Abstract: Objective　To investigate the regulation of synaptic plasticity by cannabinoid receptor 1 (CB1R) and its effects on autism spectrum disorder (ASD)-like behavior. Methods 　CB1R-knockout (KO) mice and valproic acid (VPA)-induced ASD model mice (VPA mice) were used as study subjects. Behavioral experiments were used to assess the effects of CB1R on ASD-like behavior in mice, neuronal structural integrity and dendritic density were detected by microtubule-associated protein 2 (MAP2) staining experiments, and the expression of synapse-associated proteins was detected by Western blot, to assess the effects of CB1R on synaptic plasticity. Results Behavioral result showed that VPA mice demonstrated significant ASD-like behavior, while CB1R^{-/ -} mice spent a significantly smaller proportion of residence time in the central region of the open field (P < 0. 0001), showed significant increases in the number of marbles buried and self-grooming time (P<0. 01), significantly less time spent socializing with unfamiliar mice 2 and exploring unfamiliar objects (P<0. 001), and significantly more time exploring old objects (P<0. 05). The relative dwelling time was significantly reduced in CB1R^{+/ -} mice (P<0. 001), and the number of marbles buried and self-grooming time were significantly increased (P<0. 05). Synaptic plasticity assays revealed significant synaptic plasticity impairment in VPA mice. Hippocampal MAP2-positive neuron densities were significantly reduced in CB1R^{-/ -} and CB1R^{+/ -} mice, and expression levels of synapsin-1 were significantly increased (P<0. 05). Conclusions 　CB1R KO leads to ASD-like behavior such as anxiety and repetitive stereotyped behavior,social and cognitive impairments, as well as neuronal damage, dendritic dysplasia and disrupted synaptic protein expression in mice, suggesting that CB1R is involved in regulating synaptic plasticity as a pathological mechanism for the development of ASD-like behavior.

Abstract: Objective　To explore the role of Erianin in atopic dermatitis (AD) and its regulatory mechanism involving the high-mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE)-Ras homolog gene family member A (RhoA)/Rho-associated protein kinase 1 (ROCK1) signaling pathway. Methods An AD model was induced in BALB/c mice using 1-chloro-2,4-dinitrobenzene (DNCB). Skin thickness and spleen and lymph node weight were measured and pathological changes in the back skin and ears were detected using methylamine blue and hematoxylin and eosin staining. Inflammatory factors were detected by enzyme linked immunosorbent assay. An in vitro model of AD was established in HaCaT cells stimulated by tumor necrosis factor (TNF)-α. Cellular reactive oxygen species (ROS) were detected by flow cytometry and mitochondrial ROS (mtROS) were detected by immunofluorescence assay. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling. HMGB1, RAGE, RhoA, and ROCK1 proteins were detected by Western blot. Results　Erianin inhibited the increase in skin thickness, reduced the spleen and lymph node weights, improved the infiltration of inflammatory cells and the degranulation of mast cells, and reduced the levels of inflammatory factors(P<0.05). Erianin also reduced the production of cellular ROS and mtROS induced by TNF-α in vitro(P<0.01), and decreased the protein expression of HMGB1, RAGE, RhoA, and ROCK1(P<0.01). Treatment of HMGB1stimulated HaCaT cells with a RAGE-specific blocker (TFA) had no effect on HMGB1 expression, while expression levels of RAGE, RhoA, and ROCK1 were decreased(P<0.01). Cells treated with the Rho kinase inhibitor Y-27632 +r-HMGB1 group showed similar result to the TFA+r-HMGB1 group, except for RAGE. Conclusions 　Erianin relieves AD by regulating the HMGB1/RAGE-RhoA/ROCK signaling pathway.

Abstract: Objective　To study the effect of Liangxue Tuizi Formula (LXTZF) on reactive oxygen species (ROS)-mediated NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome activation in Henoch-Sch?nlein purpura (HSP) rats, and to explore its possible mechanism in the treatment of HSP. Methods Twenty-four rats were divided randomly into four groups: control, model, LXTZF, and compound glycyrrhizin (CG) groups. Except for the control group, a model of HSP was established in the other groups by heat drugs combined with egg albumin. After successful modeling, rats in the LXTZF group were given LXTZF solution 7.47 g/kg, rats in the CG group were given CG solution 13.5 mg/kg by gavage, and rats in the control and model groups were given normal saline solution by gavage once a day for 4 weeks. Samples were collected 8 hours after the last gavage. Skin histopathology changes were observed by hematoxylin and eosin (HE) staining. Serum interleukin (IL)-18 and IL-1β levels were detected by enzyme-linked immunosorbent assay(ELISA). Changes in ROS levels in the skin were detected by immunofluorescence. Apoptosis-associated speckle-like protein (ASC), NLRP3, cysteinyl aspartate specific protease-1 (Caspase-1) mRNA and protein expression levels in rat skin were detected by real-time quantitative polymerase chain reaction (RT-PCR) and immunohistochemistry and Western blot, respectively. Results The skin pathology in the model group showed obvious inflammatory cell infiltration compared with the control group. Serum IL-18 and IL-1β levels were significantly increased (P<0.05), skin ROS levels were significantly increased (P<0.05), and skin ASC, NLRP3, Caspase-1 mRNA and protein expression levels were significantly increased (P<0.05). Inflammatory cell infiltration in the skin tissues of rats was alleviated in the LXTZF and CG groups compared with the model group, while serum levels of IL-18 and IL-1β were significantly decreased (P<0.05). ROS levels in the skin were significantly decreased (P<0.05), and mRNA and protein levels of ASC, NLRP3, and Caspase-1 in the skin were significantly decreased (P<0.05). Conclusions 　The mechanism of LXTZF in HSP may be related to the inhibition of ROS-mediated NLRP3 inflammasome activation.

Abstract: Objective　To investigate the neuroprotective effect of Dendrobium nobileLindl (DNL) extract in a Caenorhabditis elegans (C.elegans)model of Parkinson’s disease (PD). Methods　C. elegans NL5901 and 6 hydroxydopamine (6-OHDA)induced N2, BZ555, PD4521, and CB7272 C. elegans strains were treated with DNL 7.5, 15, and 30 mg/L. The survival rate, basal slowing response rate, α-synuclein (α-syn) aggregation, dopaminergic neurons (DNs), mitochondrial distribution density of body wall muscle cells, and protein levels in the membrane were observed. In addition, reactive oxygen species(ROS), superoxide dismutase(SOD) and glutathione (GSH) in 6-OHDA induced N2 was detected to explore the effect of DNL on the antioxidative stress ability of PD C. elegans models. Results　Compared with that in the model group, the DN fluorescence intensity was significantly increased in nematodes treated with DNL and levodopa(L-DOPA) (P<0.05, P<0.0001), α-syn aggregation was significantly decreased (P<0.05, P<0.001, P<0.0001), the basal slowing rate (P<0.05, P<0.01, P<0.001), mitochondrial density (P<0.05, P<0.01, P<0.001), mitochondrial intima protein content (P<0.05, P<0.001, P<0.0001), SOD content (P<0.05), and GSH content were all increased. The ROS content was reduced in nematodes(P<0.01). The lifespans of N2 wild-type and PD C. elegans models were prolonged after DNL treatment (P<0.05, P<0.01, P<0.001). Conclusions 　DNL can effectively improve motor paralysis in a C. elegans PD model, improve DN degradation, inhibit α-syn aggregation and neuronal damage, increase the antioxidative stress ability, and slow the aging process in C. elegans.

Abstract: Objective　To construct and evaluate a mouse model of renal fibrosis (RF) combined with Qi deficiency and dampness stasis, and investigate the changes in protein and metabolic pathways using multiomics. Methods　Twenty-four C57BL/6J mice were divided randomly into normal (N), model (M), and RF and syndrome combined groups (BZ) (n=8/group). The experiment lasted 6 weeks. A mouse model of RF with Qi deficiency and dampness stasis was established by “cyclosporine A+high-fat diet+swimming exhaustion+constant temperature and humidity”. The model was evaluated by detecting general signs, renal function, tongue RGB (red, green, blue) values, hemorheology indexes, blood lipids, and inflammation and oxidation indexes, combined with hematoxylin and eosin, Masson, periodic acid-Schiff, and Oil red O staining, terminal deoxynucleotidyl transferase dUTP nick end labeling apoptosis, and transforming growth factor-β immunofluorescence analysis of renal tissue. Differential proteins and metabolites were screened by renal proteomics combined with serum metabolomics and subjected to pathway enrichment analysis. Results　Body mass of mice in the BZ group began to decline at week 3 (P<0.05) and decreased significantly at week 4 (P<0.01), while food and water consumption decreased, the fur became messy and less glossy, mood and activity decreased, and stools became watery. Serum creatinine, blood urea nitrogen, urine albumin-creatinine ratio, and N-acetyl-beta-glucosaminidase (NAG) were significantly higher in the BZ group compared with those in the N group (P<0.05, P<0.01), and serum creatinine and NAG levels were significantly different compared with those in the M group. The R value of tongue images was significantly lower in the BZ group compared with that in the N group (P<0.01), while the B value was significantly higher (P<0.05). The viscosity of the whole blood multi-shear rate and the hematocrit were higher in the BZ group compared with those in the N and M groups, and the platelet volume was higher than in the N group (P<0.05, P<0.01). Total cholesterol, low-density lipoprotein cholesterol, C-reactive protein, interleukin-6, and malondialdehyde levels were significantly increased in the BZ group compared with those in the N and M groups (P<0.01), and superoxide dismutase activity was significantly decreased compared with that in the N group (P<0.05). Renal tubule vacuolation, inflammatory cell infiltration, glomerular basement membrane thickening, collagen fiber hyperplasia, and lipid accumulation were evident, and renal cell apoptosis and transforming growth factor-β deposition were increased in the BZ group. There were 299 differential proteins in the BZ and N groups, including 180 up-regulated and 119 down-regulated proteins, and 323 differential metabolites, including 205 up-regulated and 118 down-regulated. Primary bile acid biosynthesis, taurine and hypotaurine metabolism, and biosynthesis of unsaturated fatty acids were co-enriched in differential proteins and differential metabolites, involving three differential proteins and nine differential metabolites. Among these, docosapentaenoic acid (22n-3), eicosapentaenoic acid, taurine, 3-sulfinoalanine, taurocholic acid, Acnat1, Acnat2, and Hsd17b12 showed high prediction accuracy. Conclusions 　We successfully constructed an RF animal model of Qi deficiency and dampness stasis using the “cyclosporine A +high-fat diet+exhaustion of swimming+constant temperature and humidity” method. Biosynthesis of unsaturated fatty acids and taurine and hypotaurine metabolism may play important roles in this RF mouse model of Qi deficiency and dampness stasis.

Abstract: Objective　To investigate the protective effect and mechanism of Polygonatum sibiricum polysaccharides (PSP) on diabetic cardiomyopathy (DCM). Methods　Forty SPF-grade male Sprague-Dawley rats were divided randomly into Control, Model, PSP, and metformin groups. After 4 weeks of feeding a high-fat diet, streptozotocin was injected intraperitoneally to establish a rat model of diabetes mellitus. The drug was administered by gavage for 12 weeks, and body mass and blood glucose were recorded every 2 weeks. Cardiac function was detected by non-invasive echocardiography at week 16. Myocardial histopathological changes and the degree of myocardial fibrosis were assessed by hematoxylin and eosin and Masson staining. Serum interleukin (IL)-6, IL-1β, IL-18, tumor necrosis factor-α (TNF-α), triglycerides, total cholesterol, low-density lipoprotein, and high-density lipoprotein were detected by enzyme-linked immunosorbent assay. Expression levels of the fibrosis-related proteins transforming growth factor (TGF)-β1, Smad2, Collagen-Ⅰ, Collagen-Ⅲ, and the pyroptosis-related proteins NOD-like receptor thermal protein domain associated protein 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and Caspase-1 were detected in rat myocardial tissues by Western blot. Cellular experiments were performed by exposing H9c2 cells to high glucose (40 mmol/L) to mimic the in vitro DCM model, cell viability was detected by Cell Counting Kit-8 assay, and the apoptotic cell ratio was detected by flow cytometry. Results　Rats in the treatment group had significantly lower blood glucose, lipid, and serum inflammatory factor levels compared with the model group (P<0.05), significantly higher ejection fraction and fractional shortening values (P<0.05), and improved cardiac function. Myocardial fibers were better aligned and collagen fiber accumulation was reduced, and myocardial tissue levels of NLRP3, ASC, Caspase-1, Collagen-Ⅰ, Collagen-Ⅲ, TGF-β1, and Smad2 were significantly reduced (P<0.05). In the cellular assay, PSP increased the viability and decreased the proportion of apoptotic cells in high glucose-induced H9c2 cardiomyocytes. Conclusions 　PSP can improve glucose-lipid metabolism, protect cardiac function, and delay the occurrence of myocardial fibrosis in diabetic rats, and can also improve the viability of cardiomyocytes. Its mechanism of action may be related to the inhibition of cellular pyroptosis and delayed occurrence of ventricular remodeling.

Abstract: Objective　To investigate the role of cholinergic receptor muscarinic 3 (Chrm3) in regulating lipopolysaccharide (LPS)-induced inflammation in peritoneal macrophages in lipopolysaccharide binding protein (LBP)-knockout (Lbp^-/-) mice. Methods　Peritoneal macrophages were isolated from wild-type and Lbp^-/- mice to establish an LPS-induced inflammation model. Chrm3 expression in Lbp^-/- mouse peritoneal macrophages was inhibited by 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (4-damp) and small interfering (siRNA) and Chrm3 overexpression was achieved by lentivirus transfection. For 4-damp inhibition, cells were divided into control, LPS, and inhibitor groups, and for siRNA transfection, cells were divided into control, LPS, si-normal control group, and si-Chrm3 groups. For overexpression, cells were divided into control, LPS, negative control, and overexpression groups. Changes in Chrm3 in response to LPS stimulation were verified by Western blot. The effects of 4-damp, siChrm3, and lentivirus on cell inflammation and survival were confirmed by Cell Counting Kit-8, quantitative polymerase chain reaction, and Western blot assays. Results　Chrm3 protein expression was significantly elevated in Lbp^-/- peritoneal macrophages post-LPS stimulation (P<0.001), whereas there was no notable change in wild-type cells. The cell survival rate was significantly increased in the 4-damp and si-Chrm3 groups (P<0.05, P<0.01), and cell survival was significantly reduced in the overexpression group (P<0.01). Furthermore, 4-damp and si-Chrm3 significantly reduced expression levels of the inflammatory factors tumor necrosis factor (TNF)-α, interleukin (IL)1β, IL-6 (P<0.01, P<0.001), and phospho-extracellular signal-regulated kinase (p-ERK) (P<0.01, P<0.001), which are associated with cell damage and inflammation. In contrast, TNF-α, IL-1β, IL-6 (P<0.001), and p-ERK protein (P<0.001) were significantly elevated in the overexpression group. Conclusions 　LPS stimulation upregulated the expression of Chrm3 and proinflammatory cytokines in Lbp^-/- peritoneal macrophages. Specific downregulation of Chrm3 by 4-damp and si-Chrm3 significantly decreased LPS-induced proinflammatory cytokines in Lbp^-/- peritoneal macrophages, while upregulation of Chrm3 using overexpressing lentivirus significantly elevated the expression of related inflammatory factors. Chrm3 is implicated in the regulation of the LPS-induced inflammation response in peritoneal macrophages in Lbp-/- mice.

Abstract: Objective　To explore time-related changes in renal function, renal injury biomarkers, and renal pathology in rats entering a low-pressure and low-oxygen (LPLO) environment simulating moving from the plains to a plateau. Methods　Thirty male Sprague-Dawley rats were divided randomly into five groups (n=6 rats per group). Rats in the Control group were placed outside the chamber under normal pressure and oxygen conditions. Rats in the experimental groups were placed in an LPLO chamber to simulate a plateau environment at 5000 m above sea level, and were maintained in the chamber for 3, 7, 14, and 28 days, respectively. Serum levels of creatinine (CRE), cystatin C (CysC), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and interleukin-18 (IL-18) were measured as biomarkers of renal injury. Pathological changes in the kidney were observed by hematoxylin and eosin and periodic acid-Schiff staining, with quantitative assessment of the following parameters: average glomerular diameter, peritubular capillary (PTC) density per tubule, tubular injury score, and outer medulla (OM) congestion score. Results　NGAL, KIM-1, CysC, and CRE were significantly increased in the experimental compared with the Control group (all P<0.05). The average glomerulus diameter was significantly reduced in the LPLO 3 d group and significantly increased in the LPLO 14 d group (both P<0.05). The peritubular capillary (PTC)/tubule ratio was significantly decreased. The renal tubular injury and OM congestion scores were significantly increased (both P<0.05). Regression analysis showed that PTC/tubule was linearly negatively correlated with the LPLO duration, while CRE, CysC, and pathological indicators (mean glomerular diameter, OM congestion score, renal tubular injury score) were curvilinearly correlated with the duration of LPLO (all P<0.05). Variables with a curvilinear correlation were analyzed using restricted cubic splines(RCS). Each curve exhibited an inverted-L shape, with inflection points on day 7, indicating that the rate of increase of all indicators was highest within the first 7 days of LPLO, and the rate of increase then slowed from 7 days to 28 days. Conclusions 　A simulated move from a plains to a plateau environment was associated with significant structural and functional renal damage, but the kidneys then showed a self-adaptive adjustment process towards the plateau environment.

Abstract: Objective　We aimed to investigate the effects of different non-surgical embryo transfer devices, number of transferred embryos, embryo stage, and embryos obtained from different mouse strains on the efficiency of non-surgical embryo transfer in mice, and to compare the efficiencies of surgical and non-surgical embryo transfer, in order to establish a stable non-surgical embryo transfer technology system. Methods　Mouse embryo transfer was carried out using non-surgical method . Results　The pregnancy rates using two different non-surgical transfer devices were (75.00±0.00)% and (66.67±14.43)%,and the birth rates were (46.11±6.31)% and (18.89±0.96)%,respectively. Transfer of 10, 15, and 20 embryos resulted in pregnancy rates of (66.67±11.55)%, (80.00± 0.00)%, and (66.67±23.09)%, and birth rates of (29.33±4.16)%, (38.67±4.81)%, and (17.00±3.46)%, respectively. When blastocysts and morulae were transferred non-surgically, the resulting pregnancy rates were (80.00±0.00)% and (46.67±11.55)% and the birth rates were (38.67±4.81)% and (10.22±2.77)%, respectively. Four strains (C57BL/6J, ICR, genetically modified mice A, genetically modified mice B) were used as donors for non-surgical embryo transfer, with resulting pregnancy rates of (66.67±11.55)%, (80.00±0.00)%, (73.33±11.55)%, and (80.00±0.00)%, and birth rates of (26.67±2.67)%, (38.67±4.81)%, (32.00±3.53)%, and (29.34±2.31)%, respectively. Fifteen pseudo-pregnant mice were transplanted surgically and 15 were transplanted non-surgically, with pregnancy rates of (80.00±0.00)% and (86.67±11.55)%, and birth rates of (38.67±4.81)% and (36.00±5.82)%, respectively. Conclusions 　Transfer device A resulted in a higher birth rate in this study. The embryo transfer efficiency was higher when 15 embryos were transferred into unilateral uterine horns of pseudo-pregnant 2.5-day recipients. Blastocyst-stage embryo transfer was more efficient than morula-stage transfer. There was no significant difference in efficiency between surgical and non-surgical embryo transfer procedures.

Abstract:Atherosclerosis is the main pathological basis of coronary heart disease, and is thus of great importance in terms of the prevention and treatment of coronary heart disease. Neuropilin-1 (NRP1), a member of the neuropilin receptor family, is closely associated with various growth factors, including vascular endothelial growth factor (VEGF) and transforming growth factor-β (TGF-β). NRP1 influences the progression of atherosclerosis through its crucial roles in angiogenesis and inflammatory responses, and sensing of wall shear stress on the vascular endothelium. This review thus explores the mechanisms underlying the role of NRP1 in atherosclerosis and the development of NRP1-targeted therapeutic strategies, to provide new insights into the diagnosis and treatment of atherosclerosis.

Abstract:Mitochondria are the center of intracellular energy metabolism. Mitochondrial dynamics refers to the dynamic process of mitochondrial fusion and fission, which plays an important role in maintaining mitochondrial homeostasis and central nervous system function. Optic atrophy 1 (OPA1) is a key factor involved in mitochondrial dynamics. OPA1 acts by regulating mitochondrial fusion and fission, reducing oxidative stress, inhibiting apoptosis, and promoting mitochondrial autophagy, to maintain the dynamic changes in mitochondrial quantity, structure, and biological function. Numerous studies have shown that OPA1-mediated mitochondrial dynamics plays an important role in ischemic stroke, Alzheimer’s disease, Parkinson’s disease, spinal cord injury, multiple sclerosis, and other central nervous system diseases. Here we review the regulatory mechanism of OPA1 in terms of mitochondrial dynamics and the important role of mitochondrial function mediated by OPA1 in central nervous system diseases, to provide new ideas for clinical treatment.

Abstract:The heart serves as the “energy factory” of the human body and is responsible for maintaining blood circulation and oxygen supplies. Its normal functioning thus relies on the generation of substantial amounts of ATP to support its mechanical activities. Under pathological conditions such as myocardial infarction, coronary artery sclerosis, and pulmonary hypertension, however, an insufficient blood supply leads to a reduced oxygen supply, subsequently activating a series of compensatory protective mechanisms. Hypoxia-inducible factor-1α (HIF-1α), as a nuclear transcription factor stably expressed under hypoxic conditions, has been shown to regulate oxygen transport by promoting angiogenesis and vasodilation, and to optimize oxygen utilization by regulating the balance of glucose and lipid metabolisms, thus participating in the regulation of various cardiac diseases. HIF-1α plays a crucial role in regulating cardiac energy metabolism and oxidative stress. This review systematically summarizes recent research regarding the various mechanisms of action of HIF-1α in reprogramming cardiac energy metabolism, explores its potential clinical applications in cardiovascular diseases, and proposes future research directions and possible treatment strategies. By comprehensively summarizing the mechanism of HIF-1α in ischemic heart disease, this article aims to provide new ideas and therapeutic targets for the prevention and treatment of cardiovascular diseases.

Abstract:The need for suitable interventions for progressive pulmonary vascular lesions has become a bottleneck and a consequent focus in the prevention and treatment of clinical pulmonary hypertension. Plexiform lesions in pulmonary arterioles are the typical pathological manifestation of irreversible abnormal pulmonary vascular remodeling and the criterion for stage Ⅳ pulmonary vascular remodeling. There is currently no effective clinical intervention for such pathophysiological lesions, highlighting the need for corresponding animal models. This review considers new progress in the stereology of plexiform lesions and highlights plexiform-lesion models in mice and rats induced by multifactor stimulation, such as two-hit models and genetic engineering. It also evaluates the characteristics and applications of these models to provide a reference for animal experimental studies and to clarify the mechanism of pulmonary hypertension with pulmonary vascular plexiform lesions.

Abstract:Ferroptosis is closely related to iron metabolism, lipid metabolism, and amino acid metabolism, which contribute to the production of reactive oxygen species, mitochondrial damage, and cell death. Ferroptosis has recently been recognized as a key regulatory mechanism during tumor development, including in acute leukemia. This review considers the inhibitory effects of drugs on the occurrence and development of acute leukemia, by regulating key proteins or factors involved in the above three metabolic pathways of ferroptosis and by interfering with the production of lipid peroxides. We also point out the deficiencies in current research and describe the role of ferroptosis in acute leukemia. The application of these findings in clinical trials will provide new ideas for future research and the treatment of leukemia.

Abstract:The endoplasmic reticulum quality control (ERQC) system is a core mechanism for maintaining cellular homeostasis, which primarily mediates the degradation of misfolded proteins in the endoplasmic reticulum (ER) through the ER-associated degradation (ERAD) and ER autophagy (ER-phagy) pathways. Tripartite motif 13 (TRIM13) is a protein located on the ER membrane, which plays a critical role in ERAD via its E3 ubiquitin ligase activity. TRIM13 also acts as a non-classical ER-phagy receptor to mediate the occurrence of ER-phagy. TRIM13 has recently received extensive attention in the field of ERQC. Here we review the structure and function of TRIM13 and the mechanisms by which it contributes to ERQC, and summarize its abnormal expression and regulatory role in diseases, with the aim of providing new strategies for the treatment of related diseases.

Abstract:The pathogenesis of Alzheimer’s disease (AD) is a key research focus in the field of life sciences. Exercise serves as an important intervention for ameliorating neurodegenerative diseases, and aerobic exercise, resistance training, and multimodal exercise combinations have been shown to significantly improve AD. Studies have shown that the pathogenesis of AD is closely associated with the regulatory effects of exercise in suppressing inflammatory responses, optimizing the activation of astrocytes and microglia, promoting hippocampal neurogenesis, and improving blood-brain barrier function. This article reviews the effects and mechanisms of different exercise method in improving AD and discusses future prospects, with the aim of providing a theoretical and experimental basis for the role of exercise in the prevention and treatment of AD.