Protective effects of caffeic acid phenylethyl ester, a main component of propolis against cyclosporine A-induced nephrotoxicity in rats

The present study was designed to investigate the possible protective effects of Caffeic acid phenylethyl ester [CAPE] against Cyclosporine A [C5A] induced nephrotoxicity in rats. Through antioxidant, free radical scavenger and anti-inflammatory effects of CAPE and CsA. Thirty two male Sprague-Dawley rats were divided into four groups of eight rats in each one; first group served as control [treated with vehicle]. The other groups were treated intraperitoneally with CsA alone [20 mg/kg/24 hours], CAPE alone [10 micro mol/kg/24 hours] and CAPE plus CsA for 21 days. The treatment with CAPE started two days before the first dose of CsA. Estimation of urine volume, serum creatinine and urea concentrations, creatinine clearance, kidney tissue malondialdehyde [MDA] and glutathione [GSH] contents were carried out after the last dose of CsA. Also, the lysosomal enzymes [N-acetyl-beta-glucosaminidase [NAG] and beta-glucuronidase [beta-GLU]] and antioxidant enzymes [glutathione peroxidase [GSH-Px], catalase [CAT] and superoxide dismutase [SOD]] activities were estimated in kidney homogenates. Kidneys were also examined for histological changes. CsA caused a marked nephrotoxicity as evidenced by significant increases in urine volume [295%], serum creatinine [194%] and urea [167%] and a significant decrease in creatinine clearance [Ccr] [24%]. Pre-treatment with CAPE produced amelioration in biochemical indices of nephrotoxicity in serum and urine. Furthermore, CAPE prevented the CsA-induced increase in the renal levels of oxidative stress markers [MDA, NAG and beta-GLU] and prevent the decrease in the antioxidant enzymes [SOD, CAT and GSH-Px] activities. In addition, co-administration of CAPE was found to reduce the degree of kidney tissue damage in histopathological findings. CAPE as a natural antioxidant might have protective effects against CsA-induced nephrotoxicity and oxidative stress in rats. However, clinical studies are warranted to investigate such an effect in human subjects

Circulating levels of adhesion molecules and oxidative stress markers in smokers

Objective: To examine whether oxidative stress markers were correlated with adhesion molecules [sICAM-1, sVCAM-1 and sP-selectin] derived from endothelial/platelet activation in a group of smokers as well as to study the influence of smoking index on the above mentioned markers

Subjects and Methods: Plasma levels of sICAM-1 , sVCAM-l , sP-selectin, 8-isoprostane [8-IP] and protein carbonyl content were assessed by ELISA technique and colorimetric method. Antioxidant status, assessed by measuring the glutathione [GSH], and vitamin C levels in 38 smokers and 20 nonsmokers serving as control. Smokers were divided into three groups: mild, moderate and heavy smokers according to smoking index

Results: Smokers showed significant higher levels of sICAM-1 , sVCAM-1 , sP-sclectin, 8-IP and protein cathonyl content and this increase was directly proportional to the degree of smoking. Smokers showed also significantly lower levels of GSH and vitamin C than nonsmokers. In comparing groups of smokers to each other, significant decreased levels were observed in GSH, vitamin C in the following order heavy > moderate > mild smokers. A positive correlation was detected between the circulating adhesion molecules [sICAM-1, sVCAM-1 , sP-sclectm.] and oxidative stress markers; 8-IP [r[2] =0.927, 0.919 and 0.969 respectively] and protein carbonyl [r[2] = 0.924, 0.923 and 0.845 respectively] in plasma of smokers

Conclusion: Adhesion molecules [sICAM-1 , sVCAM-1 , sP-selectin ] increase in smokers may be a secondary response to inflammation and oxidative stress. Smoking: stimulate the release of adhesion molecules by creating oxidative stress through decrease of the antioxidant status including both vascuiar and systemic complications in smokers