Remifentanil preconditioning confers cardioprotection via c-Jun NH 2 -terminal kinases and extracellular signal regulated kinases pathways in ex-vivo failing rat heart

Jin, Shiyun; Huang, Jun; Zhu, Haijuan; Wu, Hao; Xu, Shijie; Irwin, Michael G.; He, Songqing; Zhang, Ye

doi:10.1016/j.ejphar.2018.03.030

Cited by 12 publications

(4 citation statements)

References 41 publications

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“…Remifentanil (Ultiva™) is a selective μ‐opioid receptor agonist, which is used clinically for analgesia and as part of general anaesthesia 11‐13 . Remifentanil reportedly protects the heart from I/R injury via post‐conditioning 14 and reduces hepatic I/R injury in rats 15 . However, the molecular mechanism by which remifentanil attenuates hepatic I/R injury is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Remifentanil up‐regulates HIF1α expression to ameliorate hepatic ischaemia/reperfusion injury via the ZEB1/LIF axis

Zhou

Mei

et al. 2020

J Cellular Molecular Medi

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Ischaemia/reperfusion (I/R)‐induced hepatic injury is regarded as a main reason of hepatic failure after transplantation or lobectomy. The current study aimed to investigate how the opioid analgesic remifentanil treatment affects I/R‐induced hepatic injury and explore the possible mechanisms related to HIF1α. Initially, an I/R‐induced hepatic injury animal model was established in C57BL/6 mice, and an in vitro hypoxia‐reoxygenation model was constructed in NCTC‐1469 cells, followed by remifentanil treatment and HIF1α silencing treatment. The levels of blood glucose, lipids, alanine transaminase (ALT) and aspartate transaminase (AST) in mouse serum were measured using automatic chemistry analyser, while the viability and apoptosis of cells were detected using CCK8 assay and flow cytometry. Our results revealed that mice with I/R‐induced hepatic injury showed higher serum levels of blood glucose, lipids, ALT and AST and leukaemia inhibitory factor (LIF) expression, and lower HIF1α and ZEB1 expression (P < .05), which were reversed after remifentanil treatment (P < .05). Besides, HIF1α silencing increased the serum levels of blood glucose, lipids, ALT and AST (P < .05). Furthermore, hypoxia‐induced NCTC‐1469 cells exhibited decreased HIF1α and ZEB1 expression, reduced cell viability, as well as increased LIF expression and cell apoptosis (P < .05), which were reversed by remifentanil treatment (P < .05). Moreover, HIF1α silencing down‐regulated ZEB1 expression, decreased cell viability, and increased cell apoptosis (P < .05). ZEB1 was identified to bind to the promoter region of LIF and inhibit its expression. In summary, remifentanil protects against hepatic I/R injury through HIF1α and downstream effectors.

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Section: Introductionmentioning

confidence: 99%

Remifentanil up‐regulates HIF1α expression to ameliorate hepatic ischaemia/reperfusion injury via the ZEB1/LIF axis

Zhou

Mei

et al. 2020

J Cellular Molecular Medi

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“…Indeed, activation of opioid receptors, including kappa‐opioid receptors (KOR), delta opioid receptors (DOR), and mu opioid receptors (MOR) inhibited myocardial ischemia‐reperfusion injury (IRI) and cardiomyocyte death (Roth et al., 2021 ). Noteworthy, MOR is generally absent in healthy and non‐ischemic hearts; however, it specifically upregulated in ischemic and heart failure conditions (Jin et al., 2018 ). It has been suggested that non‐coding RNAs are responsible for the inhibition of apoptosis and protective effects of opioids against IRI (Melo et al., 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Evaluating the association between opium abuse, blood lead levels, and the complexity of coronary artery disease

Khameneh Bagheri,

Mousavi,

Mehrad‐Majd

et al. 2024

Physiological Reports

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Opium abuse and exposure to heavy metals elevate the risk of coronary artery disease (CAD). Therefore, we aimed to determine the association between opium abuse and blood lead levels (BLLs) and the CAD complexity. We evaluated patients with acute coronary symptoms who underwent coronary angiography, and those with >50% stenosis in at least one of the coronary arteries were included. Furthermore, Synergy between PCI with Taxus and Cardiac Surgery I (SYNTAX I) score and BLLs were measured. Based on the opium abuse, 95 patients were subdivided into opium (45) and control (50) groups. Differences in demographics and CAD risk factors were insignificant between the two groups. The median BLLs were remarkably higher in the opium group than in controls (36 (35.7) and 20.5 μg/dL (11.45), respectively, p = 0.003). We also revealed no significant differences in SYNTAX score between the two groups (15.0 (9.0) and 17.5 (14.0), respectively, p = 0.28). Additionally, we found no significant correlation between BLLs and the SYNTAX scores (p = 0.277 and r = −0.113). Opium abuse was associated with high BLLs. Neither opium abuse nor high BLLs were correlated with the complexity of CAD. Further studies are warranted to establish better the relationship between opium abuse, BLLs, and CAD.

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“…The different concentrations of remifentanil may trigger cardioprotection or enhance myocardial injury. Studies have shown that RF postconditioning (RPC), which used a low concentration of RF (1μM), significantly reduces myocardial infarction in mice following MI/R in vitro 17 , 18 . On the other hand, some studies have suggested that HRF leads to severe cardiovascular depression 19 .…”

Section: Discussionmentioning

confidence: 99%

High-dose remifentanil exacerbates myocardial ischemia-reperfusion injury through activation of calcium-sensing receptor-mediated pyroptosis

Zhu,

Chi,

Cai

et al. 2023

Int. J. Med. Sci.

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Background: The aim of this study was to investigate whether calcium-sensing receptor (CaSR) was involved in HRF-mediated exacerbation of MI/R injury through NLRP3 inflammasome activation and pyroptosis. Methods: In vivo , a rat MI/R model was established by ligating the left coronary artery, and short-term HRF exposure was induced during reoxygenation. Then, TUNEL, H&E, Masson staining, immunohistochemical (IHC) and serum levels of lactate dehydrogenase (LDH) and creatine kinase isoenzyme (CK), as well as the expression levels of CaSR and pyroptosis-related proteins in heart tissues, were measured. H9c2 cells were cultured to create a hypoxia/reoxygenation (H/R) model and exposed to different concentrations of RF. After pretreatment with the CaSR activator gadolinium chloride (GdCl 3 ) and inhibitor NPS2143 in the H/R model and treatment with HRF, we compared cellular viability, TUNEL, cytosolic [Ca 2+ ] i , the levels of LDH and CK, pyroptosis-related proteins and CaSR in H9c2 cells. We further researched the mechanisms of CaSR-mediated pyroptosis in the H/R+HRF model by CaSR-shRNA, Ac-YVAD-CMK, MCC950 and NAC. Results: We found that HRF significantly increased CaSR expression, rate of cell death, levels of CK and LDH, and exacerbated pyroptosis in MI/R model. In vitro , HRF increased CaSR expression, decreased viability, enhanced cytosolic [Ca 2+ ] i and exacerbated pyroptosis in H/R cells. Pretreated with GdCl 3 worsen these changes, and NPS2143, MCC950, Ac-YVAD-CMK, NAC and sh-CaSR can reversed these effects. Conclusion: Exposure to HRF for a short time exacerbates MI/R-induced injury by targeting CaSR to increase cytosolic [Ca 2+ ] i and ROS levels, which mediate the NLRP3 inflammasome and pyroptosis.

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Remifentanil preconditioning confers cardioprotection via c-Jun NH 2 -terminal kinases and extracellular signal regulated kinases pathways in ex-vivo failing rat heart

Cited by 12 publications

References 41 publications

Remifentanil up‐regulates HIF1α expression to ameliorate hepatic ischaemia/reperfusion injury via the ZEB1/LIF axis

Remifentanil up‐regulates HIF1α expression to ameliorate hepatic ischaemia/reperfusion injury via the ZEB1/LIF axis

Evaluating the association between opium abuse, blood lead levels, and the complexity of coronary artery disease

High-dose remifentanil exacerbates myocardial ischemia-reperfusion injury through activation of calcium-sensing receptor-mediated pyroptosis

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