The effects of the caffeic acid phenethyl ester (CAPE) on erythrocyte membrane damage after hind limb ischaemia–reperfusion

Abstract

Reactive oxygen species have been implicated in pathogenesis injury after ischaemia-reperfusion (I/R). Caffeic Acid Phenethyl Ester (CAPE), an active component of honeybee propolis extract, exhibits antioxidant and anti-inflammatory properties. The aim of this study was to investigate the effects of CAPE on erythrocyte membrane damage after hind limb I/R. Rats were divided into two groups: I/R and I/R with CAPE pre-treatment. They were anaesthetized with intramuscular ketamine 100 mg kg(-1). A 4-h I/R period was performed on the right hind limb of all animals. In the CAPE-treated group, animals received CAPE 10 microm by intraperitoneal injection 1 h before the reperfusion. At the end of the reperfusion period, a midsternotomy was performed. A 5-ml blood sample was withdrawn from the ascending aorta for biochemical assays. Serum and erythrocyte membrane MDA levels were significantly lower in the CAPE-treated group when compared to the I/R group ( p = 0.001 and p<0.001, respectively). Erythrocyte membrane Na(+)-K(+) ATPases activity in the CAPE-treated group was significantly higher than the I/R group ( p<0.001). In conclusion, CAPE seems to be effective in protecting against oxidative stress. Therefore, we suggest that in order to decrease I/R injury, pre-administration of CAPE may be a promising agent for a variety of conditions associated with I/R.

Red Orange: Experimental Models and Epidemiological Evidence of Its Benefits on Human Health

“…It is found in all plants because it is a key intermediate in the biosynthesis of lignin, one of the principal sources of biomass [113]. The caffeic acid phenethyl ester has been found to be a potent free radical scavenger [114] and studied for its antioxidant capacities in several experimental rat models on renal impairment [115–117], retinal oxidative stress [118], myocardial oxidative stress [119], age-related vascular remodeling and cardiac damage [120], and at the same time helping to prevent the metabolic consequences in diabetes mellitus [121, 122], erythrocyte membrane ischemia/reperfusion injury [123], cerebral damage induced by ischemia reperfusion [124], and oxidative stress [125]. The mechanisms by which caffeic acid phenethyl ester exerts its anti-inflammatory action seems to depend on its effect on lipid peroxidation (LPO) and the inhibition of antioxidant enzymes such as superoxide dismutase and catalase [126].…”

Caffeic acid phenethyl amide improves glucose homeostasis and attenuates the progression of vascular dysfunction in Streptozotocin-induced diabetic rats

“…Oral administration of CAPE (30 mg/kg) for 12 weeks ameliorated the atherosclerosis progress in apolipoprotein E-deficient mice [23]. In addition, intraperitoneally injected CAPE (10 μM) 1 h before reperfusion attenuated ischemia-reperfusion injury by exerting antioxidant activity in Wistar rats [24]. CAPE significantly decreased the fasting blood levels of glucose, alanine aminotransferase, cholesterol, and triglyceride induced by diabetes [25].…”

Prevention of Pulmonary Complications of Pneumoperitoneum in Rats

“…However, the free oxygen radicals (H 2 O 2 , O 2 - , and OH - ) and proteases released from the accumulated inflammatory cells, especially neutrophils can increase the systemic availability of inflammatory mediators, leading to leukocyte activation and endothelial adhesion molecule expression and vascular endothelial damage of remote organs. The free oxygen radicals are capable of reacting with proteins, nucleic acids, and lipids resulting in lipid peroxidation of biological membranes [11]. …”