The widely used anesthetic agent propofol can replace α‐tocopherol as an antioxidant

Aarts, Leon; Hee, Regine van der; Dekker, Ingrid; Jong, Jan de; Langemeijer, Han J.; Bast, Aalt

doi:10.1016/0014-5793(94)01337-z

Cited by 149 publications

(79 citation statements)

References 16 publications

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“…Previous studies indicated that the well-known anti-oxidant properties of propofol might be related to its chemical structure, which is similar to that of phenol-based scavengers such as tocopherols. 1,9,[42][43][44] Indeed, a-tocopherol is reported to have a strong anti-oxidizing effect. 42 Similarly, propofol's inhibitory effect on COX might be ascribable to its structural similarity to c-tocopherol.…”

Section: Lps Pretreatmentmentioning

confidence: 99%

Propofol inhibits cyclo-oxygenase activity in human monocytic THP-1 cells

Inada

Kubo

Kambara

et al. 2009

Can J Anesth/J Can Anesth

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Purpose Monocytes/macrophages are key players in innate and adaptive immunity. Upon stimulation, they secrete prostanoids, which are produced by cyclooxygenase from arachidonic acid. Prostanoids influence inflammation and immune responses. We investigated the effect of propofol on prostaglandin E 2 and thromboxane B 2 production by the human monocytic cell line THP-1. Methods The THP-1 cells were cultured with lipopolysaccharide (1 lg ml -1 ) in the presence of clinically relevant sedative/anesthetic concentrations of propofol (0-30 lM) for 18 h, and the concentration of prostaglandin E 2 and thromboxane B 2 in culture supernatants was measured using an enzyme immunoassay. Intracellular cyclooxygenase protein expression was measured by flow cytometry. Cyclooxygenase activity was assessed by measuring production of prostaglandin E 2 and thromboxane B 2 by THP-1 cells after arachidonic acid (10 lM) substrate provision. Results Propofol decreased the production of prostaglandin E 2 (75.4 ± 6.4 pg ml -1 at 0 lM vs. 28.5 ± 11.2 pg ml -1 at 30 lM; P \ 0.001) and thromboxane B 2 (282.4 ± 79.2 pg ml -1 at 0 lM vs. 40.4 ± 21.7 pg ml -1at 30 lM; P \ 0.001). The inhibition was not due to the decreased cyclooxygenase protein expression because intracellular staining of this enzyme was not affected by propofol. After arachidonic acid provision, prostaglandin E 2 and thromboxane B 2 production from activated THP-1 cells was significantly (P \ 0.001) decreased with propofol, indicating direct suppression of cyclooxygenase activity with propofol.

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Section: Lps Pretreatmentmentioning

confidence: 99%

Propofol inhibits cyclo-oxygenase activity in human monocytic THP-1 cells

Inada

Kubo

Kambara

et al. 2009

Can J Anesth/J Can Anesth

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“…Propofol (2,6-diisopropylphenol) is a lipidsoluble anesthetic agent that has a chemical structure similar to that of phenol-based free radical scavengers such as vitamin E (Aarts et al, 1995;Kokita et al, 1998). It is commonly used as an intravenous anesthetic in cardiac surgery and has been shown to decrease postischemic myocardial dysfunction (Kokita and Hara, 1996), infarct size (Ebel et al, 1999), and histologic degeneration (Ko et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective effects of anesthetic preconditioning in rats with ischemia-reperfusion injury: propofol versus isoflurane

Xing

Lü

et al. 2009

J. Zhejiang Univ. Sci. B

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Abstract:Objective: We compare the cardioprotective effects of anesthetic preconditioning by propofol and/or isoflurane in rats with ischemia-reperfusion injury. Methods: Male adult Wistar rats were subjected to 60 min of anterior descending coronary artery occlusion followed by 120 min of reperfusion. Before the long ischemia, anesthetics were administered twice for 10 min followed by 5 min washout. Isoflurane was inhaled at 1 MAC (0.016) in I group, whereas propofol was inhaled intravenously at 37.5 mg/(kg⋅h) in P group. A combination of isoflurane and propofol was administered simultaneously in I+P group. Results: In control (without anesthetic preconditioning, C group), remarkable myocardial infarction and apoptosis accompanied by an increased level of cardiac troponin T were noted 120 min after ischemia-reperfusion. As compared to those of control group, I and P groups had comparable cardioprotection. In addition, I+P group shares with I and P groups the comparable cardioprotective effects in terms of myocardial infarction and cardiac troponin T elevation. Conclusion: A combination of isoflurane and propofol produced no additional cardioprotection.

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“…Propofol is one of the intravenous agents searched for its antioxidising effect. Chemical structure of propofol (2,6-diisoproyl phenol) mimics butilised hydroxy toluen (BHT) and endogenous antioxidising agent alpha-tocopherol (vitamin E) which are phenol containing free oxygen radical scavengers and contains a phenolic hydroxy group [13]. All these molecules form complexes with either the cellular membranes or its structural components resulting in a less reactive molecules and each single propofol molecule can scavenger two free oxygen radicals [3,4].…”

Section: Discussionmentioning

confidence: 99%

“…And other similar models of I/R injury on neurons [19], leucocytes [4] and erythrocytes [20] prooved that propofol has a preventive effect against I/R injury. Aarts et al has reported that propofol has a preventive role in cases such as coronary artery transplantation surgery, sepsis and burns, which of all lead into a decreased ontioxidising defense mechanism [13]. Also in some recent studies propofol has been reported to be a free radical scavenger due to its antioxidising property at anesthetic doses [21][22][23].…”

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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The widely used anesthetic agent propofol can replace α‐tocopherol as an antioxidant

Cited by 149 publications

References 16 publications

Propofol inhibits cyclo-oxygenase activity in human monocytic THP-1 cells

Propofol inhibits cyclo-oxygenase activity in human monocytic THP-1 cells

Cardioprotective effects of anesthetic preconditioning in rats with ischemia-reperfusion injury: propofol versus isoflurane

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

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