middle cerebral artery (mca)  (SAS institute)

Journal: Cell Communication and Signaling : CCS

Article Title: Mechanisms of electroacupuncture-induced neuroprotection in acute stroke rats: the role of astrocyte-mediated mitochondrial transfer

doi: 10.1186/s12964-025-02287-9

Figure Lengend Snippet: Study on the time-effect relationship of EA pretreatment and EA intervention for neuronal protection in MCAO model rats. (A) Timeline of EA pretreatment and EA intervention. (B) B1: The effects of EA intervention at different time points on the mNSS and Garcia JH scores in MCAO model rats ( n = 12 per group); B2: The effects of different numbers of EA pretreatments on the mNSS and Garcia JH score in MCAO model rats ( n = 10 per group). (C) Representative TTC-stained images of MCAO rats. C1: The effects of different numbers of electroacupuncture pretreatments on the infarct volume in MCAO model rats ( n = 7 per group) C2: The effects of electroacupuncture intervention at different time points on the infarct volume in MCAO model rats ( n = 10 per group). S, sham operation group; M, model group; EA, electroacupuncture group (ns: P > 0.05; *: P < 0.05; **: P < 0.01; ****: P < 0.001). (D) The effects of electroacupuncture intervention and electroacupuncture pretreatment on the number of TUNEL-positive cells in the ischemic penumbra cortex of MCAO rats. Green: TUNEL; Blue: DAPI; merge: TUNEL + DAPI. D1: The effects of different numbers of electroacupuncture pretreatments on the apoptosis rate of neurons in the infarcted brain tissue of MCAO model rats ( n = 5 per group). D2: The effects of electroacupuncture intervention 12 h after modeling on the apoptosis rate of neurons in the infarcted brain tissue of MCAO model rats ( n = 4 per group). (One-way ANOVA was used for comparison among multiple groups, and Tukey’s post hoc test was used for pairwise comparison. ns: P > 0.05; *: P < 0.05; **). (E) E1: Electron micrographs showing the effects of EA intervention on the morphology and structure of neurons and astrocytes in the ischemic penumbra of the cerebral cortex in MCAO model rats ( n = 4 per group). E2: Electron micrographs showing the effects of EA pretreatment on the morphology and structure of neurons and astrocytes in the ischemic penumbra of the cerebral cortex in MCAO model rats ( n = 4 per group). Note : EA Acupoints: Baihui (GV20), bilateral Neiguan (PC6), and Sanyinjiao (SP6). EA Parameters: Sparse-dense waves: 2/10 Hz, Intensity: 1 mA, Duration: 20 min

Article Snippet: A middle cerebral artery occlusion (MCAO) model in Sprague-Dawley (SD) rats and an oxygen-glucose deprivation/reperfusion (OGD/R) model in vitro were employed.

Techniques: Staining, TUNEL Assay, Comparison

Journal: Cell Communication and Signaling : CCS

Article Title: Mechanisms of electroacupuncture-induced neuroprotection in acute stroke rats: the role of astrocyte-mediated mitochondrial transfer

doi: 10.1186/s12964-025-02287-9

Figure Lengend Snippet: Effects of EA on the distribution, functional activity and morphology of mitochondria in the brain of MCAO rats. (A) Multiple immunofluorescence staining, panoramic tissue quantitative analysis and the effects of EA intervention on mitochondrial functional activity. A1: Effects of EA intervention on mitochondrial aggregation near neurons in the ischemic penumbra of the cerebral cortex of MCAO rats ( n = 4 per group). A2: Effects of EA intervention on mitochondrial aggregation near astrocytes in the ischemic penumbra of the cerebral cortex of MCAO rats ( n = 4 per group). A3: Effects of EA intervention on mitochondrial membrane potential in the ischemic penumbra of the cerebral cortex of MCAO rats ( n = 4 per group). A4: Effects of EA intervention on mitochondrial activity of neurons in the ischemic penumbra of the cerebral cortex of MCAO rats ( n = 4 per group). (B) Effects of EA intervention and EA pretreatment on the morphological structure of mitochondria near neurons and astrocytes in the ischemic penumbra of the cerebral cortex of MCAO rats ( n = 4 per group). (C) Study on the process of EA regulating mitochondrial transcellular transfer based on stereotaxic brain injection. C1: Mitochondrial aggregation in the brain of MCAO model rats (Figure a shows the TTC staining results of the whole brain and brain slices; Figure b shows the results of brain tissue immunofluorescence staining, blue is DAPI, green is Tunel cell apoptosis, the scale bar is 2000 μm, and Figure d shows the results of its enlarged scale bar of 200 μm; Figure e shows the results of brain tissue immunofluorescence staining, blue is DAPI, green is NeuN (neuron), the scale bar is 200 μm, and Figure c shows the results of its reduced scale bar of 2000 μm. As can be seen from the figure, the number of neurons on the affected side is significantly less than that on the healthy side). C2: The effect of active mitochondria after acupuncture injection on the apoptosis rate of nerve cells in MCAO model rats (**: P < 0.01) ( n = 5 per group). (D) The effect of different doses of astrocytes injected into the brain on the distribution of mitochondria in the brain of MCAO model rats. D1: The effect of different doses of astrocytes injected on the apoptosis rate of neurons in MCAO rats ( n = 5 per group). D2: The effect of different doses of astrocytes injected on the distribution area of ​​mitochondria in the brain ( n = 5 per group). (E) The effect of EA on mitochondrial distribution in the brains of MCAO model rats injected with 5 μm-sized astrocytes. E1: The effect of EA on neuronal apoptosis in MCAO rats injected with astrocytes ( n = 5 per group). E2: The effect of EA on the area of mitochondrial distribution in the brains of MCAO rats injected with astrocytes ( n = 5 per group)

Article Snippet: A middle cerebral artery occlusion (MCAO) model in Sprague-Dawley (SD) rats and an oxygen-glucose deprivation/reperfusion (OGD/R) model in vitro were employed.

Techniques: Functional Assay, Activity Assay, Immunofluorescence, Staining, Membrane, Injection, TUNEL Assay

Journal: Cell Communication and Signaling : CCS

Article Title: Mechanisms of electroacupuncture-induced neuroprotection in acute stroke rats: the role of astrocyte-mediated mitochondrial transfer

doi: 10.1186/s12964-025-02287-9

Figure Lengend Snippet: Study on the regulation of mitochondrial transcellular transfer by EA in MCAO rats. (A) In vitro experimental study on mitochondrial transcellular transfer in neural cells under OGD conditions. A1:Immunofluorescence staining of neurons, microglia and astrocytes in the lower chamber of Transwell. A2: Effect of (primary) neuronal group, microglia group and astrocyte group on the apoptosis rate of neuronal cells after OGD (flow cytometry) & Results of the apoptosis assay (Annexin V/PI double staining method). A3: Lactate dehydrogenase (LDH) cellular colorimetric assay results. (B) In vitro experimental study on EA preconditioning promoting mitochondrial release from astrocytes in the ischemic penumbra of the rat cerebral cortex (Acu-Astro + Neuron group, n = 6; Astro + Neuron group, n = 5; neuron group, n = 4).B1: Mito-tracker labeled astrocytes mitochondria transferred into neurons (Mito-tracker in red, Fluorescence microscopy at 20x magnification). B2: Mitochondrial fluorescence markers that appear in the axon of neurons (Fluorescence microscopy at 40x magnification). B3: Relative cell viability of neurons wre assessed by CCK-8 after astrocytes/Acu-astrocytes treatment after OGD/R injury (** neuron vs. astro + neuron, P < 0.01;**neuron vs. Acu-astrocytes, P < 0.01). B4: Effect of EA preconditioning on positive cells percentage of TUNEL staining in OGD/R (** neuron vs. astro + neuron, P < 0.01;**neuron vs. Acu-astrocytes, P < 0.01)

Article Snippet: A middle cerebral artery occlusion (MCAO) model in Sprague-Dawley (SD) rats and an oxygen-glucose deprivation/reperfusion (OGD/R) model in vitro were employed.

Techniques: In Vitro, Immunofluorescence, Staining, Flow Cytometry, Apoptosis Assay, Double Staining, Colorimetric Assay, Labeling, Fluorescence, Microscopy, CCK-8 Assay, TUNEL Assay

Journal: Cell Communication and Signaling : CCS

Article Title: Mechanisms of electroacupuncture-induced neuroprotection in acute stroke rats: the role of astrocyte-mediated mitochondrial transfer

doi: 10.1186/s12964-025-02287-9

Figure Lengend Snippet: Mechanistic study on how EA promotes the release of mitochondria from astrocytes in the ischemic penumbra of the rat cerebral cortex. A) EA preconditioning promotes the release of mitochondria from astrocytes in the ischemic penumbra of the rat cerebral cortex by upregulating the expression of astrocytic CD38 and indirectly modulating the CD38-cADPR-Ca²⁺ pathway ( n = 8 per group). A1: Immunohistochemical observation of the expression of CD38 on neurons and astrocytes. A2: The expression of CD38 in astrocyts with or without 8-Br-cADPR. Tested by Western blot ( n = 4 per group, * P < 0.01). A3: The effect of 8-BR-CADPR on LDH release level of neurons after co-culture with EA-preconditioned astrocytes ( n = 4 per group). A4: Antagonizing CD38 inhibits the release of mitochondria from EA-preconditioned astrocytes to neurons injured by OGD. A5: Effect of 8-Br-cADPR on intracellular Ca2 + in astrocyte after co-cultured in OGD condition. (B) Molecular mechanism study on the intercellular transfer of astrocytic mitochondria via the TNT pathway induced by EA in MCAO model rats. B1: Effect of EA on F-actin expression in P region ( n = 5 per group). B2: Effect of EA on F-actin expression in CP region( n = 5 per group). B3: The effect of EA on the gene expression of F-actin, Miro 1, TRAK 1, KIF 5a, KIF5b and KIF5c ( n = 4 per group, ## P <0.01 vs. Sham; * P <0.05, ** P <0.01 vs. MCAO). B4: The effect of EA on the expression of F-actin, Miro 1, TRAK 1 and KIF 5 protein( n = 4 per group)

Article Snippet: A middle cerebral artery occlusion (MCAO) model in Sprague-Dawley (SD) rats and an oxygen-glucose deprivation/reperfusion (OGD/R) model in vitro were employed.

Techniques: Expressing, Immunohistochemical staining, Western Blot, Co-Culture Assay, Cell Culture, Gene Expression

Journal: Journal of Neuroinflammation

Article Title: Complement inhibition targets a rich-club within the neuroinflammatory network after stroke to improve radiographic and functional outcomes

doi: 10.1186/s12974-024-03316-z

Figure Lengend Snippet: Study design and analytical pipeline. a Adult C57BL/6 J mice were randomized into either a sham group or subjected to 60 min of transient middle cerebral artery occlusion (MCAO). b – c behavioral testing included neurological severity score (NSS) performed daily, corner task performed on day 4, novel object recognition task (NOR) performed on day 3, and passive avoidance (PA) performed on day 4. (c) MRI scans were conducted on day 4 post-stroke using a 7 T/30 Bruker Biospec animal scanner including T2-weighted imaging, diffusion tensor imaging (DTI) and diffusion kurtosis imaging (DKI). d Mice were sacrificed 5 days post-MCAO, and ipsilateral hemisphere representing the MCA territory was harvested, and homogenized for RNA extraction. e RNA was extracted using the RNeasy Lipid Tissue kit (Qiagen). f High-throughput analysis of immunology-related gene expression was carried out using the Nanostring Mouse Immunology Codeset comprising 561 genes. g Expression data were analyzed, and differentially expressed genes (DEGs) were identified. h Gene Ontology analysis was used to functionally annotate the DEGs. i Using gene interaction data from the STRING database and the weighted gene co-expression network analysis (WGCNA) algorithm, a gene interaction network was constructed using the identified DEGs. j Graph theory methodology was then used to identify the network hub genes, known as “rich-club” genes. k Ingenuity Pathway Analysis (IPA) software was used to identify upstream regulators of the rich-club genes, and the results were visualized using Cytoscape. l In vivo inhibition of C3 activation, an IPA-identified target, was conducted in a similar paradigm to ( a ), and the correlation between treatment and outcomes was analyzed

Article Snippet: We used the transient middle cerebral artery occlusion (MCAO) model in adult C57BL/6j mice (Jackson Laboratories) to mimic clinical stroke and mechanical reperfusion.

Techniques: Imaging, Diffusion-based Assay, RNA Extraction, High Throughput Screening Assay, Gene Expression, Expressing, Construct, Software, In Vivo, Inhibition, Activation Assay

Journal: Journal of Neuroinflammation

Article Title: Complement inhibition targets a rich-club within the neuroinflammatory network after stroke to improve radiographic and functional outcomes

doi: 10.1186/s12974-024-03316-z

Figure Lengend Snippet: Analysis of gene expression, network construction and identification of network rich-club nodes. a Heatmap showing the differential expression of immunology-related genes between sham (N = 4) and transient middle cerebral artery occlusion (MCAO, N = 9) groups. b Functional annotation for top biological processes among differentially expressed genes (DEGs) between sham and MCAO using Gene Ontology analysis. c Illustrative demonstration of random and scale-free network topology. d Curve plot showing the power law distribution of node degrees within the constructed DEGs network. e Bar plot showing significant difference between the clustering coefficient of the DEGs network as compared to 1000 random constructed networks with similar degree distribution. Permutation test *P < 0.01. f Curve plot showing the rich-club coefficient (φ) of the DEGs network (blue) and random networks (red) plotted against the left vertical axis, while normalized rich-club coefficient (ρ) (green) is plotted against right vertical axis. The gray shaded area indicated the rich-club region where ρ > 1, while the red shaded area indicated the strongest rich-club component where the DEGs network rich-club coefficient plateaus at φ = 1. Horizontal dashed lines correspond to φ and ρ = 1. g Interactive network showing the identified rich-club genes. h Bar plot showing the in degree centrality between rich-club (RC) nodes and other nodes within the DEGs network. Student’s t-test. ****P < 0.001. Shown is mean ± SD i Functional annotation for top biological processes enriched within the rich-club genes using Gene Ontology analysis

Article Snippet: We used the transient middle cerebral artery occlusion (MCAO) model in adult C57BL/6j mice (Jackson Laboratories) to mimic clinical stroke and mechanical reperfusion.

Techniques: Gene Expression, Quantitative Proteomics, Functional Assay, Construct