RESUMO
OBJECTIVES: Our previous study indicated that aerobic exercise relieves cognitive impairment in patients with vascular cognitive impairment (VCI) via regulating brain-derived neurotrophic factor (BDNF), but the mechanism is not yet clear. This study aimed to explore whether lncRNA taurine upregulated gene 1 (TUG1) participates in the process of VCI by regulating BDNF. METHODS: The expressions of TUG1 and BDNF in the serum of VCI patients were detected. The potential molecular mechanisms of TUG1 in regulating hippocampal neuronal apoptosis were explored in oxygen and glucose deprivation-induced (OGD-induced) hippocampal cell line HT22. The VCI mouse model was established, and TUG1 and BDNF were overexpressed via lentivirus injection. The cognitive impairment of mice was detected by the Morris water maze experiment after the aerobic exercise. RESULTS: The level of TUG1 was elevated in the serum of VCI patients compared with the control group. The knockdown of TUG1 in OGD-induced HT22 cells increased BDNF level and decreased cell apoptosis, and the downregulation of BDNF restored the decreased cell apoptosis. RNA immunoprecipitation and RNA pull-down assays showed that TUG1 could bind to BDNF protein. The aerobic exercise alleviated cognitive impairment and inhibited hippocampal apoptosis in VCI mice. Meanwhile, the overexpression of TUG1 reversed the therapeutic effects of aerobic exercise on cognitive impairment. CONCLUSIONS: The knockdown of TUG1 reduced hippocampal neuronal apoptosis and participates in the aerobic exercise-alleviated VCI, which was partly through regulating BDNF.
Assuntos
Apoptose , Disfunção Cognitiva , Neurônios/patologia , Condicionamento Físico Animal , RNA Longo não Codificante/genética , Animais , Fator Neurotrófico Derivado do Encéfalo , Linhagem Celular , Proliferação de Células , Disfunção Cognitiva/genética , Disfunção Cognitiva/terapia , Técnicas de Silenciamento de Genes , Hipocampo/citologia , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , RNA Longo não Codificante/sangue , TaurinaRESUMO
OBJECTIVES: Our previous study indicated that aerobic exercise relieves cognitive impairment in patients with vascular cognitive impairment (VCI) via regulating brain-derived neurotrophic factor (BDNF), but the mechanism is not yet clear. This study aimed to explore whether lncRNA taurine upregulated gene 1 (TUG1) participates in the process of VCI by regulating BDNF. METHODS: The expressions of TUG1 and BDNF in the serum of VCI patients were detected. The potential molecular mechanisms of TUG1 in regulating hippocampal neuronal apoptosis were explored in oxygen and glucose deprivation-induced (OGD-induced) hippocampal cell line HT22. The VCI mouse model was established, and TUG1 and BDNF were overexpressed via lentivirus injection. The cognitive impairment of mice was detected by the Morris water maze experiment after the aerobic exercise. RESULTS: The level of TUG1 was elevated in the serum of VCI patients compared with the control group. The knockdown of TUG1 in OGD-induced HT22 cells increased BDNF level and decreased cell apoptosis, and the downregulation of BDNF restored the decreased cell apoptosis. RNA immunoprecipitation and RNA pull-down assays showed that TUG1 could bind to BDNF protein. The aerobic exercise alleviated cognitive impairment and inhibited hippocampal apoptosis in VCI mice. Meanwhile, the overexpression of TUG1 reversed the therapeutic effects of aerobic exercise on cognitive impairment. CONCLUSIONS: The knockdown of TUG1 reduced hippocampal neuronal apoptosis and participates in the aerobic exercise-alleviated VCI, which was partly through regulating BDNF.
Assuntos
Humanos , Animais , Masculino , Camundongos , Condicionamento Físico Animal , Apoptose , Disfunção Cognitiva/genética , Disfunção Cognitiva/terapia , RNA Longo não Codificante/genética , Neurônios/patologia , Taurina , Linhagem Celular , Camundongos Knockout , Fator Neurotrófico Derivado do Encéfalo , Proliferação de Células , Técnicas de Silenciamento de Genes , RNA Longo não Codificante/sangue , Hipocampo/citologia , Camundongos Endogâmicos C57BLRESUMO
BACKGROUND AND OBJECTIVE: Pulmonary hypertension (PH) is characterized by rising pulmonary arterial pressure, decreasing right ventricular (RV) function, and ultimately, RV failure. Therefore, it is important to monitor RV function and pulmonary artery hemodynamics accurately and noninvasively. This study evaluates cardiac magnetic resonance imaging (CMRI) in assessing RV function and pulmonary artery hemodynamics in patients with PH. METHODS: Cine-MRI and phase-contrast MRI (PC-MRI) were performed in 25 PH patients and 30 healthy volunteers. Cine-MRI images were post-processed on Report Card software and the following parameters were obtained: RV end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), ejection fraction (EF), and myocardial mass (MM). Except for EF, all of the above parameters were normalized to body surface area (BSA). PC-MRI images were post-processed on Report Card software, peak velocity and distensibility of main pulmonary artery (MPA) could also be obtained. Student t test was employed for statistical assessment. RESULTS: Compared with controls, RV EDV, ESV and MM index in PH patients were significantly increased (P<0.01), EF was significantly impaired (P<0.01), peak velocity and distensibility of MPA were significantly lower (P<0.01). SV index between the two groups had no significant difference (P>0.05). CONCLUSIONS: Cardiac MRI is of great value in the assessment of RV function and MPA hemodynamic parameters in patients with PH.