Coronary artery bypass on survival in patients with moderate ischemic mitral regurgitation: meta-analysis.

OBJECTIVE: The objective of the study was to systematically evaluate the effect of coronary artery bypass grafting (CABG) or CABG combined with mitral valve surgery (cMVS) on post-operative survival in patients with moderate ischemic mitral valve regurgitation. MATERIALS AND METHODS: Databases including PubMed, Web of Science, COCHRANE LIBRARY, WanFang Data, and CNKI Data were searched from inception to January 2020. According to the inclusion criterion, relevant articles were screened. After that we extracted data, assessed quality, and performed meta-analysis using RevMan 5.2. RESULTS: A total of 4 randomized controlled trial and 14 retrospective study involving 4476 patients were included in the study. The CABG group was 2278 and the cMVS group was 1698. The results of meta-analysis showed that compared with CABG group, there were no statistically significant differences in the recent mortality (odds ratio [OR] = 0.88, p = 0.62), 1-year survival (OR = 1.03, p = 0.82), 1-year survival (OR = 1.07, p = 0.62), and long-term survival (OR = 0.95, p = 0.61) of the cMVS group. CONCLUSION: Current evidence indicates that patients in the cMVS group did not benefit from CABG group in survival after surgery.

OBJETIVO: . Evaluar sistemáticamente el efecto del injerto de derivación de la arteria coronaria (CABG) o el injerto de derivación de la arteria coronaria combinados con la cirugía de la válvula mitral (cMVS) sobre la supervivencia posoperatoria en pacientes con insuficiencia valvular mitral isquémica moderada. MATERIAL Y MÉTODOS: . Se realizaron búsquedas en bases de datos que incluyen Pubmed, Web of Science, COCHRANE LIBRARY, WanFang Data y CNKI Data desde el inicio hasta enero de 2020. De acuerdo con el criterio de inclusión, se seleccionaron los artículos relevantes. Después de eso, extrajimos los datos, evaluamos la calidad y realizamos el metanálisis con RevMan 5.2. RESULTADOS: . Se incluyó un total de 4 ensayos controlados aleatorios (ECA) y 14 estudios retrospectivos con 4476 pacientes. El grupo CABG fue 2278, el grupo cMVS fue 1698. Los resultados del metanálisis mostraron que, en comparación con el grupo CABG, no hubo diferencias estadísticamente significativas en la mortalidad reciente (OR = 0.88, p = 0.62), supervivencia a 1 año (OR = 1.03, p = 0.82), supervivencia a 1 año (OR = 1.07, p = 0.62) y supervivencia a largo plazo (OR = 0.95, p = 0.61) del grupo cMVS. CONCLUSIÓN: . La evidencia actual indica que los pacientes del grupo cMVS no se beneficiaron del grupo CABG en la supervivencia después de la cirugía.

Neuroprotective effects of an Nrf2 agonist on high glucose-induced damage in HT22 cells.

BACKGROUND: Oxidative stress is the hallmark of diabetic encephalopathy, which may be caused by hyperglycaemic toxicity. We aimed to discover pharmacologic targets to restore redox homeostasis. We identified the transcription factor Nrf2 as such a target. METHODS: HT22 cells were cultured in 25 or 50 mM D-glucose with various concentrations of sulforaphane (SFN) (from 1.25 to 5.0 µM). Cell viability was tested with the Cell Counting Kit-8 assay. Reactive oxygen species (ROS) production was detected with an inverted fluorescence microscope using the dichlorodihydrofluorescein-diacetate fluorescent probe. The expression of NF-E2-related factor 2 (Nrf2), haem oxygenase-1 (HO-1) and nuclear factor-κB (NF-κB) at the mRNA and protein levels was detected by reverse transcription quantitative polymerase chain reaction and western blotting. RESULT: We found that a high glucose concentration (50 mM) increased the generation of ROS, downregulated the expression of Nrf2/HO-1 and upregulated the expression of NF-κB. Moreover, HT22 cell viability significantly decreased after culture in high-glucose medium for 24, 48 and 72 h, whereas the activation of the Nrf2/HO-1 pathway using a pharmacological Nrf2 activator abrogated this high-glucose-induced toxicity. CONCLUSION: This study suggests that the activation of the Nrf2-ARE signalling pathway might be a therapeutic target for the treatment of diabetic encephalopathy.

Neuroprotective effects of an Nrf2 agonist on high glucose-induced damage in HT22 cells

BACKGROUND: Oxidative stress is the hallmark of diabetic encephalopathy, which may be caused by hyperglycaemic toxicity. We aimed to discover pharmacologic targets to restore redox homeostasis. We identified the transcription factor Nrf2 as such a target. METHODS: HT22 cells were cultured in 25 or 50 mM D-glucose with various concentrations of sulforaphane (SFN) (from 1.25 to 5.0 µM). Cell viability was tested with the Cell Counting Kit-8 assay. Reactive oxygen species (ROS) production was detected with an inverted fluorescence microscope using the dichlorodihydrofluorescein-diacetate fluorescent probe. The expression of NF-E2-related factor 2 (Nrf2), haem oxygenase-1 (HO-1) and nuclear factor-κB (NF-κB) at the mRNA and protein levels was detected by reverse transcription quantitative polymerase chain reaction and western blotting. RESULT: We found that a high glucose concentration (50 mM) increased the generation of ROS, downregulated the expression of Nrf2/HO-1 and upregulated the expression of NF-κB. Moreover, HT22 cell viability significantly decreased after culture in high-glucose medium for 24, 48 and 72 h, whereas the activation of the Nrf2/HO-1 pathway using a pharmacological Nrf2 activator abrogated this high-glucose-induced toxicity. CONCLUSION: This study suggests that the activation of the Nrf2-ARE signalling pathway might be a therapeutic target for the treatment of diabetic encephalopathy.