Rutin alleviates hypoxia/reoxygenation-induced injury in myocardial cells by up-regulating SIRT1 expression

Han, Yang; Wang, Chao; Zhang, Lingyan; Lv, Jun; Ni, Hongzao

doi:10.1016/j.cbi.2018.10.016

Cited by 37 publications

(18 citation statements)

References 26 publications

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“…Accordingly, the level of LDH in the supernatant of the culture medium may reflect the degree of cardiomyocyte injury ( 30 – 32 ). In corroboration with the results of the present study, previous studies have demonstrated that the level of LDH is significantly higher in the H/R-induced I/R injury compared with the control in cardiomyocytes ( 33 – 35 ). The inflammatory factors TNF-α, IL-1β and IL-6 are commonly recognized as inflammatory indicators ( 36 ).…”

Section: Discussionsupporting

confidence: 93%

Protective effects of dexmedetomidine on hypoxia/reoxygenation injury in cardiomyocytes by regulating the CHOP signaling pathway

Shi

Liu

2020

Mol Med Rep

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Hypoxia/reoxygenation (H/r) injury in myocardial cells occurs frequently during cardiac surgery and affects the prognosis of patients. The present study aimed to investigate the protective effects of dexmedetomidine (dex) on H/r injury and its association with the c/eBP-homologous protein (cHoP) signaling pathway. an H/r model was constructed in H9c2 cells to investigate the effects of dex on H/r injury. cell viability, apoptosis and lactate dehydrogenase (LDH) levels were determined by MTT, flow cytometry and 2,4-dinitrophenylhydrazine colorimetric assays, respectively. The expression levels of inflammatory factors were measured by reverse transcription-quantitative Pcr (rT-qPcr), and cHoP and glucose-regulated protein-78 (Grp78) expression levels were detected by rT-qPcr and western blotting. cHoP was overexpressed or knocked down to detect the cell viability, apoptosis, LDH level and the expression levels of inflammatory factors and Grp78. The results demonstrated that in the H/r group, cell viability was lower and apoptosis was higher, and that higher levels of LDH and inflammatory factors were present compared with those in the dex+H/r group. Silencing of CHOP significantly reversed the H/R-reduced cell viability, high apoptotic rate and ldH levels, as well as the elevated expression levels of inflammatory factors and Grp78 caused by H/r injury, whereas the overexpression of cHoP inhibited cell viability and promoted apoptosis, elevated ldH level and expression of inflammatory factors and Grp78 compared with the negative control. additionally, pretreatment with Dex significantly alleviated the H/R injury; thus, Dex may protect H9c2 cells against H/r induced cell injury, possibly by suppressing the cHoP signaling pathway.

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Section: Discussionsupporting

confidence: 93%

Protective effects of dexmedetomidine on hypoxia/reoxygenation injury in cardiomyocytes by regulating the CHOP signaling pathway

Shi

Liu

2020

Mol Med Rep

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“…Myocardial ischemia/reperfusion (I/R), known to restore blood supply to ischemic area, causes further damage such as oxidative stress, arrhythmia, cell apoptosis, and cell death . Hypoxia/reoxygenation (H/R) is an important pathological process in the I/R phase of acute myocardial infarction . It is widely believed that reconstitution of blood ischemic myocardial tissue has become one of the most viable treatments for ischemic heart disease .…”

Section: Introductionmentioning

confidence: 99%

MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

Zhang

2019

The Kaohsiung J of Med Scie

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MiR‐27 prevents atherosclerosis by inhibiting inflammatory responses induced by lipoprotein lipase. Overexpression of miR‐27b attenuates angiotensin‐induced atrial fibrosis. Nevertheless, studies have rarely investigated on the effect of miR‐27 in cardiomyocyte injury. H9c2 cells were transfected with miR‐27 mimic/inhibitor. Then the cell proliferation was tested by MTT assay and the cell apoptosis was detected by flow cytometry. The luciferase activity assay was utilized to analyze the relationship between miR‐27 and TGFBR1. Quantificational real‐time polymerase chain reaction and western blot were utilized to detect the cardiomyocyte differentiation marker and nuclear factor kappa B (NF‐κB) pathway. Our outcomes demonstrated that miR‐27 expression was downregulated cardiomyocyte injury subjected to hypoxia/reoxygenation (H/R). Additionally, overexpression of miR‐27 could significantly alleviate cardiomyocyte injury by regulating cell activity and apoptosis. The luciferase activity assay confirmed that transforming growth factor ß receptor 1 (TGFBR1) is a direct hallmark of miR‐27. Besides, overexpression of miR‐27 promoted the expression of TGFBR1 in H/R model. After transfection with miR‐27 mimic/inhibitor, the expression of NF‐κB pathway‐related proteins was decreased/increased. Taken together, our data manifested that miR‐27 repressed cardiomyocyte injury induced by H/R via mediating TGFBR1 and inhibiting NF‐κB signaling pathway. Furthermore, miR‐27/ TGFBR1 might be utilized as hopeful biomarkers for myocardial ischemia diagnosis and treatment.

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“…These data highlighted the important role of SIRT1 in mediating ANRIL protection against H/R injury. To date, it is known that SIRT1 exhibits cardioprotective effects on H/R injury by comprehensive means, including inhibition of oxidative and endoplasmic reticulum stress ( 34 , 35 ), and orchestration of autophagy induction ( 36 ). Examining the specific contribution of these underlying mechanisms to the effects of ANRIL is one of the future research topics that deserves further investigation.…”

Section: Discussionmentioning

confidence: 99%

Critical role of SIRT1 upregulation on the protective effect of lncRNA ANRIL against hypoxia/reoxygenation injury in H9c2 cardiomyocytes

et al. 2021

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Dysregulation of long non-coding RNA (IncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) is associated with the risk of myocardial infarction (MI). Therefore, the present study aimed to determine the mechanisms underlying this association, which is currently poorly understood, to the best of our knowledge. The current study used an in vitro myocardial ischemia and reperfusion (MI/R) model, in which H9c2 cardiomyocytes were exposed to hypoxia/reoxygenation (H/R), which demonstrated that ANRIL expression was downregulated and that ANRIL positively regulated sirtuin 1 (SIRT1) expression following H/R injury. Subsequently, it was demonstrated that ANRIL upregulated SIRT1 expression by sponging microRNA-181a (miR-181a). In addition, ANRIL overexpression reduced lactate dehydrogenase release and apoptosis of H9c2 cardiomyocytes exposed to H/R, indicating that ANRIL prevented H/R-induced cardiomyocyte injury. Moreover, both miR-181a overexpression and SIRT1 knockdown significantly decreased the protective effects of ANRIL on H/R-induced cardiomyocyte injury, thus demonstrating that SIRT1 upregulation via sponging miR-181a is a critical mechanism that mediates the function of ANRIL. These results provided a novel mechanistic insight into the role of ANRIL in H/R-injured cardiomyocytes and suggested that the ANRIL/miR-181a/SIRT1 axis may be a therapeutic target for reducing MI/R injury.

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Rutin alleviates hypoxia/reoxygenation-induced injury in myocardial cells by up-regulating SIRT1 expression

Cited by 37 publications

References 26 publications

Protective effects of dexmedetomidine on hypoxia/reoxygenation injury in cardiomyocytes by regulating the CHOP signaling pathway

Protective effects of dexmedetomidine on hypoxia/reoxygenation injury in cardiomyocytes by regulating the CHOP signaling pathway

MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

Critical role of SIRT1 upregulation on the protective effect of lncRNA ANRIL against hypoxia/reoxygenation injury in H9c2 cardiomyocytes

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