Sufentanil preconditioning protects against myocardial ischemia/reperfusion injury via miR-125a/DRAM2 axis

Wu, Qiaoling; Shang, You; Bai, Yanli; Wang, Hao; Tu, Shen

doi:10.1080/15384101.2021.1875668

Cited by 21 publications

(14 citation statements)

References 28 publications

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“…In the process of exploring the prevention and treatment of IRI, the potential targets and preventive bene ts of drugs based on narcotic drugs have become the subject of a large number of studies. So far, many narcotic drugs have been shown to have a protective effect including Dex [21] propofol [25] sevo urane [26] and sufentanil [27], etc. Among them, Dex has attracted the attention of many researchers.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine preconditioning alleviates H2O2-induced oxidative stress and apoptosis in human umbilical vein endothelial cells via p38MAPK signaling pathway

Long

Zhong

Zhao

et al. 2022

Preprint

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Background: Ischemia-reperfusion injury (IRI) is the main cause of perioperative organ injury, and the morbidity increase constantly in population. Due to a lack of effective treatment, IRI is associated with a high mortality rate. Thus, we need to discover an effective means to alleviate IRI.Methods: HUVECs were treated with different concentrations of H2O2 alone and in combination with Dex to explore the dose-effect relationship of different concentrations of H2O2 and Dex on HUVEC. In order to explore the relationship between Dex and p38MAPK signal pathway, HUVEC was treated with SB202190, an inhibitor of p38MAPK signal pathway. Cell viability was detected by CCK-8 method. ELISA kit was used to detect lactate dehydrogenase (LDH). Fluorescence probe DCFH-DA staining was used to detect ROS level. Flow cytometry analysis with Propidium Iodide (PI) was used to determine the rate of cell apoptosis. And the protein expression of p-p38MAPK, total p38MAPK, p-ERK1/2 and caspase9 was detected by western blot.Results: 1）H2O2 could damage HUVEC and lead to the release of LDH. The higher the concentration of H2O2, the more severe the injury. 2）Dex pretreatment attenuated H2O2-induced oxidative stress injury and apoptosis of HUVEC. The cell activity of HUVEC increase as Dex concentration increase, the release of LDH decreased, the intracellular ROS level and apoptosis rate decreased, the protein expression of p-p38MAPK and caspase9 decreased, while the protein expression of p-ERK1/2 increased. 3）Dex had the same effect as SB202190, an inhibitor of p38MAPK signaling pathway. After the application of SB202190, the activity of HUVECs increased significantly, while LDH, intracellular ROS and apoptosis rate decreased significantly. Western blot showed that the protein expression of p-p38MAPK and caspase9 decreased significantly, while the protein levels of p-ERK1/2 increased significantly.Conclusion: 1）Dex attenuates H2O2-induced oxidative stress injury and apoptosis of HUVEC in a concentration-dependent. 2）Dex may attenuate H2O2-induced oxidative stress injury and apoptosis of HUVEC by inhibiting p38MAPK signal pathway.

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Section: Discussionmentioning

confidence: 99%

Dexmedetomidine preconditioning alleviates H2O2-induced oxidative stress and apoptosis in human umbilical vein endothelial cells via p38MAPK signaling pathway

Long

Zhong

Zhao

et al. 2022

Preprint

View full text Add to dashboard Cite

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“…In another study, cigarette smoke-induced EVs were enriched in let-7d, miR-191, miR-126, and miR125a. The last two can alleviate the IRI by reducing apoptosis and the myocardial area after reperfusion, as mentioned above [ 308 , 309 ] ( Table 1 ). The other two miRNA should be investigated as they may play a role in the IRI of other organs or may be important factors in cardiovascular diseases [ 310 , 311 , 312 ].…”

Section: Cardiovascular Risk Factorsmentioning

confidence: 99%

“…MiR-125a has a potential cardioprotective effect by ameliorating cardiomyocyte autophagy and oxidative injury. These mechanisms are activated by promoting gene expression dysregulation involved in cell death and apoptosis [ 308 , 309 ]. Furthermore, miR-34a, which is also dysregulated in DM and obesity, may play a role in IRI.…”

Section: Cardiovascular Risk Factorsmentioning

confidence: 99%

Impact of the Main Cardiovascular Risk Factors on Plasma Extracellular Vesicles and Their Influence on the Heart’s Vulnerability to Ischemia-Reperfusion Injury

Majka

Kleibert

Wojciechowska

2021

Cells

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The majority of cardiovascular deaths are associated with acute coronary syndrome, especially ST-elevation myocardial infarction. Therapeutic reperfusion alone can contribute up to 40 percent of total infarct size following coronary artery occlusion, which is called ischemia-reperfusion injury (IRI). Its size depends on many factors, including the main risk factors of cardiovascular mortality, such as age, sex, systolic blood pressure, smoking, and total cholesterol level as well as obesity, diabetes, and physical effort. Extracellular vesicles (EVs) are membrane-coated particles released by every type of cell, which can carry content that affects the functioning of other tissues. Their role is essential in the communication between healthy and dysfunctional cells. In this article, data on the variability of the content of EVs in patients with the most prevalent cardiovascular risk factors is presented, and their influence on IRI is discussed.

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“… 8 In addition, SUF has also been found to alleviate myocardial ischemia-reperfusion injury by activating the ERK1/2 signaling pathway or miR-125a/DRAM2 axis. 10 , 11 A clinical study also shows that SUF can alleviate ischemia-reperfusion injury in patients with coronary heart disease. 12 Therefore, we speculated that SUF may have a therapeutic effect on ischemia-reperfusion disease.…”

Section: Introductionmentioning

confidence: 99%

Sufentanil alleviates cerebral ischemia-reperfusion injury by inhibiting inflammation and protecting the blood-brain barrier in rats

Wang

et al. 2022

Eur J Histochem

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Stroke is a brain system disease with a high fatality rate and disability rate. About 80% of strokes are ischemic strokes. Cerebral ischemia-reperfusion injury (CIRI) caused by ischemic stroke seriously affects the prognosis of stroke patients. The purpose of this study is to investigate the effect of sufentanil (SUF) on CIRI model rats. We used middle cerebral artery occlusion (MCAO) to make the CIRI model in rats and monitored region cerebral blood flow (rCBF) to ensure that blood flow was blocked and recanalized. We used ELISA and RT-PCR to detect the expression of inflammatory factors in rat serum and brain tissue. In addition, we detected the expression of metalloproteinase (MMP) 2, MMP9 and collagen IV in brain tissues and performed Evans blue (EB) assay to determine the permeability of the blood-brain barrier (BBB). Finally, we clarified the apoptosis of brain tissue through the TUNEL staining and the detection of caspase3, Bcl2 and Bax. Various concentrations of SUF, especially 5, 10 and 25 μg/kg of SUF, all alleviated the infarct size, neurological function and brain edema of MCAO rats. SUF pretreatment also effectively reduced the expression of inflammatory cytokines in MCAO rats, including interleukin (IL)-1β, IL-4, IL-6, IL-8, IL-10 and tumor necrosis factor (TNF)-α. In addition, SUF also inhibited MMP2 and MMP9 and promoted the expression of collagen IV, indicating that SUF attenuated the destruction of the BBB. SUF also inhibited caspase3 and Bax rats and promoted Bcl2 in MCAO rats, thus inhibiting cell apoptosis. SUF pretreatment effectively improved the neurological function and cerebral infarction of MCAO rats, inhibited excessive inflammation in rats, protected the BBB, and inhibited cell apoptosis in brain tissue.

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Sufentanil preconditioning protects against myocardial ischemia/reperfusion injury via miR-125a/DRAM2 axis

Cited by 21 publications

References 28 publications

Dexmedetomidine preconditioning alleviates H2O2-induced oxidative stress and apoptosis in human umbilical vein endothelial cells via p38MAPK signaling pathway

Dexmedetomidine preconditioning alleviates H2O2-induced oxidative stress and apoptosis in human umbilical vein endothelial cells via p38MAPK signaling pathway

Impact of the Main Cardiovascular Risk Factors on Plasma Extracellular Vesicles and Their Influence on the Heart’s Vulnerability to Ischemia-Reperfusion Injury

Sufentanil alleviates cerebral ischemia-reperfusion injury by inhibiting inflammation and protecting the blood-brain barrier in rats

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