knockdown group in comparison to both the blank control and negative control groups (P<0.05). Compared with those in the blank control + DDP and negative control + DDP groups, the tumor volume and weight in the knockdown + DDP group were significantly reduced (P<0.05). Conclusions　GBA knockdown suppresses the proliferation, migration, and invasion of DDP-resistant OC cells significantly as well as the growth of subcutaneous xenografts derived from A2780/DDP cells in nude mice. These effects may be mediated through the inhibition of the EGFR/MAPK/ERK signaling pathway.

Abstract: Objective　To construct a model of knee osteoarthritis (KOA) through the co-culture of dorsal root ganglia (DRG) and fibroblast-like synoviocytes (FLSs). To investigate the effects of transient receptor potential vanilloid type 1 (TRPV1) desensitization of sensory neurons induced by mechanical stimulation, including the alleviation of the FLSs inflammatory response. Methods　DRG neuronal cells were identified through immunofluorescence. The stress loading of DRG neurons was realized using the FX-6000T cell stress system, and the effect of mechanical strain on the activity of DRG neurons was measured using the CCK-8 method. Ca²⁺ ion flux in DRG neurons was studied through flow cytometry. A Transwell chamber and FLSs were used to establish a co-culture system. The contents of the pro-inflammatory factors IL-1β, TNF-α, and TGF-β in the supernatant were determined by ELISA. Gene and protein expression levels of TRPV1 and its desensitizing negative regulatory proteins PP2B, CaM, IL-1β, TNF-α, TGF-β, and α-SMA in DRG neurons were evaluated using RT-qPCR and Western blot, respectively. Results　The Ca²⁺ ion flux in DRG neurons increased under inflammatory conditions, and low intensity (sinusoidal, 2%, 1 Hz, 6 h) thumb-pressing-induced mechanical stimulation did not alter Ca²⁺ ion flux (P>0.05). However, middle intensity (sinusoidal, 4%, 1 Hz, 6 h) and high intensity (sinusoidal, 8%, 1 Hz, 6 h) stimulation increased Ca²⁺ ion flux significantly (P<0.05). Notably, high intensity stimulation did not lead to a further increase in Ca²⁺ ion flux over that for middle intensity stimulation (P>0.05). There was no significant effect of low intensity stimulation on TRPV1, PP2B, or CaM gene or protein expression in DRG neurones, on IL-1β, TNF-α, or TGF-β concentrations in the supernatant of co-cultured cells, or on IL-1β, TNF-α, TGF-β, or α-SMA gene or protein expression in FLSs (P>0.05).Middle and high intensity mechanical stimulation up-regulated TRPV1 at the gene and protein expression levels in DRG neurons in the inflammatory group (P<0.05) but down-regulated PP2B and CaM at the gene and protein expression levels(P<0.05). Middle and high intensity mechanical stimulation decreased IL-1β, TNF-α, and TGF-β levels in the supernatants of co-cultured cells (P<0.05) and decreased the gene and protein expression levels of IL-1β, TNF-α, TGF-β, and α-SMA in FLSs (P<0.05). Conclusions　Middle and high intensity thumb-pressing-induced mechanical stimulation induced TRPV1 desensitization of rat sensory neurons, reduced the release of pain mediators, and suppressed the FLSs inflammatory response through downregulating IL-1β, TNF-α, and TGF-β.

Abstract: Objective　To establish a model of indirectly induced respiratory tract infection with influenza A subtypes H1N1 and H3N2 in animals, to screen influenza virus hosts, and to provide theoretical support for the clinical control of influenza viruses. Methods　Fifty BALB/c mice and 50 Hartley guinea pigs were randomly divided into five groups (10 animals/group for each species): normal control group, virus infects 1 group, virus infects 2 group, close transmission 1 group, and close transmission 2 group. Mice and guinea pigs in virus infects 1 and 2 groups were administered influenza A (H1N1) and influenza A (H3N2) viruses via nasal drip. For both virus infects 1 and 2 groups, animals were housed together with those in the close transmission group at a 1 ∶ 1 ratio on the following day. On day 7, the lung function, viral titer and viral load of the nasal tissue, trachea, and lung tissue of each group were measured, and pathological changes of the trachea and lung tissue of animals in the close transmission group were evaluated. Results　In mice, the viral titers and viral loads of nasal, tracheal, and lung tissues of virus infects 1 and 2 and the closely transmitted groups 1 and 2 were significantly higher (P<0.01), pathological scores of the trachea and lung tissues were significantly higher (P<0.01), and the FVC and FEV₂₀ of virus infects 1 and 2 groups were significantly lower (P<0.01) than those in the normal control group. The nasal tissue, trachea and lung tissues of guinea pigs in virus infects 1 and 2 groups and close transmission groups 1 and 2 showed significantly higher viral titers and viral loads (P<0.01), significantly higher trachea and lung histopathological scores (P<0.01), and significantly lower FVC and FEV₂₀₀ (P<0.01) than those of the normal control group. Conclusions　In this study, influenza A subtypes H1N1 and H3N2 were used to indirectly induce respiratory tract infections in mice and guinea pigs for analyses of animal lung function, respiratory viral titers, viral load, and pathology. The animal models of the indirect transmission of influenza viruses in the respiratory tract had certain limitations; for example, influenza viruses were transmitted less efficiently among mice than among guinea pigs. The guinea pig model was stable. These findings confirm that guinea pigs are suitable hosts for efficient virus replication and transmission.

Abstract:Animal models of cardiac arrhythmia are important tools for analyses of antiarrhythmic drug mechanisms and medical laboratory teaching. In this study, two major models, namely, barium chloride-induced arrhythmia in rabbits and ouabain-induced arrhythmia in guinea pigs, were systematically compared in terms of technical principles, modeling method, and indexes. By optimizing electrocardiographic parameters, standardizing arrhythmia grading criteria, and introducing quantitative analysis method, we revealed differences between the two models in terms of ion channel mechanisms, drug targets, and applicability to teaching. The barium chloride model was characterized by rapidly induced ventricular arrhythmia, which is suitable for the observation of acute drug efficacy. The ouabain model simulated the development of progressive arrhythmia, which is suitable for the study of the preventive effects of anti-arrhythmic drugs. This study provides a technical reference for the selection of arrhythmia models, optimization process, and mechanistic analyses in medical experimental teaching and is of great significance for improving the electrophysiology experimental skills of medical students.

Abstract:Alzheimer’s disease (AD) is a typical progressive neurodegenerative disease, mainly manifesting as severe cognitive dysfunction, and involving memory, thought processes, and emotion. The kynurenine pathway (KP) is one of the main metabolic pathways of tryptophan, which can be divided into neurotoxicity and neuroprotective branches. Increasing evidence has suggested that KP is involved in the pathogenesis of AD. This review considers the role of KP in the pathogenesis of AD, with reference to the relevant literature on KP interventions in AD in the PubMed database. The result will provide an important reference for the use of KP as a target for AD drug development.

Abstract:With population aging worldwide, Alzheimer’s disease (AD) has become a serious human health issue. Owing in part to the complexity of the pathogenesis of AD, effective therapeutic options are lacking. Mesenchymal stem cell-derived exosomes (MSC-Exos) have powerful regenerative properties and repair functions, providing a new direction for treatment. They are donor-derived, easily stored, natural carriers, with low immunogenicity and a low risk of tumor formation. They have shown great potential in the treatment of AD and post treatment rehabilitation. This article introduces the pathological mechanisms of AD and characteristics of MSC-Exos, provides a detailed review of the roles of MSC-Exos in the treatment of AD, including anti-inflammatory effects,immunomodulatory effects, and related signaling pathway modulation, and summarizes recent research progress, with the aim of providing a basis for the development of novel therapeutic approaches to AD.

Abstract:Neural remodeling is the key to neurological recovery after intracerebral hemorrhage (ICH). The early stage of stroke is a sensitive period for brain plasticity, during which the brain initiates complex processes such as neurogenesis, synaptic remodeling, and angiogenesis to promote collateral circulation and achieve structural and functional remodeling. Acupuncture, as a critical traditional Chinese medicine approach for treating brain disorders, has demonstrated significant efficacy in promoting neurological recovery after ICH in both clinical and experimental studies; however, systematic reviews of the mechanisms by which acupuncture regulates neural remodeling after ICH remain limited. This review thus provides a multi-dimensional summary of the mechanisms by which acupuncture facilitates neural remodeling after ICH, including (1)promoting neurogenesis and synaptic remodeling; (2) modulating the damaged microenvironment; (3)optimizing neuroelectrophysiology; (4)improving hemodynamics; (5)facilitating angiogenesis. This review systematically summarizes these mechanisms to highlight the therapeutic potential of acupuncture and advance its further research and application in the field of neuroscience.

Abstract:Parkinson’s disease (PD), the second most common neurodegenerative disorder, involves dopaminergic neuron degeneration, abnormal α-synuclein aggregation, and energy metabolic disruption. AMP activated protein kinase (AMPK), a key cellular energy metabolic regulator, has multiple roles in PD progression. This paper explores the structure and function of AMPK and its regulatory mechanisms in PD, including its roles in modulating neuronal energy metabolism, mediating mitochondrial function, inhibiting oxidative stress, inducing autophagy, and regulating neuroinflammation and apoptosis. Potential AMPK-based PD therapies are also reviewed, including natural products (e.g., resveratrol, curcumin), gene therapy, and targeted delivery systems, while noting the need to precisely control the dual effects of AMPK (e.g., overactivation causes energy stress). Future research should focus on clarifying interactions between AMPK and other pathways (e.g., SIRT1 and NF-κB) and improving the spatiotemporal specificity of targeted treatments for clinical translation. This study offers crucial theoretical support for understanding mechanisms underlying PD and developing AMPK-targeted therapies.

Abstract:Homing pigeons and many other animals have exquisite geomagnetic sensing ability and can accurately find appropriate paths and directions during long-distance migration. Homing pigeons are the preferred animal model for studies of biological geomagnetic navigation. Despite substantial progress in research on bio geomagnetic navigation over the past few decades, the biological mechanism is still unclear. In this paper, we review recent advancements in research on biological magnetoreception using homing pigeons. We focus on the magnetic sensing mechanisms of the magnetoreceptor models based on nanoscale ferromagnetic particles and the light-dependent radical pair model. Key directions for biological magnetoreception research are proposed. This review provides an improved theoretical basis for the study of geomagnetic navigation using homing pigeons as well as insight into the operating principles of the biological magnetic perception system.

Abstract:Parkinson’s disease (PD) is a common progressive neurodegenerative disease mainly affecting the motor system. Various genetic factors and cellular mechanisms underlying PD have recently been discovered. Emerging evidence suggests that epigenetic modifications play a very important role in the pathogenesis, prevention, and treatment of PD. Epigenetic modification mediates genetic and environmental interactions mainly through complex interactions of DNA methylation, histone modification, and non-coding RNA, thereby affecting expression in the absence of changes in DNA sequence. In this review, we summarize the epigenetic modification mechanisms involved in the pathogenesis of Parkinson’s disease. In this review, we summarize the epigenetic modification mechanisms involved in the pathogenesis of Parkinson’s disease.Recent studies have found that traditional Chinese medicine can participate in the regulation of abnormal epigenetic modifications in the treatment of PD. Traditional Chinese medicine benefits from its multi-level and multi-target regulatory effects, and various traditional Chinese medicine monomers, compound prescriptions, and techniques have been evaluated, confirming that this is a promising approach for improving symptoms in PD. This review summarizes the mechanisms by which epigenetic modifications contribute to PD, explores the role of traditional Chinese medicine, and provides new ideas for clinical treatment and drug development in PD through epigenetic intervention.

Abstract:Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide, characterized primarily by cognitive impairment and memory dysfunction. Its pathological mechanisms involve the toxic accumulation of amyloid β-protein (Aβ), hyperphosphorylation of Tau protein leading to neurofibrillary tangles, mitochondrial dysfunction, synaptic impairment, cholinergic system dysfunction, neuroinflammation, and oxidative stress. Current clinical treatments for AD include acetylcholinesterase inhibitors and N-methyl-D-aspartate antagonists, which can improve cognitive function but fail to slow disease progression and often have side effects. Research indicates that traditional Chinese medicine (TCM) may regulate the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, promoting neuronal survival, inhibiting neuroinflammation, reducing oxidative stress, preventing apoptosis, and decreasing Aβ deposition, thus improving the symptoms of AD. This review summarizes the mechanisms by which individual TCM components, extracts, and formulas may regulate the PI3K/AKT pathway in the treatment of AD, with the aim of providing a theoretical foundation for the application of TCM in AD therapy.