Effects of ketamine, propofol, and ketofol on proinflammatory cytokines and markers of oxidative stress in a rat model of endotoxemia-induced acute lung injury.

Abstract

Intravenous lipopolysaccharide (LPS) leads to acute lung injury (ALI) in rats. The purpose of this study was to examine the anti-inflammatory and antioxidant efficacy of ketamine, propofol, and ketofol in a rat model of ALI. We induced ALI in rats via intravenous injection of LPS (15 mg kg -1 ). The animals were randomly separated into five groups: control, LPS only, LPS + ketamine (10 mg·kg -1 ·h -1 ), LPS + propofol (10 mg·kg -1 ·h -1 ), LPS + ketofol (5 mg·kg -1 ·h -1 ketamine + 5 mg·kg -1 ·h -1 propofol). LPS resulted in an increase in the release of proinflammatory cytokines, mRNA expression related with inflammation, production of nitric oxide, and lipid peroxidation. Ketamine prevented the increase in markers of oxidative stress and inflammation mediators, both in plasma and lung tissue. Propofol decreased the levels of cytokines in plasma and lung tissue, whereas it had no effect on the IL-1-beta level in lung tissue. Ketamine downregulated mediators of lung tissue inflammation and reduced the level of circulating cytokines and protected lung tissue against lipid peroxidation. Ketofol decreased the level of TNF-α and IL-1β in plasma, as well as expression of cyclooxygenase-2 mRNA and the nitrate/nitrite level in lung tissue. The results of this investigation support the hypothesis that ketamine may be effective in preventing ALI.

Protective Effect of Ketamine against Acetic Acid-Induced Ulcerative Colitis in Rats

“…Ketamine treatment inhibits TNF production which may be due to inhibition of its synthesis or release. Our results parallel recent investigations showing anti-inflammatory properties of ketamine [24].…”

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

“…Propofol was previously reported to protect cells against oxidative stress induced by hydrogen peroxide (31,32), oxygen glucose deprivation (33) and endotoxemia (34), and to inhibit lipid peroxidation in various experimental cell models (35). The present results suggested that propofol significantly increased cell viability under normal culture conditions in a concentration-dependent manner, and the protective effects of propofol pretreatment against CoCl 2 hypoxiainduced injury were greatest at a concentration of 50 µg/ml.…”

Angiotensin II-induced mouse hippocampal neuronal HT22 cell apoptosis was inhibited by propofol: Role of neuronal nitric oxide synthase and metallothinonein-3

“…Further, it is indicated that its neuroprotec-446 tive effects were mediated via anti-oxidative and anti-447 apoptotic properties (Krzisch et al, 2013). In the present 448 study, we reported that MT-3 was down-regulated by 449 Ang II, suggesting that Ang II caused hippocampal (Chen et al, 2010(Chen et al, , 2011Gokcinar et al, 2013). 461 However, the effects of propofol on the brain are quite Alzheimer's disease transgenic mice (Shao et al, 2014).…”