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TargetMol y-27632
Y 27632, supplied by TargetMol, used in various techniques. Bioz Stars score: 95/100, based on 99 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/y+27632/Y-27632/custom%40t1870%4042784458
Average 95 stars, based on 99 article reviews

y-27632 - by Bioz Stars, 2026-10

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Article Title: A Human Neural Tube Model Using 4D Self‐Folding Smart Scaffolds
Article Snippet: .. Cells were then centrifuged at 200 x g for 3 min. After pellet resuspension, cells were counted and plated at a density of 0.7 × 10 5 cells cm −2 in neural induction medium (DMEM‐F12/Neurobasal mixture 1:1, 1% N2, 2% B27, 20 μg mL −1 insulin, 1% MEM‐nonessential amino acids, 1% L‐glutamine, 0.1% 2‐mercaptoethanol) supplemented with Dual SMAD inhibition factors, i.e., 10 μ m SB431542 (TargetMol; #T1726), 100 n m LDN193189 (STEMCELL Technologies; #72144), 2 μ m XAV939 (STEMCELL Technologies; #72674), and 10 μ m Y‐27632 (TargetMol; #T1725) to increase cell survival. ..

Article Title: A Human Neural Tube Model Using 4D Self-Folding Smart Scaffolds.
Article Snippet: .. Cells were then centrifuged at 200 x g for 3 min. After pellet resuspension, cells were counted and plated at a density of 0.7 × 105 cells cm−2 in neural induction medium (DMEM-F12/Neurobasal mixture 1:1, 1% N2, 2% B27, 20 μg mL−1 insulin, 1% MEM-nonessential amino acids, 1% L-glutamine, 0.1% 2-mercaptoethanol) supplemented with Dual SMAD inhibition factors, i.e., 10 μm SB431542 (TargetMol; #T1726), 100 nm LDN193189 (STEMCELL Technologies; #72144), 2 μmXAV939 (STEMCELL Technologies; #72674), and 10 μm Y-27632 (TargetMol; #T1725) to increase cell survival. ..

Cell Culture:

Article Title: BHLHE40 Cooperates with GATA2/3 to Control Human Syncytiotrophoblast Lineage Differentiation
Article Snippet: .. TSCs were cultured in Matrigel‐coated (354277, Corning) plates and maintained in Advanced DMEM/F‐12 medium with 0.2% fetal bovine serum (FBS), 0.3% bovine serum albumin (BSA; Sigma–Aldrich, A9418), 1% ITS‐X (Gibco, 51500), 50 ng mL −1 recombinant human epidermal growth factor (EGF; Peprotech, AF‐100‐15), 2 μM m CHIR99021 (TargetMol, T2301), 0.5 μM m A83‐01 (PeproTech, 90943360), 5 μM Y‐27632 (TargetMol, T1870), 1 μM m SB431542 (TargetMol, T1726), 0.8 mM m valproic acid (TargetMol, T7064), 1.5 mg mL −1 L‐ascorbic acid (TargetMol, T0928), 0.1 mM m β‐mercaptoethanol (Thermo Fisher Scientific, 21985023), and 0.5% penicillin‐streptomycin. .. For cell passages, TSCs were washed with phosphate‐buffered saline (PBS) and dissociated by TrypLE Express (Thermo Fisher Scientific) for 5 min, followed by seeding at a 1:3 to 1:4 ratio.

Recombinant:

Centrifugation:

Article Title: Cell-of-Origin, not Oncogenic Effect, Determines Desmoplastic Immune Exclusion in KRAS-Driven Liver Cancer
Article Snippet: [ ] The pBabe-KrasG12D plasmid was reconstructed from pBabe-Kras G12D -puro (Addgene #58902) by removing the puromycin resistance gene through digestion with HindIII-HF and BspDI, blunt-ended by Klenow and re-ligation to restore plasmid circularity. .. After quenching with cold DMEM and centrifugation, cells were resuspended in chol GF+ media with 10μM of Y-27632 (TargetMol, #TMO-T1725-50mg) and plated at 450 μL/well in a 48-well plate. .. The Lenti-CRISPR-sgRNA( Trp53 ), pBabe- Kras G12D , or Lenti-luciferase-P2A-Neo plasmid (Addgene #105621) was co-transfected with packaging plasmid psPAX2 and pMD2.G (both from PlasmidFactory GmbH & Co. KG, Bielefeld, Germany) into HEK293T cells by TransIT LT1 transfection reagent according to the manufacturer’s instructions (Mirus Bio, Madison, WI, USA).

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LSS triggers m/lEV release via Ca 2+ ‐CaMKII‐MLC signalling. (A) LSS (15 dyn/cm 2 for 300 s) induced Piezo1 translocation to the cell periphery colocalising with the microvesicle formation site ( n = 3). PKH26, a lipophilic membrane dye for labelling the membrane structures of EVs and cells. (B) Piezo1 reduction by siRNA suppressed LSS‐induced Piezo1 translocation to the cell periphery ( n = 3). (C) Inhibition of Ca 2+ signal through Thapsigargin (TG, 1 µM) and BAPTA (10 µM) blocked Yoda1 (Piezo1 agonist, 2 µM)‐induced Piezo1 translocation to the cell periphery ( n = 3). (D) TG and BAPTA inhibited Yoda1‐induced m/lEV release as imaged by confocal microscope ( n = 200 cells from three independent experiments). (E) TG and BAPTA suppressed Yoda1‐induced m/lEV release as detected by Western blot ( n = 3). (F) TG and BAPTA inhibited Yoda1‐induced MLC phosphorylation in HUVECs ( n = 3). (G) MLC reduction did not affect the Yoda1‐induced Piezo1 translocation to the cell periphery ( n = 3). (H) MLC reduction reduced Yoda1‐induced m/lEV release as visualized by confocal microscope ( n = 200 cells from three independent experiments). (I) MLC reduction attenuated Yoda1‐induced m/lEV release as detected by Western blot ( n = 3). (J) MLC reduction decreased Yoda1‐induced MLC phosphorylation ( n = 3). (K) Pharmacological inhibition of MLC phosphorylation by Y27632 (2 µM) did not affect the Yoda1‐induced Piezo1 translocation to the cell periphery ( n = 3). (L) Y27632 reduced Yoda1‐induced m/lEV release as visualized by confocal microscope ( n = 200 cells from three independent experiments). (M) Y27632 attenuated Yoda1‐induced m/lEV release and MLC phosphorylation as detected by Western blot ( n = 3). (N) KN‐62 (CaMKII inhibitor, 1 µM), but not PD150606 (Calpain inhibitor, 10 µM), blocked Yoda1‐induced Piezo1 translocation to the cell periphery ( n = 3). (O) KN‐62 reduced Yoda1‐induced m/lEV release as imaged by confocal microscope ( n = 200 cells from three independent experiments). (P) KN‐62 attenuated Yoda1‐induced m/lEV release and MLC phosphorylation as detected by Western blot ( n = 3). (Q) Schematic diagram showing that Piezo1 activation‐induced Piezo1 translocation to the cell periphery and m/lEV release are mediated by Ca 2+ ‐CaMKII signalling. In imaging experiments and subsequent quantitative analysis, HUVECs were subjected to either 15 dyn/cm 2 LSS for 300 s or Yoda1 for 10 min. For Western blot analysis, HUVECs were treated with Yoda1 for 24 h to ensure adequate EV collection. The quantified results of the Western blot were shown in Figure . All inhibitors were added 5 min prior to Yoda1 stimulation. Data are presented as mean ± SEM. ** p < 0.01.

Journal: Journal of Extracellular Vesicles

Article Title: Shear Stress‐Stimulated Trafficking of Endothelial Piezo1 to Splenic Capsule Boosts Spleen Contraction and Exercise Endurance

doi: 10.1002/jev2.70375

Figure Lengend Snippet: LSS triggers m/lEV release via Ca 2+ ‐CaMKII‐MLC signalling. (A) LSS (15 dyn/cm 2 for 300 s) induced Piezo1 translocation to the cell periphery colocalising with the microvesicle formation site ( n = 3). PKH26, a lipophilic membrane dye for labelling the membrane structures of EVs and cells. (B) Piezo1 reduction by siRNA suppressed LSS‐induced Piezo1 translocation to the cell periphery ( n = 3). (C) Inhibition of Ca 2+ signal through Thapsigargin (TG, 1 µM) and BAPTA (10 µM) blocked Yoda1 (Piezo1 agonist, 2 µM)‐induced Piezo1 translocation to the cell periphery ( n = 3). (D) TG and BAPTA inhibited Yoda1‐induced m/lEV release as imaged by confocal microscope ( n = 200 cells from three independent experiments). (E) TG and BAPTA suppressed Yoda1‐induced m/lEV release as detected by Western blot ( n = 3). (F) TG and BAPTA inhibited Yoda1‐induced MLC phosphorylation in HUVECs ( n = 3). (G) MLC reduction did not affect the Yoda1‐induced Piezo1 translocation to the cell periphery ( n = 3). (H) MLC reduction reduced Yoda1‐induced m/lEV release as visualized by confocal microscope ( n = 200 cells from three independent experiments). (I) MLC reduction attenuated Yoda1‐induced m/lEV release as detected by Western blot ( n = 3). (J) MLC reduction decreased Yoda1‐induced MLC phosphorylation ( n = 3). (K) Pharmacological inhibition of MLC phosphorylation by Y27632 (2 µM) did not affect the Yoda1‐induced Piezo1 translocation to the cell periphery ( n = 3). (L) Y27632 reduced Yoda1‐induced m/lEV release as visualized by confocal microscope ( n = 200 cells from three independent experiments). (M) Y27632 attenuated Yoda1‐induced m/lEV release and MLC phosphorylation as detected by Western blot ( n = 3). (N) KN‐62 (CaMKII inhibitor, 1 µM), but not PD150606 (Calpain inhibitor, 10 µM), blocked Yoda1‐induced Piezo1 translocation to the cell periphery ( n = 3). (O) KN‐62 reduced Yoda1‐induced m/lEV release as imaged by confocal microscope ( n = 200 cells from three independent experiments). (P) KN‐62 attenuated Yoda1‐induced m/lEV release and MLC phosphorylation as detected by Western blot ( n = 3). (Q) Schematic diagram showing that Piezo1 activation‐induced Piezo1 translocation to the cell periphery and m/lEV release are mediated by Ca 2+ ‐CaMKII signalling. In imaging experiments and subsequent quantitative analysis, HUVECs were subjected to either 15 dyn/cm 2 LSS for 300 s or Yoda1 for 10 min. For Western blot analysis, HUVECs were treated with Yoda1 for 24 h to ensure adequate EV collection. The quantified results of the Western blot were shown in Figure . All inhibitors were added 5 min prior to Yoda1 stimulation. Data are presented as mean ± SEM. ** p < 0.01.

Article Snippet: Pantethine (150 mg/kg, HY‐B1028, MCE, USA) or Y27632 (5 mg/kg, HY‐10071, MCE, USA) was dissolved in saline and injected intraperitoneally at 30 min before each exercise.

Techniques: Translocation Assay, Membrane, Inhibition, Confocal, Microscopy, Western Blot, Phospho-proteomics, Activation Assay, Imaging, Analysis

$Inhibition of m/lEV release inhibits the effects of shear stress on promoting endothelial function. (A) Treatment with Yoda1 (Piezo1 agonist, 2 µM) for 24 h increased m/lEV release, whereas both pantethine and Y27632 attenuated this effect ( n = 5). (B, C) Inhibition of m/lEV release by pantethine (50 µM) and Y27632 (2 µM) abolished Yoda1‐induced benefits in HUVECs, as determined by cell migration (B) and cell viability (C) ( n = 5). HUVECs were pre‐treated with pantethine or Y27632 for 5 min followed by Yoda1 treatment for 24 h. (D) Pantethine (150 mg/kg, i.p.) and Y27632 (5 mg/kg, i.p.) were used to test whether inhibiting m/lEV release causes vascular endothelial dysfunction in vivo. Pantethine or Y27632 was injected to mice at 30 min prior to each exercise. The mice were subjected to treadmill exercise at 18 m/min, 60 min/d, 5 days a week, for 1 month. All indices were tested after 1 month of exercise. (E) Schematic diagram of plasma m/lEV isolation and purification. (F) The presence of the EV markers Annexin A1, CD9, MMP2 and TSG101 were determined in SEC fractions 7–9 (500 µL/fraction) using Western blotting. Fractions 7–9 were identified as the m/lEV‐rich fractions ( n = 4). (G) Both pantethine and Y27632 blocked the upregulation of circulating m/lEVs induced by exercise, as determined by NTA ( n = 8). (H) The exercise‐induced increase in exhaustion distance on the treadmill was abolished by pantethine and Y27632 ( n = 8). (I) Pantethine or Y27632 suppressed exercise‐promoted endurance of forelimb grip strength ( n = 6). (J) Pantethine and Y27632 reduced the effect of exercise on decreasing aortic intima‐media thickness ( n = 8). (K) Treatment with pantethine or Y27632 blocked the effect of exercise on reducing blood pressure ( n = 8). (L) Pantethine and Y27632 suppressed the effect of exercise on improving endothelium‐dependent vasodilation in isolated arteries ( n = 6). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01.$

Journal: Journal of Extracellular Vesicles

Article Title: Shear Stress‐Stimulated Trafficking of Endothelial Piezo1 to Splenic Capsule Boosts Spleen Contraction and Exercise Endurance

doi: 10.1002/jev2.70375

Figure Lengend Snippet: Inhibition of m/lEV release inhibits the effects of shear stress on promoting endothelial function. (A) Treatment with Yoda1 (Piezo1 agonist, 2 µM) for 24 h increased m/lEV release, whereas both pantethine and Y27632 attenuated this effect ( n = 5). (B, C) Inhibition of m/lEV release by pantethine (50 µM) and Y27632 (2 µM) abolished Yoda1‐induced benefits in HUVECs, as determined by cell migration (B) and cell viability (C) ( n = 5). HUVECs were pre‐treated with pantethine or Y27632 for 5 min followed by Yoda1 treatment for 24 h. (D) Pantethine (150 mg/kg, i.p.) and Y27632 (5 mg/kg, i.p.) were used to test whether inhibiting m/lEV release causes vascular endothelial dysfunction in vivo. Pantethine or Y27632 was injected to mice at 30 min prior to each exercise. The mice were subjected to treadmill exercise at 18 m/min, 60 min/d, 5 days a week, for 1 month. All indices were tested after 1 month of exercise. (E) Schematic diagram of plasma m/lEV isolation and purification. (F) The presence of the EV markers Annexin A1, CD9, MMP2 and TSG101 were determined in SEC fractions 7–9 (500 µL/fraction) using Western blotting. Fractions 7–9 were identified as the m/lEV‐rich fractions ( n = 4). (G) Both pantethine and Y27632 blocked the upregulation of circulating m/lEVs induced by exercise, as determined by NTA ( n = 8). (H) The exercise‐induced increase in exhaustion distance on the treadmill was abolished by pantethine and Y27632 ( n = 8). (I) Pantethine or Y27632 suppressed exercise‐promoted endurance of forelimb grip strength ( n = 6). (J) Pantethine and Y27632 reduced the effect of exercise on decreasing aortic intima‐media thickness ( n = 8). (K) Treatment with pantethine or Y27632 blocked the effect of exercise on reducing blood pressure ( n = 8). (L) Pantethine and Y27632 suppressed the effect of exercise on improving endothelium‐dependent vasodilation in isolated arteries ( n = 6). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01.

Article Snippet: Pantethine (150 mg/kg, HY‐B1028, MCE, USA) or Y27632 (5 mg/kg, HY‐10071, MCE, USA) was dissolved in saline and injected intraperitoneally at 30 min before each exercise.

Techniques: Inhibition, Shear, Migration, In Vivo, Injection, Clinical Proteomics, Isolation, Purification, Western Blot

LSS‐induced m/lEV release maintains endothelial Piezo1 homeostasis. (A) Immunoelectron microscope visualized that Piezo1 was packaged into the m/lEVs ( n = 15 cells from three independent experiments). (B) Left panel: Confocal microscope visualized that LSS (15 dyn/cm 2 for 300 s) increased the content of Piezo1 in m/lEVs ( n = 60 cells from six independent experiments). Right panel: LSS increased the percentage of Piezo1‐positive m/lEVs ( n = 6). (C) Both LSS and Yoda1increased the content of Piezo1 in m/lEVs ( n = 4). (D) Dual stimulation with Yoda1 (Piezo1 agonist, 2 µM) and m/lEV release inhibitor (500 nM pantethine or 2 µM Y27632) induced Piezo1 over accumulation in HUVECs ( n = 4). HUVECs were pre‐treated with pantethine or Y27632 for 5 min followed by Yoda1 treatment for 24 h. (E) Dual stimulation with Yoda1 and m/lEV release inhibitor induced Ca 2+ overload in HUVECs ( n = 5). (F) Piezo1 overexpression (OE) reduced the phosphorylation of eNOS and VEGFR2 ( n = 3). Plasmid transfection for Piezo1 OE was performed 60 h prior to the cell functional analysis. (G) Piezo1 OE impaired EC migration ( n = 5). (H) Piezo1 OE impaired EC tube formation ( n = 5). (I) Piezo1 OE impaired ACh‐induced NO production ( n = 5). (J) Piezo1 OE induced Ca 2+ overload in ECs ( n = 5). (K) Treatment with either pantethine (150 mg/kg, i.p.) or Y27632 (5 mg/kg, i.p.) abolished the effect of exercise on upregulating Piezo1 in circulating m/lEVs from mice ( n = 6). The experimental schemes for m/lEV release inhibitor treatment and the exercise model were showed in Figure . (L) Chronic exercise mildly upregulated Piezo1 expression, whereas treatment with either pantethine or Y27632 induced Piezo1 over accumulation in aorta from mice with exercise ( n = 6). (M) Schematic diagram showing that LSS‐induced m/lEV release contributes to intracellular Piezo1 homeostasis. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01.

Journal: Journal of Extracellular Vesicles

Article Title: Shear Stress‐Stimulated Trafficking of Endothelial Piezo1 to Splenic Capsule Boosts Spleen Contraction and Exercise Endurance

doi: 10.1002/jev2.70375

Figure Lengend Snippet: LSS‐induced m/lEV release maintains endothelial Piezo1 homeostasis. (A) Immunoelectron microscope visualized that Piezo1 was packaged into the m/lEVs ( n = 15 cells from three independent experiments). (B) Left panel: Confocal microscope visualized that LSS (15 dyn/cm 2 for 300 s) increased the content of Piezo1 in m/lEVs ( n = 60 cells from six independent experiments). Right panel: LSS increased the percentage of Piezo1‐positive m/lEVs ( n = 6). (C) Both LSS and Yoda1increased the content of Piezo1 in m/lEVs ( n = 4). (D) Dual stimulation with Yoda1 (Piezo1 agonist, 2 µM) and m/lEV release inhibitor (500 nM pantethine or 2 µM Y27632) induced Piezo1 over accumulation in HUVECs ( n = 4). HUVECs were pre‐treated with pantethine or Y27632 for 5 min followed by Yoda1 treatment for 24 h. (E) Dual stimulation with Yoda1 and m/lEV release inhibitor induced Ca 2+ overload in HUVECs ( n = 5). (F) Piezo1 overexpression (OE) reduced the phosphorylation of eNOS and VEGFR2 ( n = 3). Plasmid transfection for Piezo1 OE was performed 60 h prior to the cell functional analysis. (G) Piezo1 OE impaired EC migration ( n = 5). (H) Piezo1 OE impaired EC tube formation ( n = 5). (I) Piezo1 OE impaired ACh‐induced NO production ( n = 5). (J) Piezo1 OE induced Ca 2+ overload in ECs ( n = 5). (K) Treatment with either pantethine (150 mg/kg, i.p.) or Y27632 (5 mg/kg, i.p.) abolished the effect of exercise on upregulating Piezo1 in circulating m/lEVs from mice ( n = 6). The experimental schemes for m/lEV release inhibitor treatment and the exercise model were showed in Figure . (L) Chronic exercise mildly upregulated Piezo1 expression, whereas treatment with either pantethine or Y27632 induced Piezo1 over accumulation in aorta from mice with exercise ( n = 6). (M) Schematic diagram showing that LSS‐induced m/lEV release contributes to intracellular Piezo1 homeostasis. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01.

Article Snippet: Pantethine (150 mg/kg, HY‐B1028, MCE, USA) or Y27632 (5 mg/kg, HY‐10071, MCE, USA) was dissolved in saline and injected intraperitoneally at 30 min before each exercise.

Techniques: Microscopy, Confocal, Over Expression, Phospho-proteomics, Plasmid Preparation, Transfection, Functional Assay, Analysis, Migration, Expressing

Piezo1 transportation to the splenic capsule promotes spleen contraction and maintains exercise endurance. (A) Schematic diagram of the ultrasonographic measurements before and after acute exercise. (B) Inhibition of Piezo1 transportation through EC‐specific KO (Piezo1 EC −/− ) and Y27632 (5 mg/kg, i.p., 30 min prior to exercise) abolished the effect of exercise on upregulating splenic Piezo1 contents ( n = 6). (C) Piezo1 EC −/− , Y27632 and GsMTx4 (10 mg/kg, i.p., 30 min prior to exercise) suppressed exercise‐induced spleen contraction ( n = 10). Left panel: Representative ultrasound images of the spleen pre‐ and post‐exercise. Middle panel: Quantification of spleen area pre‐ and post‐exercise from ultrasound images. Right panel: Percentage change in spleen contraction in response to exercise. (D) Piezo1 EC −/− , Y27632 and GsMTx4 decreased circulating blood volume during exercise ( n = 6). (E) Piezo1 EC −/− , Y27632 and GsMTx4 showed no significant effect on motor coordination quantified from average latency to fall from rotarod ( n = 8). (F, G) Piezo1 EC −/− , Y27632 and GsMTx4 decreased exercise endurance in mice, as detected by cumulative numbers of falls binned every 5 min of mice during 1 h rotarod endurance test (F), and distance and time run to exhaustion during a treadmill endurance test (G) ( n = 8). (H) α1AR antagonist (Prazosin, 1 mg/kg, i.p., 30 min prior to exercise) abolished exercise‐induced spleen contraction ( n = 10). (I) Schematic illustration of splenic denervation via absolute ethanol ablation. (J) Representative images of sham‐operated (upper) and denervated (lower) spleens 5 weeks post‐surgery. Tyrosine hydroxylase (TH) was used to label neural fibers. (K) Splenic denervation abolished exercise‐induced spleen contraction ( n = 10). (L) Yoda1 (2 mg/kg, i.p.) induced spleen contraction even with ablation of the splenic nerve plexus ( n = 10). Ultrasonographic measurements were performed before and at 1 h after Yoda1 injection. Data are presented as mean or mean ± SEM. * p < 0.05, ** p < 0.01.

Journal: Journal of Extracellular Vesicles

Article Title: Shear Stress‐Stimulated Trafficking of Endothelial Piezo1 to Splenic Capsule Boosts Spleen Contraction and Exercise Endurance

doi: 10.1002/jev2.70375

Figure Lengend Snippet: Piezo1 transportation to the splenic capsule promotes spleen contraction and maintains exercise endurance. (A) Schematic diagram of the ultrasonographic measurements before and after acute exercise. (B) Inhibition of Piezo1 transportation through EC‐specific KO (Piezo1 EC −/− ) and Y27632 (5 mg/kg, i.p., 30 min prior to exercise) abolished the effect of exercise on upregulating splenic Piezo1 contents ( n = 6). (C) Piezo1 EC −/− , Y27632 and GsMTx4 (10 mg/kg, i.p., 30 min prior to exercise) suppressed exercise‐induced spleen contraction ( n = 10). Left panel: Representative ultrasound images of the spleen pre‐ and post‐exercise. Middle panel: Quantification of spleen area pre‐ and post‐exercise from ultrasound images. Right panel: Percentage change in spleen contraction in response to exercise. (D) Piezo1 EC −/− , Y27632 and GsMTx4 decreased circulating blood volume during exercise ( n = 6). (E) Piezo1 EC −/− , Y27632 and GsMTx4 showed no significant effect on motor coordination quantified from average latency to fall from rotarod ( n = 8). (F, G) Piezo1 EC −/− , Y27632 and GsMTx4 decreased exercise endurance in mice, as detected by cumulative numbers of falls binned every 5 min of mice during 1 h rotarod endurance test (F), and distance and time run to exhaustion during a treadmill endurance test (G) ( n = 8). (H) α1AR antagonist (Prazosin, 1 mg/kg, i.p., 30 min prior to exercise) abolished exercise‐induced spleen contraction ( n = 10). (I) Schematic illustration of splenic denervation via absolute ethanol ablation. (J) Representative images of sham‐operated (upper) and denervated (lower) spleens 5 weeks post‐surgery. Tyrosine hydroxylase (TH) was used to label neural fibers. (K) Splenic denervation abolished exercise‐induced spleen contraction ( n = 10). (L) Yoda1 (2 mg/kg, i.p.) induced spleen contraction even with ablation of the splenic nerve plexus ( n = 10). Ultrasonographic measurements were performed before and at 1 h after Yoda1 injection. Data are presented as mean or mean ± SEM. * p < 0.05, ** p < 0.01.

Article Snippet: Pantethine (150 mg/kg, HY‐B1028, MCE, USA) or Y27632 (5 mg/kg, HY‐10071, MCE, USA) was dissolved in saline and injected intraperitoneally at 30 min before each exercise.

Techniques: Inhibition, Injection

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