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Phenethyl Ester (phenethyl + ester)
Kinds of Phenethyl Ester Selected AbstractsThe effects of the caffeic acid phenethyl ester (CAPE) on erythrocyte membrane damage after hind limb ischaemia,reperfusionCELL BIOCHEMISTRY AND FUNCTION, Issue 5 2004Lülüfer Tamer 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,,m 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 A 5-ml blood sample was withdrawn from the ascending aorta for biochemical assays.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. Copyright © 2004 John Wiley & Sons, Ltd. [source] Effects of melatonin and caffeic acid phenethyl ester on testicular injury induced by myocardial ischemia/reperfusion in ratsFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2005Mukaddes E Abstract Experimental studies indicate that ischemia/reperfusion (I/R) causes remote organ injury although the molecular mechanism has not been clearly defined. In this report, the role of oxidative injury on testicular damage following myocardial I/R injury and the effects of antioxidant agents, melatonin and caffeic acid phenethyl ester (CAPE), on testicular injury were investigated. As far as we know, this is the first report demonstrating that myocardial I/R induces damage to the testes. Thirty-two male Wistar rats were randomly divided into four groups: sham operation (SO), I/R + vehicle, I/R + melatonin, and I/R + caffeic acid phenethyl ester. To produce cardiac damage, the left main coronary artery was occluded for 30 min, followed by 120 min reperfusion, in anesthetized rats. Serum nitric oxide (NO) and malondialdehyde (MDA) levels and morphological changes were examined. I/R was accompanied by a significant increase in serum MDA and NO levels, whereas, melatonin and CAPE administration significantly reduced these values. Melatonin was more efficient in reducing MDA levels than CAPE (P < 0.05). I/R induced myocardial damage, manifested as the histopathological evidence of intracellular vacuolization, interstitial edema, neutrophil infiltration and coagulative necrosis. I/R + vehicle group showed many histological alterations such as focal tubular atrophy, and degeneration and disorganization of the seminiferous epithelium in testes. The number of atrophic tubules and degenerating cells was significantly higher in I/R + vehicle group than that of SO group. Melatonin and CAPE significantly reduced the number of degenerating cells; additionally, melatonin reduced the number of atrophic tubules (P < 0.05). Our results indicate that myocardial I/R induces severe testicular damage and antioxidant agents, especially melatonin, have protective effects on testicular injury after myocardial I/R. Our data emphasize that oxygen-based reactants may play a central role in remote organ injury. [source] Alcohol potentiates hepatitis C virus replicon expressionHEPATOLOGY, Issue 1 2003Ting Zhang Alcohol consumption accelerates liver damage and diminishes the anti-hepatitis C virus (HCV) effect of interferon alfa (IFN-,) in patients with HCV infection. It is unknown, however, whether alcohol enhances HCV replication and promotes HCV disease progression. The availability of the HCV replicon containing hepatic cells has provided a unique opportunity to investigate the interaction between alcohol and HCV replicon expression. We determined whether alcohol enhances HCV RNA expression in the replicon containing hepatic cells. Alcohol, in a concentration-dependent fashion, significantly increased HCV replicon expression. Alcohol also compromised the anti-HCV effect of IFN-,. Investigation of the mechanism(s) responsible for the alcohol action on HCV replicon indicated that alcohol activated nuclear factor ,B (NF-,B) promoter. Caffeic acid phenethyl ester (CAPE), a specific inhibitor of the activation of NF-,B, abolished alcohol-induced HCV RNA expression. In addition, naltrexone, an opiate receptor antagonist, abrogated the enhancing effect of alcohol on HCV replicon expression. In conclusion, alcohol, probably through the activation of NF-,B and the endogenous opioid system, enhances HCV replicon expression and compromises the anti-HCV effect of IFN-,. Thus, alcohol may play an important role in vivo as a cofactor in HCV disease progression and compromise IFN-,-based therapy against HCV infection. [source] Caffeic acid phenethyl ester decreases cholangiocarcinoma growth by inhibition of NF-,B and induction of apoptosisINTERNATIONAL JOURNAL OF CANCER, Issue 3 2009Paolo Onori Abstract Caffeic acid phenethyl ester (CAPE) inhibits the growth of tumor cells and is a known inhibitor of nuclear factor kappa beta (NF-,B), which is constitutively active in cholangiocarcinoma (CCH) cells. We evaluated the effects of CAPE on CCH growth both in vitro and in vivo. Inhibition of NF-,B DNA-binding activity was confirmed in nuclear extracts treated with CAPE at 50, 40 and 20 ,M. CAPE decreases the expression of NF-,B1 (p50) and RelA (p65). CAPE decreased the growth of a number of CCH cells but not normal cholangiocytes. Cell cycle decrease was seen by a decrease in PCNA protein expression and the number of BrdU-positive cells treated with CAPE at 20 ,M compared to vehicle. Inhibition of growth and increased cell cycle arrest of Mz-ChA-1 cells by CAPE were coupled with increased apoptosis. Bax expression was increased, whereas Bcl-2 was decreased in cells treated with CAPE compared to vehicle. In vivo studies were performed in BALB/c nude (nu/nu) mice implanted subcutaneously with Mz-ChA-1 cells and treated with daily IP injections of DMSO or CAPE (10 mg/kg body weight in DMSO) for 77 days. Tumor growth was decreased and tumor latency was increased 2-fold in CAPE compared to vehicle-treated nude mice. In tumor samples, decreased CCH growth by CAPE was coupled with increased apoptosis. CAPE both in vivo and in vitro decreases the growth of CCH cells by increasing apoptosis. These results demonstrate that CAPE might be an important therapeutic tool in the treatment of CCH. © 2009 UICC [source] Tumor necrosis factor-alpha (TNF-,) regulates Toll-like receptor 2 (TLR2) expression in microgliaJOURNAL OF NEUROCHEMISTRY, Issue 4 2007Mohsin Md. Abstract Microglia represent one effector arm of CNS innate immunity as evident by their role in pathogen recognition. We previously reported that exposure of microglia to Staphylococcus aureus (S. aureus), a prevalent CNS pathogen, led to elevated Toll-like receptor 2 (TLR2) expression, a pattern recognition receptor capable of recognizing conserved structural motifs associated with gram-positive bacteria such as S. aureus. In this study, we demonstrate that the proinflammatory cytokine tumor necrosis factor-, (TNF-,) enhances TLR2 expression in microglia, whereas interleukin-1, has no significant effect. To determine the downstream signaling events responsible for elevated microglial TLR2 expression in response to TNF-,, a series of signal transduction inhibitors were employed. Treatment with caffeic acid phenethyl ester, an inhibitor of redox-mediated nuclear factor-kappa B activation, significantly attenuated TNF-,-induced TLR2 expression. Similar results were observed with the IKK-2 and I,B-, inhibitors SC-514 and BAY 11-7082, respectively. In contrast, no significant alterations in TLR2 expression were observed with protein kinase C or p38 mitogen-activated protein kinase inhibitors. A definitive role for TNF-, was demonstrated by the inability of S. aureus to augment TLR2 expression in microglia isolated from TNF-, knockout mice. In addition, TLR2 expression was significantly attenuated in brain abscesses of TNF-, knockout mice. Collectively, these results indicate that in response to S. aureus, TNF-, acts in an autocrine/paracrine manner to enhance TLR2 expression in microglia and that this effect is mediated, in part, by activation of the nuclear factor-kappa B pathway. [source] Stability of caffeic acid phenethyl ester and its fluorinated derivative in rat plasmaBIOMEDICAL CHROMATOGRAPHY, Issue 4 2007Xinyu Wang Abstract The stability of caffeic acid phenethyl ester (CAPE) and its fluorinated derivative (FCAPE) in rat plasma and conditions preventing their degradation are reported. Reverse-phase high-pressure liquid chromatography (HPLC) using taxifolin as an internal standard was applied for the quantitative determination of CAPE and FCAPE in rat plasma extracted with ethyl acetate. The assay was validated over a linear range of 0.25,10 µg/mL plasma (r2 > 0.9990, n = 3). No endogenous interferences were observed in the chromatographic region of interest. The limits of quantification and detection were set at 0.25 and 0.1 µg/mL, respectively. The precision ranged from 0.7 to 13.7% for CAPE, and from 0.4 to 10.4% for FCAPE. Accuracy ranged from ,2.8 to 12.4% for CAPE and from ,0.6 to 6.8% for FCAPE. The stability was conducted at 4, 25 and 37°C. First-order kinetics was observed for the degradation of CAPE and FCAPE. The energies of activation of CAPE and FCAPE were found to be 17.9 and 20.1 kcal/mol, respectively. Addition of 0.4% of sodium chloride and pH adjustment to 6 prevented their degradation in rat plasma for 24 h and at least one month at ,20°C. This study provides useful information for the future pharmacokinetic study of CAPE and FCAPE in rat. Copyright © 2007 John Wiley & Sons, Ltd. [source] Caffeic acid phenethyl ester modulates Helicobacter pylori -induced nuclear factor-kappa B and activator protein-1 expression in gastric epithelial cellsBRITISH JOURNAL OF PHARMACOLOGY, Issue 8 2005Mohamed M M Abdel-Latif Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives (honeybee resin), has anti-inflammatory, anti-carcinogenic and anti-bacterial properties. This study was designed to investigate the anti-inflammatory effects of CAPE on Helicobacter pylori -induced NF- ,B and AP-1 in the gastric epithelial cell line AGS. Electrophoretic mobility shift assay was used to measure NF- ,B- and AP-1-DNA binding activity. Western blotting was used to detect I,B- , and COX-2 expression in AGS cells cocultured with H. pylori. The antiproliferative effect of CAPE was measured by MTT assay. Our results showed that caffeic phenethyl ester inhibits H. pylori -induced NF- ,B and AP-1 DNA-binding activity in a dose (0.1,25 ,g ml,1,0.35,88 ,M) and time- (15,240 min) dependent manner in AGS cells. Maximum inhibition by CAPE was observed at concentrations of 25 ,g ml,1 (,88 ,M) CAPE prevented H. pylori - and cytokine-induced degradation of I,B- , protein. Pretreatment of AGS cells with CAPE also blocked cytokine- and mitogen-induced NF- ,B and AP-1 expression. Furthermore, CAPE suppressed H. pylori -induced cell proliferation and production of the cytokines TNF- , and IL-8. In addition, CAPE blocked H. pylori -induced COX-2 expression. The inhibition of such transcription by CAPE could result in suppression of many genes during H. pylori -induced inflammation, and also provide new insights into the anti-cancer and anti-inflammatory properties of CAPE. British Journal of Pharmacology (2005) 146, 1139,1147. doi:10.1038/sj.bjp.0706421 [source] Effect of caffeic acid phenethyl ester on treatment of experimentally induced methicillin-resi,stant Staphylococcus epidermidis endophthalmitis in a rabbit modelCELL BIOCHEMISTRY AND FUNCTION, Issue 6 2007Özlem Y Abstract This study investigated the anti-inflammatory effects of caffeic acid phenethyl ester (CAPE), a natural bee-produced compound, and compared it with corticosteroids in the treatment of experimentally induced methicillin-resistant Staphylococcus epidermidis (MRSE) endophthalmitis in addition to intravitreal antibiotics. An experimental endophthalmitis model was produced in 24 New Zealand albino rabbits by unilateral intravitreal injection of 0.1,ml of 4.7,×,104 colony-forming units (CFU) methicillin-resistant S. epidermidis. The animals were then divided randomly into three treatment groups and a control group, group 1 (six rabbits), received only intravitreal vancomycin (1.0,mg/0.1,ml); group 2 (six rabbits), received both intravitreal vancomycin (1.0,mg/0.1,ml) and intravitreal dexamethasone (400,µg/0.1,ml) and group 3 (six rabbits), received both intravitreal vancomycin (1.0,mg/0.1,ml) and subtenon CAPE (10,mg/0.3,ml) after 24,h post-infection. No treatment was given to the control group. Treatment efficacy was assessed by clinical examination, vitreous culture and histopathology. There were no statististically significant differences between clinical scores of all groups in examinations at 24 and 48,h post-infection (p,=,0.915 and p,=,0.067 respectively), but in examinations at 72,h post-infection and after 7 days post-infection, although the clinical scores of treatment groups were not significantly different from each other, they were significantly lower than the control group (p,<,0.05). The culture results of all groups were sterile. As a result, CAPE was found to be as effective as dexamethasone in reducing inflammation in the treatment of experimental MRSE endophthalmitis when used with antibiotics. More studies are needed to determine the optimal administration route and effective dosage of this compound. Copyright © 2006 John Wiley & Sons, Ltd. [source] The effects of the caffeic acid phenethyl ester (CAPE) on erythrocyte membrane damage after hind limb ischaemia,reperfusionCELL BIOCHEMISTRY AND FUNCTION, Issue 5 2004Lülüfer Tamer 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,,m 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. Copyright © 2004 John Wiley & Sons, Ltd. [source] Effects of caffeic acid phenethyl ester and alpha-tocopherol on reperfusion injury in rat brainCELL BIOCHEMISTRY AND FUNCTION, Issue 3 2003M. Kemal Irmak Abstract Oxygen-derived free radicals have been implicated in the pathogenesis of cerebral injury after ischaemia,reperfusion. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant properties. The purpose of the present study was to investigate the effects of ischaemia and subsequent reperfusion on rat brain and to investigate the effects of two free radical scavengers, CAPE and alpha-tocopherol, on this in vivo model of cerebral injury. Ischaemia was induced by bilateral occlusion of the carotid arteries for 20,min and reperfusion was achieved by releasing the occlusion to restore the circulation for 20,min. Control rats underwent a sham operation. CAPE at 10,,;mol,kg,1 or alpha-tocopherol at 25,,mol,kg,1 was administered intraperitoneally before reperfusion. Reperfusion led to significant increase in the activity of xanthine oxidase and higher malondialdehyde levels in the brain. Acute administration of both CAPE and alpha-tocopherol suppressed ischaemia,reperfusion-induced cerebral lipid peroxidation and injury, but CAPE seems to offer a better therapeutic advantage over alpha-tocopherol. Copyright © 2003 John Wiley & Sons, Ltd. [source] Caffeic acid phenethyl ester changes the indices of oxidative stress in serum of rats with renal ischaemia,reperfusion injuryCELL BIOCHEMISTRY AND FUNCTION, Issue 4 2001Hüseyin Özyurt Abstract Oxygen-derived free radicals have been implicated in the pathogenesis of renal injury after ischaemia,reperfusion. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant properties. To investigate whether treatment with either CAPE or alpha-tocopherol modifies the levels of the endogenous indices of oxidant stress, we examined their effects on an in vivo model of renal ischaemia,reperfusion injury in rats. CAPE at 10,,mol,kg,1 or alpha-tocopherol at 10,mg,kg,1 was administered intraperitoneally before reperfusion. Acute administration of both CAPE and alpha-tocopherol altered the indices of oxidative stress differently in renal ischaemia,reperfusion injury. Copyright © 2001 John Wiley & Sons, Ltd. [source] Caffeic acid phenetyl ester accelerates cutaneous wound healing in a rat model and decreases oxidative stressCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 6 2007G. Serarslan Summary Background., Cutaneous injury causes a depression in antioxidant status, as reactive oxygen species (ROS) are produced in response to injury., Aim., To determine the effects of caffeic acid phenethyl ester (CAPE), an antioxidant and anti-inflammatory agent, on wound healing in rats. Methods., In total, 40 male rats were divided into two groups: one group treated with CAPE (n = 20) and a second untreated control group (n = 20). A linear full-thickness incision was performed on the back of each rat and sutured. After incision, CAPE was given to the treatment group and saline to the control group. On days 1, 3, 7 and 14, five animals in each group were killed, and wound tissues dissected for biochemical and histopathological analysis. Results., Wound tissues showed a significant increase in glutathione and nitric oxide levels, and a significant decrease in malondialdehyde levels and superoxide dismutase levels in the CAPE group compared with the control group. Histopathology of the wound tissues displayed rapid epithelium development in the CAPE group compared with the control group. Conclusion., This study has demonstrated that CAPE partly accelerates full-thickness wound healing by its antioxidant and ROS-scavenging capabilities. [source] | |||||||||||||