With the growing aging population, strokes have become the second leading cause of mortality worldwide 1 , causing a huge financial burden on society, as well as on patients and their families. Rehabilitation is a routine and effective therapeutic strategy that is used in clinical practices for stroke patients. It can facilitate functional recovery by repairing damaged brain tissue and preventing post-stroke complications 2,3 . Some scholars believe that rehabilitation should begin as early as possible, once the patient's condition is stable 4,5 . Exercise training is one type of physical therapy commonly used after stroke. Matsuda et al and Yang et al reported that early treadmill training could significantly reduce brain infarct volume and improve neurologic function in rodent models of stroke 6,7 . Our previous studies also revealed that early exercise training (24 hours after ABSTRACT: Background: The current study explored the effects of treadmill exercise intensity on functional recovery and hippocampal phospho-NR2B (p-NR2B) expression in cerebral ischemic rats, induced by permanent middle cerebral artery occlusion (MCAO) surgery. Method: Adult male Sprague-Dawley rats were randomly divided into four groups, including sham, no exercise (NE), low intensity training (LIT, v = 15 m/min), and moderate intensity training groups (MIT, v = 20 m/min). At different time points, the hippocampal expressions of p-NR2B and total NR2B were examined. In addition, neurological deficit score (NDS), body weight, and 2,3,5-triphenyltetrazolium chloride (TTC) staining were used to evaluate brain infarct volume as assessments of post-stroke functional recovery. In order to investigate the effect of exercise on survival, the mortality rate was also recorded. Results: The results showed that treadmill exercise significantly decreased hippocampal expression of p-NR2B but didn't change the total NR2B, compared to the NE group on the 3rd, 7th, and 14th days following MCAO surgery. The effect on changes in p-NR2B levels, body weight, and brain infarct volume were more significant in the LIT compared to the MIT group. Discussion and Conclusion: The current findings demonstrate that physical exercise can produce neuroprotective effects, in part by down-regulating p-NR2B expression. Furthermore, the appropriate intensity of physical exercise is critical for post-stroke rehabilitation.RÉSUMÉ: Les effets de l'intensité de l'exercice sur l'expression de p-NR2B dans l'ischémie cérébrale chez le rat. Contexte : Cette étude explore les effets de l'intensité de l'exercice sur un tapis roulant sur la récupération fonctionnelle et sur l'expression du phospho-NR2B (p-NR2B) dans l'hippocampe dans l'ischémie cérébrale induite par l'occlusion chirurgicale permanente de l'artère cérébrale moyenne (OACM) chez le rat. Méthode : Des rats Sprague-Dawley mâles adultes ont été répartis au hasard en 4 groupes. Chacun des groupes recevait soit une intervention factice, pas d'exercice (PE), entraînement de faible intensité (EFI, v = 15 m/min), ou entraînemen...
Background: ANG (angiogenin) is essential for cellular adaptation to endoplasmic reticulum (ER) stress, a process closely associated with cardiovascular diseases, including atherosclerosis. We aimed to investigate the role of ANG in the progression of atherosclerosis and elucidate its underlying molecular mechanisms. Methods: We constructed adenoassociated virus 9 ANG overexpression vectors and endothelial ANG- and ApoE (apolipoprotein E)-deficient mice to determine the effects of ANG on ER stress and atherosclerotic lesions. RNA sequencing of endothelial ANG- and ApoE-deficient mice identified ANG-dependent downregulation of ST3GAL5 (ST3 beta-galactoside alpha-2,3-sialyltransferase 5) expression, and the direct regulation of ST3GAL5 by ANG was verified by chromatin immunoprecipitation sequencing and luciferase reporter assay results. Results: Reanalysis of expression profiling datasets indicated decreased ANG levels in patients’ atherosclerotic lesions, and these data were validated in aortas from ApoE − /− mice. ER stress marker and adhesion molecule levels, aortic root lesions and macrophage deposition were substantially reduced in ApoE −/− mice injected with an adenoassociated virus 9 ANG without signal peptide (ANG-ΔSP) overexpression vector compared with empty and full-length ANG overexpression vectors. Endothelial ANG deficiency significantly elevated ER stress and increased adhesion molecule expression, which aggravated atherosclerotic lesions and enhanced THP-1 monocyte adhesion to endothelial cells in vivo and in vitro, respectively. Furthermore, ANG-ΔSP overexpression significantly attenuated oxidized low-density lipoprotein-induced ER stress and THP-1 monocyte adhesion to endothelial cells, which were reversed by ST3GAL5 inhibition. Conclusions: These results suggest that endothelial intracellular ANG is a novel therapeutic against atherosclerosis and exerts atheroprotective effects via ST3GAL5-mediated ER stress suppression.
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