Effect of propofol on oxidative stress in an in vitro model of anoxia-reoxygenation in the rat brain

Cruz, J. P. De La; Villalobos, M.A.; Sedeno, G.; Cuesta, Felipe Sánchez de la

doi:10.1016/s0006-8993(98)00516-2

Cited by 54 publications

(27 citation statements)

References 26 publications

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“…The results of the present study indicated that the levels of pJNK in groups P1 and P2 were markedly lower than those in the ischemia/reperfusion group. 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).…”

Section: Discussionmentioning

confidence: 99%

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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Section: Discussionmentioning

confidence: 99%

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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“…As in the case of others studies, 2,9,24,25 these authors propose that propofol would inhibit, or at least decrease lipid peroxidation. Studies on antioxidant defensive cell enzyme systems by De La Cruz et al, 24,25 suggest that, at clinically relevant doses, apart from inhibiting lipid peroxidation, propofol may also act on enzyme systems (in particular on the glutathione system) which would lead to a decrease in the activity of glutathione peroxidase and an increase in the activities of glutathione reductase and glutathione transferase. This effect would yield an increase in cellular deposits of reduced glutathione, and hence in defensive cellular deposits of antioxidants, thereby protecting tissues from oxidative stress.…”

Section: Discussionmentioning

confidence: 62%

“…22 Several in vitro studies demonstrate that propofol inhibits lipid peroxidation in human liver microsomes 23 and in different tissues of Wistar rats in which, additionally, increases in reduced glutathione levels have been reported. 24,25 Corcoran et al, 26 showed that the administration of propofol before aortic cross-clamp release in patients undergoing elective coronary artery bypass graft surgery decreases myocardial lipid peroxidation, attenuates the inflammatory response to myocardial reperfusion, and limits the inflammatory cascade.…”

Section: Discussionmentioning

confidence: 99%

“…5,20,[22][23][24]27 Several studies suggest that it is the active principle of propofol and not its solvent (Intralipid ® ) which exerts the antioxidant action. 26 Certain immunomodulatory effects of propofol, such as suppression of respiratory bursts of neutrophils by propofol, may be caused by intralipid, while other actions, such as the ability to scavenge free radicals, appear to be a property of propofol itself.…”

Section: Discussionmentioning

confidence: 99%

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Laboratory investigation: Effects of propofol on the systemic inflammatory response during aortic surgery

Rodríguez-López

Conde

Lozano

et al. 2006

Can J Anesth/J Can Anesth

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Purpose: A laboratory investigation was undertaken to assess the effects of propofol on renal function, through modulation of the systemic inflammatory response, in an in vivo experimental model of aortic surgery in comparison with sevoflurane.Methods: Twenty young male piglets were anesthetized with either propofol 4 mg·kg -1 ·hr -1 (n = 10) or sevoflurane 1.5% end-tidal concentration (n = 10). Animals were subjected to aorta-aortic bypass with suprarenal aortic clamping for 30 min. At specific intervals (basal -before the start of surgery; reperfusion 15 min after unclamping the aorta; at 24, 48 and 72 hr after surgery, and on the seventh day after surgery) the levels of the following were determined: plasma creatinine, renal myeloperoxidase, tumour necrosis factor-α, interleukin 1-ß, and interferon-γ; kidney superoxide anion and its detoxifying enzyme superoxidase dismutase, kidney malondialdehyde and the activity of inducible nitric oxide synthase. Seven days after surgery, the animals were anesthetized using the described techniques, and after blood withdrawal and kidney sampling they were sacrificed. Results:In comparison with sevoflurane, propofol was associated with a lower concentration of plasma creatinine (P < 0.05) together with lower concentrations of myeloperoxidase, tumour necrosis factor-α, interleukin 1-ß, interferon-γ, superoxide anion and superoxidase dismutase, malondialdehyde and inducible nitric oxide synthase (P < 0.05). Conclusion:In an experimental model of aortic reconstructive surgery, and compared with sevoflurane, propofol anesthesia is associated with less neutrophil infiltration, lower plasma proinflammatory cytokine levels, lower production of oxygen free radicals, less lipid peroxidation, and reduced inducible nitric oxide synthase activity. These observations suggest a possible renal protective effect of propofol in this surgical setting. Objectif

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“…Its also reported that propofol functions as both peroxynitrite scavenger which is produced by superoxide radicals binding to nitric oxide physiologically and inhibiting lipid peroxidation on cellular membranes [14,15]. Another function of propofol is increasing the function of gluthatione antioxidising system [16,17].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Dexmedetomidine and Propofol on Oxidative Stress and Antioxidizing System Studied on Liver Ischemia-reperfusion Model on Rats

Urfalıoğlu¹,

Cantürk²,

Akçaboy³

et al. 2013

J Anesthe Clinic Res

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Surgical procedureAnesthesia was induced with Ketamine to rats, (Ketalar flk, Eczacıbaşı) with a dose of 90 mg/kg. Under sterile cover, laporatomy was performed via midline incision. Hepatoduodenal ligament was Materials and methods: 24 rats were randomly divided into four groups. Following anesthesia laparotomy was done and hepatoduodenal ligament was explorated. Tissue samples were taken for both biochemical (MDA, SOD, GPx) and histological study.Results: MDA level was hisghest in Group II and was significantly lower in Group III and Group IV. GPx level was lowest in Group II, the level of GPx was higher in Group III and Group IV with respect to Group II. SOD level was lowest in Group II and was highest in Group IV. SOD levels in Group II and Group III did not show statistical significance. In the histopathological study, in Group I the liver parenchyme and membrane integrity was protected; in Group II the hepatocyte cellular membrane integrity was distorted, microvesicule number increased and the liver sinusoids were shrunken; in Group III the hepatocyte membrane and nucleus was near normal and well protected; and in Group IV the cellular component structures were protected, hepatocyte cell membrane was protected in normal thickness. Discussion:The results show that dexmedetomidine and propofol decrease the level of MDA in similarly; the effect of dexmedetomidine on GPx level was slightly lower than propofol and its effect on SOD level was lower than propofol. As a result, we believe that either propofol or dexmedetomidine can be effective in protecting hepatocytes from I/R injury especially in log term procedures but the former drug having dominance in this protective role.

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Effect of propofol on oxidative stress in an in vitro model of anoxia-reoxygenation in the rat brain

Cited by 54 publications

References 26 publications

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

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

Laboratory investigation: Effects of propofol on the systemic inflammatory response during aortic surgery

The Effect of Dexmedetomidine and Propofol on Oxidative Stress and Antioxidizing System Studied on Liver Ischemia-reperfusion Model on Rats

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