Abstract: Objective To observe changes in voltage-dependent anion channel 3(VDAC3) in a mouse model of sepsis-induced myocardial injury and to explore its potential mechanism. Methods Twenty male C57BL / 6J mice were divided randomly into a Sham group and Sepsis group, respectively (n = 10 mice per group). Sepsis was induced by the cecal ligation and puncture (CLP). Serum levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α, creatine kinase MB (CK-MB), and cardiac troponin T ( cTnT) were detected by enzyme-linked immunosorbent assay. Pathological changes in heart tissue were observed by hematoxylin and eosin staining. Structural and functional changes in the heart were evaluated by echocardiography. Changes in total glutathione, reduced glutathione (GSH),oxidized glutathione, and malondialdehyde ( MDA) in heart tissue were detected by spectrophotometry. The morphological structure of mitochondria in mouse cardiomyocytes was observed by transmission electron microscopy.Expression levels of IL-6, IL-1β, VDAC3, glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), lipocalin-2 ( LCN2), and prostaglandin-endoperoxide synthase 2 ( PTGS2) mRNA were detected by real-time quantitative polymerase chain reaction and the localization and expression of VDAC3 and GPX4 proteins in mouse heart tissue were detected by immunofluorescence staining. The correlations between VDAC3 mRNA and GPX4, SLC7A11, PTGS2, LCN2, IL-6, and IL-1β mRNA were analyzed. Expression levels of VDAC3, GPX4, and SLC7A11 proteins were detected by Western blot. Results IL-6, TNF-α, CK-MB, and cTnT levels were significantly higher in the Sepsis group compared with the Sham group (P<0. 05). In the Sepsis group, myocardial fibers were torn, the ventricular wall was thickened and edematous, the mitochondrial membrane was ruptured, and mitochondrial cristae were broken or absent. GSH levels were significantly reduced in the Sepsis group (P<0. 05) and the lipid peroxide MDA was increased in the Sepsis group (P<0. 05) compared with the Sham group. VDAC3, GPX4 and SLC7A11 mRNA and protein levels were all lower in the Sepsis group compared with the Sham group (P<0. 05),while expression levels of IL-6, IL-1β, LCN2, and PTGS2 mRNA were increased (P<0. 05). VDAC3 mRNA was positively correlated with GPX4 and SLC7A11 mRNA levels, and negatively correlated with LCN2, PTGS2, IL-6,and IL-1β. Conclusions VDAC3 expression decreases in myocardial injury, and it may participate in the occurrence of sepsis-induced myocardial injury by regulating ferroptosis.

Abstract: Objective　To explore the effects and therapeutic mechanism of electroacupuncture on the levels of polarization markers and inflammatory factors interleukin (IL)-6, IL-4, tumor necrosis factor-alpha (TNF-α), and IL-10 in rats with para-chlorophenylalanine-induced insomnia (PCPA). Methods　Fifty healthy specific-pathogen free grade Sprague-Dawley rats, half male and half female, were randomly divided into a blank group (n=10) and a model reserve group (n=40), in which insomnia was induced by intraperitoneal injection of a 500 mg/kg PCPA suspension. Using the random number table method, the 30 successfully modeled rats were divided into three treatment groups of 10 rats/group: model, electroacupuncture, and estazolam. The estazolam group was given estazolam 0.2 mg/(kg·d) by gavage; the electroacupuncture group was given once-daily electroacupuncture at the “Shenmen” and “Sanyinjiao” acupoints, and stimulation at the “Baihui” and “Benshen” acupoints, 20 minutes each time, for 7 consecutive days. Following treatment, serum and hypothalamic levels of TNF-α, IL-6, IL-4, and IL-10 were detected using ELISA and Western blot, while immunofluorescence staining was used to detect the presence of Iba-1 in hypothalamic microglia and the co-expression of CD86 and CD163, which are markers for the M1 and M2 subtypes of microglial cells, respectively. Results　Compared with the blank group, the model group exhibited prolonged sleep latency (SL) (P<0.01), shortened sleep duration (ST) (P<0.05), significantly higher serum and hypothalamic protein levels of IL-6 and TNF-α (P<0.01), and significantly lower levels of IL-4 and IL-10 (P<0.01). Compared with the model group, the electroacupuncture and estazolam groups exhibited significantly shorter SL (P<0.01), prolonged ST (P<0.01), significantly lower serum and hypothalamic protein levels of IL-6 and TNFα (P<0.01), and significantly higher IL-4 and IL-10 levels (P<0.01). IL-6 content was lower in the electroacupuncture group than in the estazolam group (P<0.05). Compared with the blank group, the model group exhibited significantly enhanced Iba-1/CD86 (M1 type) co-expression (P<0.01) alongside significantly weakened Iba-1/CD163 (M2 type) co-expression (P<0.01). Under electroacupuncture or estazolam intervention, Iba-1/CD86 co-expression was significantly weakened (P<0.01), and Iba-1/CD163 co-expression was significantly enhanced in the model group (P<0.05). Conclusions　Electroacupuncture effectively improved sleep disturbances in rats, with an underlying mechanism that may involve regulation of microglial polarization, downregulation of pro-inflammatory cytokine levels, upregulation of anti-inflammatory cytokine levels, and alleviation of neuroinflammation, thereby ameliorating sleep.

Abstract: Objective　To explore the molecular mechanisms of moxibustion in improving osteoporosis in rats using high-throughput micro-RNA (miRNA) sequencing analysis. Methods　A total of 18 female Sprague-Dawley (SD) rats were randomly divided into an operation group (12 rats), which was subjected to ovariectomy to induce osteoporosis, and a sham operation control (SO) group (6 rats). The 12 osteoporosis model rats were randomly divided into a model (OVX) group and a moxibustion (MOX) group (6 rats per group), which were treated with once-daily moxibustion at the “Shenshu” (BL23) and “Guanyuan” (CV4) acupoints for 20 minutes each time, for 12 weeks. Micro-computed tomography (CT) scans of the rat femur were taken to analyze the trabecular bone thickness (Tb.Th), trabecular separation (Tb.Sp), and bone volume total volume (BV/TV) ratio of the trabecular bone. Hematoxylin and eosin staining was used for morphological observation of tibial tissues. Serum alkaline phosphatase (ALP) and osteocalcin (OCN) levels were measured using ELISA. Three randomly selected rats from each group were used for miRNA high-throughput sequencing to screen for differentially expressed miRNAs, which were subjected to functional enrichment analysis and target gene prediction. Results　Micro-CT images showed that, compared with the OVX group, the MOX group had superior bone density, significant increases in the Tb.Th and BV/ TV score, and a significant decrease in Tb.Sp (P<0.05). ELISA indicated that, compared with the OVX group, the MOX group showed a significant decrease in serum ALP activity and a significant increase in serum OCN content (P<0.05). The miRNA sequencing result showed that 34 miRNAs were commonly expressed between the OVX group and the intervention group, and 15 miRNAs were commonly expressed between the OVX group and the intervention group. KEGG pathway enrichment analysis showed that the differentially expressed genes were mainly enriched in signaling pathways involving MAPK, Ras, FoxO, TNF, and cancer-related microRNAs. For the top five most differentially expressed microRNAs, namely miR-153-5p, miR-201-5p, miR-449c-5p, miR-451-3p, and miR-153-3p, target gene predictions yielded 10 major targets: Ebf2, Rtn4, Fbxl3, Naa15, Vamp2, Daam1, Akap6, Camta1, Ptprz1, and Lamp1. Conclusions　Acupuncture slowed the progression of osteoporosis, improved bone microstructure, and balanced bone metabolism in rats. This therapeutic effect may be achieved through regulation of the expression of microRNAs and their target genes; however, the underlying mechanism requires further exploration.

Abstract: Objective　To design melatonin (Mel)-based nanomedicines (Mel-NMs) and evaluate their therapeutic effects on myocardial ischemia-reperfusion injury in mice. Methods　Melatonin self-assembled peptides (Mel-NMs) were synthesized and their structure was characterized by transmission electron microscopy. Mice were divided randomly into five groups: Sham, Model, Mel, NMs, and Mel-NMs, and a myocardial ischemia-reperfusion injury model was established. Mel (5 mg/kg), NMs, or Mel-NMs (containing Mel 5 mg/kg) were administered intraperitoneally 10 minutes prior to reperfusion, and the sham group was treated with an equal volume of solvent. Cardiac function, apoptosis, and oxidative stress markers were assessed 24 hours after reperfusion. Results Transmission electron microscopy revealed that Mel-NMs formed worm-like structures. Treatment with Mel and Mel NMs significantly improved cardiac function, reduced lactate dehydrogenase and malondialdehyde levels, and enhanced glutathione peroxidase and superoxide dismutase activities (P<0.05), while also decreasing cardiomyocyte apoptosis (P<0.05), with greater effects in the Mel-NMs group (P<0.05). Conclusions　Mel-NMs can effectively mitigate myocardial oxidative stress and apoptosis, offering a more potent cardioprotective effect than Mel alone.

Abstract: Objective　To investigate the effect of Jiawei Simiao powder on the Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway through miR-146a in monosodium urate (MSU) crystal-induced RAW264.7 macrophage inflammation models, and to explore its anti-inflammatory mechanism. Methods　A cell model of gouty arthritis was established by inducing RAW264.7 cells with MSU crystals. Cells were divided into control, model, Jiawei Simiao powder, and colchicine groups and cell viability was assessed using the CCK-8 method. Levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were measured by enzyme-linked immunosorbent assay. Expression levels of miR-146a miRNA and TLR4, myeloid differentiation factor 88 (MyD88), TNF receptor-associated factor 6 (TRAF6), and NF-κB p65 mRNA were detected by quantitative real-time polymerase chain reaction amplification technology, and protein expression levels of TLR4, MyD88, TRAF6, and phospho (p)-NF-κB p65 were evaluated by Western blot. Results　miR-146a expression was significantly decreased in the model group compared with the control group (P<0.01), while mRNA and protein expression levels of TLR4, MyD88, and TRAF6, and protein expression of p-NF-κB p65, IL-1β, IL-6, and TNF-α were significantly increased (P<0.01). In contrast, miR-146a expression was significantly increased (P<0.01) and mRNA and protein expression of TLR4, MyD88, and TRAF6, and p-NF-κB p65 protein expression(P<0.01), as well as IL-1β, IL-6, and TNF-α levels (P<0. 05) were significantly decreased in the Jiawei Simiao powder and colchicine groups. Conclusions　Jiawei Simiao powder may alleviate MSU crystal-induced macrophage inflammatory responses by upregulating miR-146a, suppressing TLR4/NF-κB signaling pathway activation, and decreasing secretion of inflammatory factors.

Abstract: Objective　To investigate the effects of the polymer pharmaceutical excipient methoxy poly ethylene glycol poly-lactic acid (mPEG-PLA) in Sprague-Dawley (SD) rats and Beagle dogs and its toxicological reactions, to provide a reference for its safe clinical use. Methods　SD rats and Beagle dogs (male:female ratios, 1 ∶ 1) were divided randomly into control group and low, medium, and high dose mPEG-PLA groups (70, 210, 700 mg/kg). Animals received intravenous mPEG-PLA once a day for 90 days, followed by a 28-day recovery period. Indicators including clinical observations, food intake, body weight, hematology, blood biochemistry, immune function, and pathological examination were recorded. Results　Compared with the control group, (1)food intake was decreased (P<0.01) and body weight was increased (P<0.05 or P<0.01) after 90 days of continuous administration, with similar changes in the medium and high dose groups in both rats and dogs. In addition, MONO/ MONO%, RBC, MCH, MCHC, HCT, HGB, PLT, TP, ALB, GLB, and Fbg were all decreased (P<0.05 or P<0.01) and coagulation indexes (e.g., APTT) were increased (P<0.05 or P<0.01). Organ weights and the organ to-body/brain weight ratios of the liver and spleen were increased (P<0.05 or P<0.01), and histopathology indicated numerous foam-like macrophages in the hepatic sinuses, red spleen pulp, and lymph node medulla. DBIL and TBIL also increased in rats in the high dose group (P<0.05 or P<0.01), while the dogs experienced skin swelling or scabs, abdominal swelling, vomiting, decreased activity, high albuminuria, and ascites, and the renal glomerular cells showed vacuoles. (2)After 28 days of recovery, rats and dogs in the medium and high dose groups showed a few foam-like macrophages in the hepatic sinuses, red spleen pulp, and lymph node medulla, as well as decreased of food intake in dogs. The MCHC, PLT, and TP decreased in dogs in the high dose group (P<0.05), and the liver and spleen weights and organ coefficients in rats increased (P<0.05 or P<0.01), while the MONO% decreased in male rats in the medium dose group (P<0.05). Conclusions　Administration of mPEG-PLA 210 and 700 mg/kg for 90 days caused blood mononuclear cells to enter and aggregate in the liver, spleen, lymph nodes, and other tissues in SD rats and Beagle dogs, leading to secondary tissue structural damage. Protein and fibrinogen synthesis and bilirubin metabolism in the liver decreased, leading to abnormal coagulation function, and decreased intravascular colloid osmotic pressure resulted in edema and bleeding. The result suggest that the liver, spleen, kidney, and lymph nodes are target organs for mPEG-PLA toxicity, with dose-dependent and reversible effects and species differences, but no significant sex differences. Clinical monitoring of related organ functions is needed to avoid secondary damage.

Abstract: Objective　To investigate the mechanism underlying the effect of intra-articular injection of ozonated water on cartilage repair in knee osteoarthritis (KOA) rats via the miR-214-3p/nuclear factor (NF)-κB signaling pathway, to provide a theoretical basis for the clinical application of ozonated water. Methods　Sixty male Sprague-Dawley rats were divided randomly into ozonated and experimental groups. Rats in the experimental group were further divided randomly into model, ozonated water, ozonated water + AAV-NC, and adeno-associated virus with ozonated water+AAV-miR-214-3p inhibitor groups. The articular cartilage repair status was evaluated after the respective treatments, using articular cartilage surface gross scoring, hematoxylin/eosin staining, and modified Mankin’s score. Expression levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and matrix metalloproteinase (MMP)-13 were detected by enzyme-linked immunosorbent assay (ELISA). Protein expression levels of IκB kinase (IKK) β, p65, and phospho (p)-IκBα were detected in cartilage tissues by Western blot, and gene expression levels of IKKβ, p65, IκBα, and miR-214-3p were detected by real-time polymerase chain reaction (RT-PCR). Results　Rats in all groups showed different degrees of cartilage damage compared with the control group, and the scores were significantly lower in the ozonated water and ozonated water+AAV-NC groups compared with the ozonated water+AAV-miR-214-3p inhibitor group (P<0.05). IL-1β, TNF-α, and MMP-13 levels detected by ELISA were significantly lower in cartilage tissues from rats in the ozonated water and ozonated water+AAV-NC groups compared with the model and ozonated water+AAV-miR-214-3p inhibitor groups (P<0.05). According to RT PCR, IKKβ and p65 mRNA levels were significantly down-regulated while IκBα mRNA was significantly up-regulated in cartilage tissues from rats in the ozonated water and ozonated water+AAV-NC groups compared with the model and ozonated water+AAV-miR-214-3p inhibitor groups (P<0.05). Similarly, IKKβ, p65, and p-IκBα protein expression levels detected by Western blot were significantly down-regulated while IκBα protein expression levels were up regulated in cartilage tissues from rats in the ozonated water and ozonated water+AAV-NC groups compared with the model and ozonated water+AAV-miR-214-3p inhibitor groups (P<0.05). Conclusions Ozone hydrotherapy significantly ameliorated cartilage damage in KOA rats, possibly via inhibiting activation of the NF-κB signaling pathway through up-regulation of miR-214-3p expression and promoting cartilage repair in KOA rats.

Abstract: Objective　To investigate the vasodilatory effect of luteolin on isolated denuded-endothelium rat thoracic aorta (DRTA) vascular rings, and the mechanistic role of the Kv7 ion channel. Methods　The tension of DRTA vascular rings was measured using an ex vivo tissue perfusion muscle-tone detection system. DRTA vascular rings were pre-contracted with 60 mmol/L KCl or 0.3 μmol/L U46619, and the effect of luteolin on vascular-ring relaxation was observed at 1, 3, 10, 30, 100 and 300 μmol/L. The effects of 4-AP, XE-991, and ML213 on luteolin-induced vasodilation were also observed. The effect of luteolin on KCNQ1-KCNQ5 expression in the thoracic aorta was detected by real-time fluorescence quantitative polymerase chain reaction. Expression levels of Kv7.1 and Kv7.4 proteins in the DRTA were detected by Western blot. Results　(1)The luteolin-induced maximum vasodilation rates in DRTA pre-contracted with 60 mmol/L KCl and 0.3 μmol/L U46619 were (97.67±8.51)% and (98.42±9.76)%, respectively. The vasodilation effect was concentration-dependent (P<0.05). (2)4-AP (3 mmol/L) significantly reduced the vasodilatory effect of luteolin on DRTA vascular rings at 10, 30, and 100 μmol/L (P<0.05), and XE-991 (3 μmol/L) significantly reduced the effect of luteolin at 30 and 100 μmol/L (P<0.05), while ML213 (1 μmol/L) significantly enhanced the vasodilatory effect of luteolin at 3, 10, and 30 μmol/L (P<0.05). (3)The relative gene expression levels of each subtype of Kv7 channel in normal DRTA were KCNQ1 > KCNQ5 > KCNQ4 > KCNQ3 > KCNQ2, with KCNQ1 being the most highly expressed. (4)Luteolin significantly enhanced the expression levels of KCNQ1 at 3, 10, 30, and 100 μmol/L, KCNQ2 at 1, 3, 10, 30, and 100 μmol/ L (P<0.05), KCNQ3 at 3, 10, 30, and 100 μmol/L, and KCNQ4 at 10, 30, and 100 μmol/L (P<0.05), but did not significantly enhance the expression of KCNQ5 at 1, 3, 10, 30, or 100 μmol/L (P>.05). (5)Luteolin significantly increased the expression of Kv7.1 protein in DRTA at 3, 10, 30, and 100 μmol/L (P<0.05) and the expression of Kv7.4 at 10, 30, and 100 μmol/L (P<0.05). Conclusions　Luteolin-induced dilation of DRTA vascular rings may be related to the enhanced gene expression of KCNQ1-4 and increased expression of Kv7.1 and Kv7.4 channel proteins.

Abstract:New quality productivity is a strategic engine for promoting high-quality development and is an inherent requirement and important focus for enhancing new driving forces and building national advantages. The cultivation of innovative talents and technological innovation are key to the development of new quality productivity. Laboratory animal science is a comprehensive interdisciplinary subject that integrates multiple disciplines including biology, medicine, pharmacy, and biomedical engineering. Teaching and research of laboratory animal science not only promotes the creation of innovative talent teams by cultivating innovative consciousness, thinking, spirit, and operational abilities, but also promotes the development of cutting-edge technologies and the transformation of disruptive research result in the fields of basic research and clinical translation of biomedicine, thus providing important guarantees for China’s scientific and technological progress and innovative development.

Abstract:Anatomy of laboratory animals plays an important role in laboratory animal science, veterinary medicine, and other life sciences. Integrating mind mapping into the entire teaching process can effectively help teachers to optimize the organization of teaching contents and stimulate students’ enthusiasm and self-motivation for learning. This manuscript aims to explore the feasibility, advantages, and challenges of applying mind-mapping tools for teaching anatomy of laboratory animals. We analyze the different application scenarios from the perspectives of both teachers and students, with the aim of providing practical teaching tools and methodologies to enhance instructional effectiveness in the teaching of anatomy of laboratory animals.

Abstract:The advent of an aging society means that bone-related diseases impose a substantial burden on the general population and on healthcare systems, highlighting the need to find new treatment method. The occurrence and progression of such diseases are closely linked to inflammatory responses. Moxibustion, as a traditional external treatment in traditional Chinese medicine (TCM), is well-known for its anti-inflammatory and analgesic effects, and it has also demonstrated remarkable therapeutic efficacy for bone-related diseases. Here we review the impact of moxibustion on inflammatory responses associated with bone-related conditions. The anti-inflammatory mechanism of moxibustion in treating bone-related diseases involves mediating pro-inflammatory and anti-inflammatory factors and related mediators, and regulating signaling pathways (e.g., nuclear factor-kappa B (NF-κB), Janus kinase (JAK)/ signal transducer and activator of transcription (STAT), mitogen-activated protein kinase (MAPK), programmed death receptor-1 (PD-1)/programmed death ligand-1 (PD-L1), adenosine monophosphate-activated protein kinase (AMPK)/UNC-51 like autophagy activating kinase (ULK1)), the hypothalamic-pituitary-adrenal axis, the activation of immune cells, and autophagy. Despite these findings however, the anti-inflammatory mechanisms underlying moxibustion treatment for bone-related diseases remain poorly understood. Further research utilizing advanced technologies is needed to gain a more comprehensive understanding of the anti-inflammatory mechanisms involved in moxibustion therapy. This approach aims to facilitate better clinical applications and contribute to safeguarding human bone health.

Abstract:Depression is a common mental disorder with adverse effects on human health and quality of life. Although its pathogenesis remains unclear, numerous recent studies have indicated a close association between depression and mitochondrial dysfunction. This review explores the critical role of mitochondrial dysfunction in the pathogenesis of depression from the aspects of energy metabolism disorders, oxidative stress and inflammatory responses, mitochondrial DNA damage and mutations, and the imbalance of the mitochondrial quality control systems.We also summarize recent advances in the use of traditional Chinese medicine (TCM) to treat depression by regulating mitochondrial function. The findings show the potential of TCM in enhancing mitochondrial energy metabolism, reducing oxidative stress and inflammatory responses, improving mitochondrial DNA, and modulating the mitochondrial quality control systems, including for the in-depth study of the pathogenesis of depression and its treatment with TCM.

Abstract:The oxygen partial pressure in high-altitude areas is low. Long-term exposure to high-altitude areas leads to a state of low-pressure hypoxia. The combination of low pressure and oxygen levels triggers a variety of mechanisms that disrupt normal bodily functions. One key response to hypoxia is hypoxic pulmonary vasoconstriction, which, when aggravated, can induce the development of high altitude heart disease (HAHD). HAHD is a clinical type of chronic mountain sickness mainly characterized by vasoconstriction and hyperproliferative remodeling of the pulmonary artery. As the pressure in the pulmonary artery continues to rise, it increases the posterior load on the right heart, causing right ventricular hypertrophy. Over time, this can lead to right heart failure or even complete heart failure. Despite extensive on HAHD in recent years, its prevalence remains high. While researchers are committed to finding an ideal treatment, this remains a huge challenge, particularly as awareness of the HAHD subtype is still limited. Here, we review the recent research on the pathogenesis and treatment of HAHD, with the aim of providing new clues for its prevention and treatment.

Abstract:Oxidative stress (OS) and dopaminergic neuron (DN) dysfunction are implicated in the pathogenesis and progression of various neurological disorders. As the primary active component of the traditional Chinese herb Scutellaria baicalensis, baicalin has garnered significant attention due to its potent antioxidant and anti inflammatory properties. Baicalin exhibits a particular affinity for the dopamine (DA) system, maintaining cerebral DA levels by regulating oxidative stress (OS)-related pathways, suggesting that the DA system serves as the “intracerebral target system” through which it exerts its neuroprotective effects. Nuclear factor erythroid 2-related factor 2 (Nrf2), a central transcription factor regulating redox homeostasis, plays a pivotal role in the anti-OS process mediated by baicalin. This systematic review covers the pharmacological effects of baicalin, providing an in-depth mechanistic analysis of the interaction between OS and DN, with a focus on the latest research progress in baicalinmediated treatment of OS through the Nrf2 signaling pathway in neurological diseases to provide theoretical references for the pharmacological and molecular mechanisms of baicalin’s anti-OS modulation of the DA system for the treatment of neurological diseases.

Abstract:Nitric oxide synthase (NOS) and its product nitric oxide are involved in learning and memory functions. Increasing evidence shows that NOS plays an important role in the pathogenesis of Alzheimer’s disease, influencing β-amyloid protein (Aβ) deposition, neuroinflammation, oxidative stress, abnormal microglia activation, synapse damage, autophagy, abnormal mitochondrial function of nerve cells, and cerebral hypoperfusion or vascular endothelial cell injury. This review summarizes the recent evidence for the role of NOS in the pathogenesis of Alzheimer’s disease and provides new feasible targets for the prevention and treatment of Alzheimer’s disease.

Abstract:Intracranial arterial dolichoectasia (IADE) is a major arterial disease characterized by artery elongation, dilatation, and curvature. Although the pathological mechanism of IADE is unclear, recent studies have suggested a close relationship with matrix metalloproteinases (MMPs). This review summarizes the possible pathological mechanism of IADE induced by MMPs in terms of MMPs activation and the occurrence and development of IADE, the correlation between MMPs activation and positive remodeling causing IADE, and the relationship between hemodynamic changes, MMPs activation and IADE and between IADE-associated diseases and MMPs, to provide potential therapeutic targets for the effective prevention and treatment of IADE.

Abstract:As the incidence of autism rises annually, its unknown pathogenesis makes it challenging to treat the varied repetitive and stereotyped behaviors that characterize its core symptoms. The striatum is an important brain region for the control of locomotor behaviors, featuring a unique mosaic structure, complex neural origin, and finely regulated developmental process that is highly susceptible to genetic and environmental influences. Both clinical and basic studies have indicated that abnormal development of the striatal nuclei may contribute to the pathogenesis of these repetitive stereotyped behaviors in autism. Clinical imaging data have primarily identified gross anatomical variations in the stratum (e. g., its general outline), but lack the resolution necessary to detect the cellular and subcellular alterations within the region. By introducing the abnormalities in the spatiotemporal development of the striatum and their links to the characteristic behaviors of autism, this review aims to advance our understanding of the role of the striatum in autism pathogenesis and to inform future animal studies and clinical research.