Propofol prevents lipid peroxidation following transient forebrain ischemia in gerbils

Sun

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

et al. 2008

This study investigated the effects of propofol on the mRNA expression of Toll-like receptor-4 (TLR4) in BV-2 cells during mimic ischemia-reperfusion (I/R) injury in vitro. BV-2 cells, a mouse microglia line, were cultured and divided into 4 groups at random: control group (group C), ischemia/reperfusion group (group I/R), low-dose propofol (25 micromol/L) intervention group (group PF(25)) and high-dose propofol (100 micromol/L) intervention group (group PF(100)). The mRNA expression of TLR4 and NF-kappaB was measured by means of RT-PCR. TNF-alpha levels in the supernatants of BV-2 cells were detected by ELISA. The results showed that the mRNA expression of TLR4 and NF-kappaB was significantly higher in groups I/R, PF(25) and PF(100) than in group C (P<0.01). And the TNF-alpha level in the supernatants was elevated in groups I/R, PF(25) and PF(100) as compared with that in group C (P<0.01). After pre-treatment with propofol, the mRNA expressions of TLR4 and NF-kappa B and the TNF-alpha level were significantly decreased in groups PF(25) and PF(100) in comparison to those in group I/R (P<0.01). And the decrease in those indicators was more significant in group PF(100) than in group PF(25) (P<0.01). It was concluded that propofol exerted brain-protecting effects during I/R injury by suppressing the mRNA expressions of TLR4 and NF-kappaB and deceasing the TNF-alpha level.

Section: Discussionmentioning

confidence: 99%

Effects of propofol on the mRNA expression of toll-like receptor 4 in BV-2 cells during mimic ischemia-reperfusion injury in vitro

Sun

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

et al. 2008

“…The antioxidant properties of propofol are well established [149]. Thus, propofol attenuated delayed neuronal death secondary to transient forebrain ischemia [150,151] by preventing lipid peroxidation through the scavenging of various free radicals [149][150][151][152].…”

Section: A-to Prevent Ros-induced Damage Via Antioxidant Treatmentmentioning

confidence: 98%

Mitochondria: A Target for Neuroprotective Interventions in Cerebral Ischemia-Reperfusion

Morin¹,

Simon

2006

CPD

192

109

Evidence obtained over the past two decades shows that reactive oxygen species (ROS) are involved in brain lesions, including those due to cerebral ischemia-reperfusion. The mitochondria are the primary intracellular source of ROS, as they generate huge numbers of oxidative-reduction reactions and use massive amounts of oxygen. When anoxia is followed promptly by reperfusion, the resulting increase in oxygen supply leads to overproduction of ROS. In ischemic tissues, numerous studies have established a direct role for ROS in oxidative damage to lipids, proteins, and nucleic acids. Thus, mitochondria are both the initiator and the first target of oxidative stress. Mitochondrial damage can lead to cell death, given the role for mitochondria in energy metabolism and calcium homeostasis, as well as the ability of mitochondria to release pro-apoptotic factors such as cytochrome C and apoptosis-inducing factor (AIF). This review discusses possible mitochondrion-targeted strategies for preventing ROS-induced injury during reperfusion. The sequence of events that follow oxidative damage provides the outline for the review: thus, we will discuss protection of oxidative phosphorylation, mitochondrial membrane integrity and fluidity, and antioxidant or mild-uncoupling strategies for diminishing ROS production. Among mechanisms of action, we will describe the modulation of mitochondrial permeability transition pore (MPTP) opening, which may not only operate as a physiological Ca(2+) release mechanism, but also contribute to mitochondrial deenergization, release of pro-apoptotic proteins, and protection by ischemic preconditioning (IPC). Finally, we will review genetic strategies for controlling apoptotic protein expression, stimulating mitochondrial oxidative defences, and increasing mitochondrial proliferation.

“…7 Propofol (2,6-diisopropylphenol), an another highly lipid-soluble anesthetic, is often used in the induction of anesthesia and in the sedation of patients bound to mechanical ventilation in intensive care unit and has been reported to have a protective effect against I/R injury in several organs: for example, muscle, 8 heart, 9 and brain. 10 The mechanism underlying this protective effect reportedly involves either radical scavenging or inhibitory effects on calcium channels during I/R injury. 11 Etomidate is commonly used for cardiac patients because of good induction properties.…”

Section: Introductionmentioning

confidence: 99%

Thiopental improves renal ischemia–reperfusion injury

et al. 2010