The effects of propofol on neutrophil function, lipid peroxidation and inflammatory response during elective coronary artery bypass grafting in patients with impaired ventricular function

Corcoran, Tomás; Engel, A.; Sakamoto, Hidetoshi; O’Shea, Aidan; O’Callaghan-Enright, S.; Shorten, George

doi:10.1093/bja/ael270

Cited by 88 publications

(56 citation statements)

References 24 publications

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“…However, propofol possesses diverse actions including anti-inflammatory properties, activation of atypical PKC isoforms, and inhibition of mitochondrial permeability transition that could confer protection against ischemia/ reperfusion [8,[17][18][19][20]. The results of the present study are consistent with our previous work, suggesting that propofol's effects cannot be explained strictly on the basis of an antioxidant mechanism.…”

Section: Discussionsupporting

confidence: 91%

Propofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation

Wang¹,

Shravah²,

Luo³

et al. 2009

Biochemical and Biophysical Research Communications

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Propofol is a widely used intravenous anesthetic agent with antioxidant properties secondary to its phenol based chemical structure. Treatment with propofol has been found to attenuate oxidative stress and prevent ischemia/reperfusion injury in rat heart. Here, we report that propofol protects cardiac H9c2 cells from hydrogen peroxide (H 2 O 2 )-induced injury by triggering the activation of Akt and a parallel up-regulation of Bcl-2. We show that pretreatment with propofol significantly protects against H 2 O 2 -induced injury. We further demonstrate that propofol activates the PI3K-Akt signaling pathway. The protective effect of propofol on H 2 O 2 -induced injury is reversed by PI3K inhibitor wortmannin, which effectively suppresses propofol-induced activation of Akt, upregulation of Bcl-2, and protection from apoptosis. Collectively, our results reveal a new mechanism by which propofol inhibits H 2 O 2 -induced injury in cardiac H9c2 cells, supporting a potential application of propofol as a preemptive cardioprotectant in clinical settings such as that during coronary bypass surgery.

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Section: Discussionsupporting

confidence: 91%

Propofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation

Wang¹,

Shravah²,

Luo³

et al. 2009

Biochemical and Biophysical Research Communications

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“…Due to their similar chemical structures, propofol has analogous biochemical functions to those of Vitamin E, including anti-oxidative, mitochondrial protective and free-radical scavenging activity (31)(32)(33). Furthermore, propofol inhibits the phosphorylation of JNK (30,34). These results therefore indicated that the mechanism underlying the inhibitory effect of propofol on AQP-4 and MMP-9 may be via inactivation of the JNK pathway.…”

Section: Discussionmentioning

confidence: 78%

Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury

Liang

Miao

et al. 2015

Molecular Medicine Reports

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Abstract. Propofol, an intravenous anesthetic, inhibits neuronal apoptosis induced by ischemic stroke, protects the brain from ischemia/reperfusion injury and improves neuronal function. However, whether propofol is able to protect the blood brain barrier (BBB) and the underlying mechanisms have remained to be elucidated. In the present study, a rat model of cerebral ischemia/reperfusion was established, using a thread embolism to achieve middle cerebral artery occlusion. Rats were treated with propofol (propofol post-conditioning) or physiological saline (control) administered by intravenous injection 30 min following reperfusion. Twenty-four hours following reperfusion, neurobehavioral manifestations were assessed. The levels of cephaloedema, damage to the BBB and expression levels of matrix metalloproteinase-9 (MMP-9), aquaporin-4 (AQP-4) and phosphorylated c-Jun N-terminal kinase (pJNK) were determined in order to evaluate the effects of propofol on the BBB. In comparison to the cerebral ischemia/reperfusion group, the levels of brain water content and Evans blue content, as well as the expression levels of MMP-9, AQP-4 and pJNK were significantly reduced in the propofol post-conditioning group. These results indicated that propofol post-conditioning improved the neurobehavioral manifestations and attenuated the BBB damage and cephaloedema induced following cerebral ischemia/reperfusion. This effect may be due to the inhibition of MMP-9 and AQP-4 expression, and the concurrent decrease in JNK phosphorylation.

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“…In contrast, the intravenous anaesthetic, propofol, may have largely protective effects 6, 11, 12, 13, mainly shown in animal and cellular models, although it has also been suggested to have some negative actions 14.…”

Section: Introductionmentioning

confidence: 99%

Cognitive decline in the elderly after surgery and anaesthesia: results from the Oxford Project to Investigate Memory and Ageing (OPTIMA) cohort

et al. 2016

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SummaryConcerns have been raised about the effects on cognition of anaesthesia for surgery, especially in elderly people. We recorded cognitive decline in a cohort of 394 people (198 women) with median (IQR) age at recruitment of 72.6 (66.6–77.8) years, of whom 109 had moderate or major surgery during a median (IQR) follow‐up of 4.1 (2.0–7.6) years. Cognitive decline was more rapid in people who on recruitment were: older, p = 0.0003; male, p = 0.027; had worse cognition, p < 0.0001; or carried the ε4 allele of apoliprotein E (APOEε4), p = 0.008; and after an operation if cognitive impairment was already diagnosed, p = 0.0001. Cognitive decline appears to accelerate after surgery in elderly patients diagnosed with cognitive impairment, but not other elderly patients.

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The effects of propofol on neutrophil function, lipid peroxidation and inflammatory response during elective coronary artery bypass grafting in patients with impaired ventricular function

Abstract: Propofol attenuates free-radical-mediated lipid peroxidation and systemic inflammation in patients with impaired myocardial function undergoing CABG.

Cited by 88 publications

References 24 publications

Propofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation

Propofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation

Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury

Cognitive decline in the elderly after surgery and anaesthesia: results from the Oxford Project to Investigate Memory and Ageing (OPTIMA) cohort

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