Tissue & cell最新文献

{"title":"Research on the molecular mechanism of intervertebral disc degeneration caused by mitochondrial dysfunction","authors":"Pandeng Hao ,&nbsp;Yuheng He ,&nbsp;Feilong Li ,&nbsp;Yingjin Luo ,&nbsp;Chao Song ,&nbsp;Zongchao Liu ,&nbsp;Zhijiang Fu","doi":"10.1016/j.tice.2025.103155","DOIUrl":"10.1016/j.tice.2025.103155","url":null,"abstract":"<div><div>Intervertebral Disc Degeneration (IVDD) is the primary pathological basis of chronic low back pain, typically characterized by degeneration of the nucleus pulposus (NP), fissures in the annulus fibrosus (AF), and calcification of the cartilage endplates. These changes ultimately lead to nerve compression and loss of spinal function. Current treatment approaches are primarily symptomatic and cannot reverse disease progression. Therefore, a detailed understanding of the molecular mechanisms of IVDD and the exploration of targeted therapeutic strategies are of considerable clinical importance.Growing evidence indicates that mitochondrial dysfunction is a key factor in the pathogenesis of IVDD. Aberrations such as excessive production of reactive oxygen species (ROS), imbalance in mitochondrial dynamics, impaired mitophagy, and abnormal metabolic reprogramming converge to disrupt cellular activities, accelerate programmed cell death, and drive the breakdown of the extracellular matrix (ECM). This article comprehensively summarizes the role of mitochondrial damage in IVDD, with a focus on oxidative stress, dysregulated autophagy, and excessive mitochondrial fission. Furthermore, it evaluates emerging preclinical strategies aimed at restoring mitochondrial quality.From the perspective of bioenergetic dysfunction, this review proposes that interventions targeting the mitochondrial quality control network may establish a novel therapeutic paradigm for IVDD, thereby laying a theoretical foundation for translational and multidisciplinary research.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103155"},"PeriodicalIF":2.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145158516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of Lycium barbarum polysaccharide on oxidative stress and sperm health in varicocele patients: A randomized clinical trial","authors":"Maryam Mehdikhanloo ,&nbsp;Abdullah Abdulsattar Raeef ,&nbsp;Neda Mohammadi ,&nbsp;Mehdi Mahmoodi ,&nbsp;Mostafa Nasirzadeh ,&nbsp;Maryam Mohammad-Sadeghipour ,&nbsp;Mohammad Reza Hajizadeh","doi":"10.1016/j.tice.2025.103160","DOIUrl":"10.1016/j.tice.2025.103160","url":null,"abstract":"<div><div>Varicocele is an abnormal enlargement of scrotal veins, significantly contributing to male infertility. The plant <em>Lycium barbarum</em>, known for its high antioxidant properties, may enhance fertility quality. This study examines the protective and antioxidant effects of <em>Lycium barbarum</em> polysaccharide on sperm health in patients with varicocele. In a double-blind clinical trial conducted in 2022 at Afzalipoor Hospital in Kerman, 80 patients with varicocele were randomly assigned to either an intervention group (n = 40) or a control group (n = 40). After collecting demographic, blood, and semen samples, the intervention group received 400 mg of <em>Lycium barbarum</em> extract orally for two months, while the control group received a placebo. Blood and semen samples were re-evaluated 90 days post-treatment for markers such as Superoxide dismutase, Glutathione peroxidase, Malondialdehyde, and Testosterone, as well as sperm health parameters. Before treatment, the Mann-Whitney test showed no significant difference between the groups (P &lt; 0.05). The intervention group exhibited effective enhancement in antioxidant enzyme activity (Superoxide dismutase, Glutathione peroxidase). The intervention with <em>Lycium barbarum</em> resulted in a significant decrease in Malondialdehyde (MDA) levels, indicating a reduction in oxidative stress. Significant improvements in Testosterone level and sperm count, motility, and morphology, indicating the intervention's positive impact on male fertility indicators, excluding semen volume (P &lt; 0.05). The volume of semen following the intervention with <em>Lycium barbarum</em> showed a slight increase post-intervention. In conclusion, the results suggest that <em>Lycium barbarum</em> polysaccharide has a positive effect on oxidative stress and sperm health. Further research with larger sample sizes is recommended to enhance the generalizability of these findings.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103160"},"PeriodicalIF":2.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MSC-derived exosomes promote chondrocyte proliferation and inhibit apoptosis by suppressing inflammation in osteoarthritis","authors":"Chaochao Ji ,&nbsp;Wendan Cheng","doi":"10.1016/j.tice.2025.103157","DOIUrl":"10.1016/j.tice.2025.103157","url":null,"abstract":"<div><h3>Background</h3><div>Osteoarthritis (OA) is marked by reduced chondrocyte proliferation, increased apoptosis, and an inflammatory microenvironment. Mesenchymal stem cell-derived exosomes (MSC-Exos) are promising modulators of chondrocyte function; however, their precise roles remain unclear. This study explores whether MSC-Exos protect chondrocytes from IL-1β-induced injury via these effects, in vitro and in a rat OA model.</div></div><div><h3>Methods</h3><div>BMSC-derived exosomes (BMSC-Exos) were isolated via ultracentrifugation and characterized (TEM, NTA, Western blotting). Chondrocyte injury was induced by IL-1β (10 ng/mL). Effects of BMSC-Exos on proliferation (CCK-8), apoptosis (Annexin V/PI), migration (wound healing/Transwell), inflammatory cytokines (ELISA), and NF-κB p65 phosphorylation (Western blotting) were evaluated. <em>In vivo</em>, OA was induced by intra-articular sodium iodoacetate in rats, and MSC-Exos were administered weekly. Histological staining (H&amp;E and Safranin O-Fast Green) was performed to assess cartilage repair, immunohistochemical (IHC) analysis for IL-1β, TNF-α, IL-6, type II collagen and aggrecan was conducted, and analysis of p65 phosphorylation in cartilage tissue was conducted.</div></div><div><h3>Results</h3><div>BMSC-Exos significantly increased chondrocyte proliferation, reduced apoptosis, suppressed TNF-α, IL-6, and IL-1β expression, and inhibited p65 phosphorylation <em>in vitro</em>. <em>In vivo</em>, BMSC-Exos attenuated cartilage erosion, subchondral bone exposure, synovial hyperplasia and inflammatory cell infiltration. IHC analysis demonstrated that BMSC-Exos treatment significantly reduced the expression of IL-1β, TNF-α, IL-6, while restoring the levels of cartilage matrix components in cartilage compared to the OA model group. Reduced phospho-p65 levels correlated with these histological and molecular improvements.</div></div><div><h3>Conclusion</h3><div>MSC-Exos protect chondrocytes from inflammatory injury via promoting proliferation, inhibiting apoptosis, reducing inflammation, and suppressing NF-κB, with therapeutic potential for OA.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103157"},"PeriodicalIF":2.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Betanin mitigates vancomycin-induced acute kidney injury in mice and molecular docking indicated inhibition of STAT3 phosphorylation","authors":"Haifa Alrshedi ,&nbsp;Sawsan A. Zaitone ,&nbsp;Reem Alshaman ,&nbsp;Mohamed A. Helal ,&nbsp;Abdullah Alattar ,&nbsp;Sarah A. Alshammari ,&nbsp;Hibah S. Bedaiwi ,&nbsp;Ghiadaa K. Sroor ,&nbsp;Ibtisam R. Alnasser ,&nbsp;Abduallh J. Ghabban ,&nbsp;Eman Serry Zayed ,&nbsp;Roba Alatawy ,&nbsp;Dina M. Khodeer","doi":"10.1016/j.tice.2025.103159","DOIUrl":"10.1016/j.tice.2025.103159","url":null,"abstract":"<div><div>Acute kidney injury (AKI) is a common, complicated disorder affecting hospitalized and critically ill patients. The signal transducer and activator of transcription-3 (STAT3) is associated with the progress of AKI. Betanin is a natural betacyanin with multiple biological activities. The contribution of STAT3 in vancomycin-induced AKI and possible protection by betanin were investigated in this study. Molecular docking and molecular dynamics simulation (MDS) studies were done to test the probability of inhibition of STAT3 phosphorylation by betanin. Further, the experiment included eighteen male albino mice were assigned as (i) saline group, (ii) AKI control group (received vancomycin 200 mg/kg) by intraperitoneal injection for 14 doses, and (iii) vancomycin + betanin (50 mg/kg) group. Serum urea and creatinine were measured. Frozen kidneys were used for measuring inflammatory markers, whereas formalin-fixed kidneys were cut into sections to prepare specimens stained with hematoxylin and eosin. Molecular docking showed that betanin can hinder STAT3 phosphorylation. Serum urea and creatinine were found elevated in the AKI group versus the saline group; but reduced in the vancomycin + betanin group. Further, histopathological examination indicated tubular degeneration and interstitial inflammation that was mitigated by betanin. Betanin attenuated vancomycin-induced AKI, enhanced kidney function parameters, and retained the integrity of renal histological structures. These effects were, at least partly, facilitated via inhibiting the phosphorylation of the upregulated STAT3. These results open an avenue to fully test the effect and mechanism of betanin in various models of kidney injuries.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103159"},"PeriodicalIF":2.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Magnesium-loaded carbon quantum dots in polycaprolactone scaffolds enhance angiogenesis and accelerate wound healing: In vitro, In Ovo, and in vivo evidence","authors":"Tannaz Afshin ,&nbsp;Saber Zahri ,&nbsp;Arash Abdolmaleki ,&nbsp;Asadolah Asadi ,&nbsp;Habibolah Eskandari","doi":"10.1016/j.tice.2025.103158","DOIUrl":"10.1016/j.tice.2025.103158","url":null,"abstract":"<div><div>Wound healing and tissue regeneration are critical challenges, particularly in chronic conditions such as diabetes, where impaired angiogenesis often delays recovery. In this study, a novel bioactive wound dressing was developed by synthesizing magnesium-loaded carbon quantum dots (Mg-CQDs) and incorporating them into polycaprolactone (PCL) electrospun scaffolds. CQDs were prepared hydrothermally and subsequently bonded with Mg²⁺ ions via ionic interaction, forming nanocomposites with enhanced fluorescence and bioactivity. Characterization confirmed their structural integrity and surface modification. In vitro scratch assays using PC12 cells demonstrated significantly improved cell migration with Mg-CQD treatment. In ovo chorioallantoic membrane (CAM) assays showed enhanced neovascularization, and in vivo wound healing studies in rats revealed accelerated tissue regeneration, increased epithelialization, and collagen deposition in Mg-CQD-treated groups compared to controls. Compared to the reference group, VLDM enhancements ranged from 0.611 % to 0.749 % for the CQD group and from 0.802 % to 1.19 % for the CQD-Mg group. These results suggest that Mg-CQD-loaded PCL scaffolds offer a multifunctional platform for promoting angiogenesis and wound repair, combining structural support with targeted ion delivery and potential theranostic applications.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103158"},"PeriodicalIF":2.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review on development in synthesis process, characteristics, and biological applications of transition metal dichalcogenides quantum dots","authors":"Surya Pratap","doi":"10.1016/j.tice.2025.103156","DOIUrl":"10.1016/j.tice.2025.103156","url":null,"abstract":"<div><div>Nowadays, transition-metal dichalcogenides (TMDs) based fluorescent quantum dots (QDs) have gained considerable interest from scientific community because of their potent applications in biological science such as photothermal therapy, bioimaging, and nanomedicine. The intrinsic properties of TMDs QDs, like high brightness, long-lasting optical properties, size-tunability, narrow-range luminescence, surface functionalisation, and emission energies of quantum states, with biocompatibility enhances the biomedical efficacy of TMDs QDs. These properties together make them suitable for biological applications. However, various limiting factors (aggregation, control over QDs, poorly understood surface chemistry, and cytotoxicity, etc.) are associated with the TMDs QDs which hinder their wide application. These challenges must be understood and more rationalised process need to be adopted for the synthesis and to enhance their biocompatibility before they are widely validated. This review provides an overview of TMDs QDs technology dealing with the currently used synthesis approaches (top-down and bottom-up approaches), characterization of physical properties, and applications in biosensors, photothermal therapy, drug delivery, and bioimaging. In addition, the influence of synthesis technique on their distinctive features, such as UV-absorbance, stable fluorescent properties with tunable bio-functionality, toxicity effects, and quantum yield (QY) has been discussed. The existing challenges need to be addressed, and future prospects have been presented in a systematic way.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103156"},"PeriodicalIF":2.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside Rg3 alleviates allergic rhinitis by regulating NLRP3-mediated inflammatory response and pyroptosis through SIRT6","authors":"Wei Wang ,&nbsp;Fang Wang","doi":"10.1016/j.tice.2025.103153","DOIUrl":"10.1016/j.tice.2025.103153","url":null,"abstract":"<div><h3>Background</h3><div>Allergic rhinitis (AR) is positively correlated with pyroptosis induced by NLR family pyrin domain containing 3 (NLRP3). Here, the effect of ginsenoside Rg3 on pyroptosis in the progression of AR was evaluated.</div></div><div><h3>Methods</h3><div>Human nasal epithelial cells (HNEPCs) were exposed to house dust mite (HDM) allergen to establish an AR cell model. Cell viability and pyroptosis were tested utilizing CCK-8 and flow cytometry. RT-qPCR and Western blot were used to detect mRNA and protein expression. Co-immunoprecipitation (Co-IP) assay was adopted to validate the molecular interaction. IgE, IL-4, IL-5, IL-13, IL-1β and IL-18 were detected by ELISA. AR mouse model was established using OVA and aluminum hydroxide. The sneezing frequency and nose rubbing frequency of mice were evaluated. HE staining was used to evaluate the pathological changes of nasal mucosa. Pyroptosis was detected by TUNEL and GSDMD staining.</div></div><div><h3>Results</h3><div>Ginsenoside Rg3 blocked NLRP3 inflammasome activation and pyroptosis induced by HDM allergen in HNEPCs, and increased cell activity inhibited by HDM. SIRT6 depletion overturned the suppressive effect of ginsenoside Rg3 on HDM-caused inflammation and pyroptosis in HNEPCs. Blocking SIRT6 diminished ginsenoside Rg3's protective role against sneezing and rubbing nose, inflammation and pyroptosis in AR mice. Furthermore, Co-IP assay confirmed that SIRT6 interacted with NLRP3 protein in HNEPCs. SIRT6 overexpression could decrease NLRP3 acetylation level and reduce NLRP3 expression.</div></div><div><h3>Conclusion</h3><div>Our results reveal that ginsenoside Rg3 mitigates AR by controlling NLRP3-triggered inflammatory response and pyroptosis via SIRT6, which provides a new therapeutic strategy for AR treatment.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103153"},"PeriodicalIF":2.5,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145226856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of Lcn2 alleviates pyroptosis in a neonatal rat model of necrotizing enterocolitis through IL-17A signaling pathway suppression","authors":"Shuyun Chen ,&nbsp;Xiaobing Sun ,&nbsp;Sen Xu ,&nbsp;Zhenhua Yang ,&nbsp;Rao Cui","doi":"10.1016/j.tice.2025.103152","DOIUrl":"10.1016/j.tice.2025.103152","url":null,"abstract":"<div><h3>Background</h3><div>Necrotizing enterocolitis (NEC) is a life-threatening gastrointestinal disease primarily affecting premature infants. However, the specific regulatory molecular mechanisms focused on pyroptosis remain unclear.</div></div><div><h3>Methods</h3><div>Lipocalin-2 (<em>Lcn2</em>) was identified as a pyroptosis-associated hub gene by bioinformatics methods. Neonatal rats were fed formula milk and subjected to hypoxia (100 % N₂, 70 s) and hypothermia (4°C, 10 min). Rat intestinal epithelial cells-6 (IEC-6) and human intestinal epithelial cells-6 (HIEC-6) were stimulated with lipopolysaccharide (LPS) to mimic NEC-induced inflammation. Histological evaluation of ileal tissues was conducted using hematoxylin and eosin (HE) staining. Survival rate, body weight, and intestinal injury scores were assessed. To investigate cell viability, apoptosis, pyroptosis, and inflammatory cytokine levels, Cell Counting Kit-8 assay, flow cytometry, western blot, and enzyme-linked immunosorbent assay were conducted.</div></div><div><h3>Results</h3><div><em>Lcn2</em> expression was significantly upregulated in NEC ileal tissues and LPS-treated IEC-6 cells. <em>Lcn2</em> knockdown alleviated intestinal injury, improved survival, and suppressed the expression of NLRP3, cleaved Caspase-1, GSDMD-N, and proinflammatory cytokines (IL-1β, IL-6, TNF-α, IL-18, and HMGB1) in a neonatal rat model of NEC. <em>Lcn2</em> knockdown restored cell viability, reduced apoptosis, and inhibited pyroptosis in LPS-stimulated IEC-6 and HIEC cells, an effect that was notably abolished by nigericin, an NLRP3 inflammasome activator. Mechanistically, <em>Lcn2</em> knockdown downregulated the expression of <em>IL-17a</em> and its receptor <em>IL-17ra</em>. Recombinant IL-17A treatment markedly reversed the protective effects of <em>Lcn2</em> silencing <em>in vitro</em> and <em>in vivo</em>.</div></div><div><h3>Conclusion</h3><div><em>Lcn2</em> knockdown inhibits intestinal inflammation and pyroptosis in NEC through the blockade of the IL-17A pathway, providing a promising therapeutic approach for NEC treatment.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103152"},"PeriodicalIF":2.5,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145158513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adiponectin attenuates atherosclerosis via macrophage polarization-mediated T Cell exhaustion by modulating the NF-κB p65/PI3K/Akt signaling pathway","authors":"Man Qin ,&nbsp;Sufang Xu ,&nbsp;Yuefeng Chen ,&nbsp;Xiaoxiao Luo ,&nbsp;Xiaolei Tang ,&nbsp;Liang Zhang ,&nbsp;Qin Xu","doi":"10.1016/j.tice.2025.103150","DOIUrl":"10.1016/j.tice.2025.103150","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to investigate the role of adiponectin (AD) in attenuating atherosclerosis (AS) by modulating macrophage polarization and inducing T cell exhaustion.</div></div><div><h3>Methods</h3><div>Male Apolipoprotein E deficient (ApoE^−/−) mice were fed a high-fat diet (HFD) to establish AS models. Mice were randomized into four groups (n = 10): Model, AD, anti-PD-1, and AD+PD-1 combination therapy. Plasma lipid profiles were quantified via ELISA. Atherosclerotic plaques were assessed by HE and Oil Red O staining. Splenic T cell subsets were analyzed using immunofluorescence, while protein expression of inhibitory receptors and NF-κB p65/PI3K/Akt pathway components was evaluated by Western blot.</div></div><div><h3>Results</h3><div>AD administration significantly improved systemic lipid metabolism, reducing serum triglycerides and low-density lipoprotein levels while elevating high-density lipoprotein. AD induced macrophage polarization toward an anti-inflammatory M2 phenotype, characterized by upregulated CD206 and CD163 expression and suppressed CD64 and CD80 levels. This shift correlated with diminished cytokines including IFN-γ, IL-4 and IL-10 production in atherosclerotic plaques. AD also induced T cell exhaustion, marked by increased the expression of inhibitory receptors (PD-1, LAG3, TIM3, CTLA-4), expansion of regulatory T cells (CD4 +Foxp3 +, CD4 +IL-4 +), and suppression of CD4 +IFN-γ+ , CD4 +IL-9 + and CD8 +IL-9 + subsets. Mechanistically, AD inhibited NF-κB p65 nuclear translocation and PI3K/Akt signaling.</div></div><div><h3>Conclusion</h3><div>AD ameliorates AS through a dual mechanism of immunometabolic regulation, which involves the stabilization of plaques via macrophage M2 polarization and the induction of T cell exhaustion. This process limits tissue damage resulting from excessive immune activation, mediated by the NF-κB/PI3K/Akt signaling pathway.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103150"},"PeriodicalIF":2.5,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145158515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Massage therapy modulates energy metabolism and alleviates skeletal muscle spasms in rats","authors":"Jiawei Sun ,&nbsp;Changhe Yu ,&nbsp;Yang Zhang ,&nbsp;Fenglin Li ,&nbsp;Yanhua Wang ,&nbsp;Eryang Liu ,&nbsp;Junming Guo ,&nbsp;Xiyou Wang ,&nbsp;Zhifeng Liu","doi":"10.1016/j.tice.2025.103151","DOIUrl":"10.1016/j.tice.2025.103151","url":null,"abstract":"<div><div>Skeletal muscle spasm is a common pathological response to trauma, exercise-induced fatigue, and neurological diseases. Massage therapy is common in relaxation and rehabilitation procedures; however, its underlying metabolic mechanisms remain unclear. We aimed to explore the effects of massage therapy on muscle metabolism in a rat model of skeletal muscle spasm. Twenty-four Sprague-Dawley rats were randomly divided into three groups: control, model, and massage. A rat model of muscle spasm in the model and massage groups was established via exercise-induced fatigue. Kneading manipulation was performed in the massage group. The pain threshold was assessed using mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL). Hemorheological parameters were measured to evaluate blood viscosity. Lactic acid (LA) and blood urea nitrogen (BUN) levels were quantified using biochemical assays. The ultrastructure of the gastrocnemius muscle was observed using transmission electron microscopy. The metabolomic profiling of the gastrocnemius muscle was performed through liquid chromatography-mass spectrometry. Compared with those in the model group, the MWT and TWL in the massage group were increased, and the oscillation frequency, blood viscosity, plasma viscosity, and LA and BUN levels were decreased. Electron microscopy revealed that the myofibrils in the massage group were more orderly arranged than those in the model group, with the massage group exhibiting clear light and dark bands and increased mitochondria. The metabolomics results showed 136 differential metabolites between the massage and model groups, which primarily participate in glycolysis, the pentose phosphate pathway, inositol metabolism, and lipid metabolism. Massage therapy effectively alleviated skeletal muscle spasms, pain, and circulatory disorders caused by muscle spasms. It improved muscle metabolism by regulating the energy-related metabolic pathways and metabolites.</div></div><div><h3>Trial registration</h3><div>Clinical Trial Number: Not applicable.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"98 ","pages":"Article 103151"},"PeriodicalIF":2.5,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145118660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}