Search

The present study was conducted to investigate whether caffeic acid phenethyl ester (CAPE), an active component of propolis extract, has a protective effect on amphotericin B induced nephrotoxicity in rat models. Male Wistar-Albino rats were randomly divided into four groups: (I) control group (n = 10), (II) CAPE group (n = 9) which received 10 μmol/kg CAPE intraperitoneally (i.p.), (III) amphotericin B group (n = 7) which received one dose of 50 mg/kg amphotericin B, and (IV) amphotericin B plus CAPE group (n = 7) which received 10 μmol/kg CAPE i.p. and one dose of 50 mg/kg amphotericin B. The left kidney was evaluated histopathologically for nephrotoxicity. Levels of malondialdehyde (MDA), nitric oxide (NO), enzyme activities including catalase (CAT), and superoxide dismutase (SOD) were measured in the right kidney. Histopathological damage was prominent in the amphotericin B group compared to controls, and the severity of damage was lowered by CAPE administration. The activity of SOD, MDA, and NO levels increased and catalase activity decreased in the amphotericin B group compared to the control group (P = 0.0001, P = 0.003, P = 0.0001, and P = 0.0001, resp.). Amphotericin B plus CAPE treatment caused a significant decrease in MDA, NO levels, and SOD activity (P = 0.04, P = 0.02, and P = 0.0001, resp.) and caused an increase in CAT activity compared with amphotericin B treatment alone (P = 0.005). CAPE treatment seems to be an effective adjuvant agent for the prevention of amphotericin B nephrotoxicity in rat models.

Caffeic acid phenethyl ester (CAPE) is an antioxidant that can scavenge free radicals and protect cellular macromolecules, including DNA and proteins, from oxidative damage induced by various agents. The protective effect of CAPE on cisplatin-induced chromosome aberrations has been determined in rat bone marrow cells. The animals were pretreated with a single dose of CAPE (10 micromol/kg body weight [b.w.]) injected intraperitoneally (i.p.) 24 hours before the administration of cisplatin and then sacrificed 24 hours after the cisplatin administration. Cisplatin was administered to rats either alone (5 mg/kg b.w., i.p.) or after CAPE treatment. CAPE has led to a statistically significant decrease in the total number of chromosomal aberrations and abnormal metaphases induced by cisplatin when compared with only cisplatin given groups. We have concluded that CAPE could prevent cisplatin-induced chromosome aberrations by establishing a potent free radical scavenger effect.

In this study, we aimed to investigate the possible protective effects of caffeic acid phenethyl ester (CAPE) on lipid peroxidation (LPO) and the activities of antioxidant enzymes in the liver of rats exposed to the 900 MHz electromagnetic field (EMF). EMF of cellular phones may affect biological systems by increasing free radical, which appear mainly to enhance LPO, and by changing the antioxidative activities of liver, thus leading to oxidative damage. CAPE, an active component of propolis extract, exhibits antioxidant properties and several studies suggest that supplementation with antioxidant can influence EMF exposure induced hepatotoxicity. Thirty male Sprague-Dawley rats were divided into three groups: control (n = 10), 900 MHz EMF (n = 10) and 900 MHz EMF + CAPE (n = 10). CAPE was injected intraperitoneally for 30 days before exposure to EMF. Liver tissue was removed to study the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), xanthine oxidase (XO) and the levels of LPO. The activities of XO, CAT and level of LPO increased in the 900 MHz electromagnetic field (EMF) group compared with the control group, although XO, CAT activities and LPO levels were decreased by 900 MHz EMF + CAPE administration. The activities of SOD and GSH-Px decreased in the 900 MHz EMF group compared with the control group, although their levels were increased by EMF + CAPE administration. It can be concluded that CAPE may prevent the 900 MHz EMF-induced oxidative changes in liver by strengthening the antioxidant defense system by reducing reactive oxygen species and increasing antioxidant enzyme activities.

The aim of this experimental study was to investigate the possible role of nitric oxide (NO) and the activities of adenosine deaminase (ADA) and xanthine oxidase (XO) in the pathogenesis of isoniazid (INH)-induced oxidative damage in red blood cells (RBCs), and also to show the effect of caffeic acid phenethyl ester (CAPE) and erdosteine, antioxidants, in decreasing this toxicity. A total of 25 adult male rats were divided into four experimental groups as follows: control group (n = 7), INH-treated group (n = 6), INH + CAPE-treated group (n = 6), and INH + erdosteine-treated group (n = 6). INH, INH-CAPE, and INH-erdosteine-treated groups were treated orally with INH 50 mg/kg daily and with the tap water for 15 days. Control group was given only tap water. CAPE was intraperitoneally injected for 15 days at a dose of 10 micromol/kg. Erdosteine was treated orally for 15 days at a dose of 10 mg/kg/day. The injection of INH led to a significant increase in the activities of ADA, XO, and NO levels in RBCs of rats. Co-treatment with CAPE caused a significant decrease in the activities of ADA and XO and the levels of NO in RBCs. In addition, co-treatment with erdosteine caused a significant decrease in the activities of ADA and XO and the levels of NO in RBCs. The results of this study showed that ADA, XO, and NO may play an important role in the pathogenesis of INH-induced oxidative stress in RBCs. CAPE and erdosteine may have protective potential in this process and they may become a promising drug in the prevention of this undesired side effect of INH.

The aim of this study was to investigate the possible protective role of caffeic acid phenethyl ester on testicular toxicity of methotrexate in rats. Nineteen male rats were divided into three groups as follows: group I, control; group II, methotrexate-treated; group III, methotrexate + caffeic acid phenethyl ester-treated. In the second day of experiment, a single dose of methotrexate was intraperitoneally administered to groups II and III, although a daily single dose of caffeic acid phenethyl ester was intraperitoneally administered to group III for 7 days. At the end of the experiment, the testes of the animals were removed and weighed. In the tissue, the level of lipid peroxidation as malondialdehyde and activities of superoxide dismutase were higher in the methotrexate group than in the control group. Lipid peroxidation levels and superoxide dismutase activities were decreased in caffeic acid phenethyl ester + methotrexate group compared with methotrexate group. The activities of catalase in the methotrexate group decreased insignificantly although its activities were significantly increased by caffeic acid phenethyl ester administration. The activity of glutathione peroxidase did not change in the groups. There was significant difference in body weight between control and methotrexate-induced groups. In conclusion, the administration of methotrexate causes elevation of oxidative stress although treatment with caffeic acid phenethyl ester has protective effects on the oxidative stress in testes.

Methotrexate (MTX), a folic acid antagonist, is widely used as a cytotoxic chemotherapeutic agent. MTX-associated neurotoxicity is an important clinical problem. The aim of this study was to investigate the role of caffeic acid phenethyl ester (CAPE) on cerebellar oxidative stress induced by MTX in rats. A total of 19 adult male rats were divided into three experimental groups as follows: MTX group (MTX treated), MTX+CAPE group (MTX+CAPE treated), and control group. MTX was administered intraperitoneally (i.p.) with a single dose of 20 mg kg(-1) on the second day of experiment. CAPE was administered i.p. with a dose of 10 micromol kg(-1) day(-1) for 7 days. Malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD) and catalase (CAT) were determined in cerebellar tissue of rats. MTX caused to significant increase in MDA levels (an important marker of lipid peroxidation) in the MTX group compared with the controls (p = 0.006). CAPE significantly reduced the MTX induced lipid peroxidation in the MTX+CAPE group compared to the MTX (p = 0.007). The activities of SOD and CAT were significantly increased in the MTX group when compared with the control group (p = 0.0001, p = 0.004, respectively). The increased activities of these enzymes were significantly reduced by CAPE treatment (p = 0.004, p = 0.034, respectively). As a result, CAPE may protect from oxidative damage caused by MTX treatment in rat cerebellum.

Isoniazid (INH) still remains a first-line drug both for treatment and prophylaxis of tuberculosis, but various organs toxicity frequently develops in patients receiving this drug. We aimed to investigate possible toxic effects of INH on rat red blood cells (RBCs), and to elucidate whether Caffeic acid phenethyl ester (CAPE) prevents a possible toxic effect of INH. Experimental groups were designed as follows: control group, INH group, INH + CAPE group. Compared with the control, the INH caused a significant increase in superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels, and a decrease in glutathione peroxidase (GSH-Px) and catalase (CAT), which are recently used to monitor the development and extent of damage due to oxidative stresses. CAPE administration to INH group ameliorated above changes due to INH.

The exact mechanisms of methotrexate-induced renal toxicity have not yet been determined. However, several hypotheses have been put forward, including oxidative stress. The aim of this study was to investigate the role of caffeic acid phenethyl ester (Caffeic Ester), a novel antioxidant, on methotrexate-induced renal oxidative stress in rats. Nineteen adult male rats were equally divided into three experimental groups as follows: control group, methotrexate-treated group, and methotrexate+Caffeic Ester-treated group. A single dose of methotrexate (20 mg/kg) was administered intraperitoneally (ip). Caffeic Ester (10 micromol/kg) was administered ip, once daily for seven days. Malondialdehyde (MDA) levels (an index of lipid peroxidation) were used as a marker of oxidative stress-induced renal injury. Similarly, the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were determined to evaluate the changes of antioxidant status in renal tissue. Methotrexate administration to control rats increased MDA levels (P<0.0001), but decreased SOD, CAT and GSH-Px activities in renal tissue (P<0.0001). Caffeic Ester+ methotrexate treatment caused a significant decrease in MDA levels (P<0.001), and caused an increase in SOD, CAT and GSH-Px activities when compared with methotrexate treatment alone (P<0.001, <0.05, <0.0001, respectively). In conclusion, methotrexate leads to a reduction in antioxidant enzymatic defense capacity and causes lipid peroxidation in renal tissue. Similarly, Caffeic Ester exhibits protective effects on methotrexate-induced renal oxidative impairment in rats.

Aims: We aimed to evaluate the effects of caffeic acid phenethyl ester (CAPE) on lithium (Li)-induced lung toxicity., Methods: Twenty-two adult male Wistar albino rats weighing between 280 and 300 g were used. The rats were randomly divided into three groups: control, Li and Li+CAPE groups. Li and CAPE were co-administered intraperitoneally twice daily for 4 weeks. Control rats were given 0.9% NaCl during the same period. All the rats were allowed to feed ad libitum until midnight after they had received the proposed treatment., Results: In the Li group, peribronchial and intraparenchymal lymphocyte and macrophage infiltration were observed. Atypical type II pneumocytes, alveolar destruction and emphysematous changes were also detected. Lymphocyte and macrophage infiltration was significantly decreased in the Li+CAPE group compared with the Li group. Alveolar destruction, emphysematous changes and intraparenchymal mononuclear cell infiltration were also recovered to a level close to the control group. Malondialdehyde (MDA) levels were increased in the Li group compared with the control group. CAPE administration decreased the MDA levels in the Li+CAPE group., Conclusions: CAPE was found to associate with histopathological changes recovery in the lungs and oxidative stress due to Li treatment.

The aim of this experimental study was to investigate the possible role of nitric oxide (NO) levels and activity of adenosine deaminase (ADA) in the pathogenesis of methotrexate (MTX)-induced neurotoxicity, to demonstrate the effect of caffeic acid phenethyl ester (CAPE), the potent antioxidant, in decreasing the toxicity. A total of 19 adult male rats were divided into three experimental groups, as follows: group I, control group; group II, MTX-treated group; group III, MTX+CAPE-treated group. In the second day of experiment, MTX was administered intraperitoneally (i.p.) with a single dose of 20mg/kg to group II and group III. CAPE was administered i.p. with a dose of 10 micromol/kg once daily for 7 days to group III. Histopathological findings of the inflammatory reaction were observed in spinal cord of MTX administered rats, compared with control rats. All parameters of inflammatory reaction were significantly decreased in MTX plus CAPE administered rats, compared with MTX administered rats. The injection of MTX caused significant increase in the activity of ADA and in levels NO levels in spinal cord of rats (p=0.007 and p=0.0001, respectively). Co-treatment with CAPE caused a significant decrease in activity of ADA and the levels of NO in spinal cord (p=0.024 and p=0.0001, respectively). Study indicate that NO and ADA may play an important role in the pathogenesis of MTX-induced oxidative spinal cord damage. CAPE may have protective aspects in this process by antioxidant and anti-inflammatory effect and it will become a promising drug in the prevention of undesired side effect of MTX.

The aim of this experimental study was to investigate the possible role of nitric oxide (NO) levels, and activities of adenosine deaminase (ADA) and xanthine oxidase (XO) in the pathogenesis of methotrexate-induced nephrotoxicity, and was the effect of caffeic acid phenethyl ester (CAPE), the potent free radical scavenger, in decreasing the toxicity. A total of 19 adult male rats were divided into three experimental groups, as follows: control group, MTX-treated group, and MTX+CAPE treated group. MTX were administered intraperitoneally (i.p.) with 20 mg/kg for single dose. CAPE was administered i.p. with a dose of 10 micromol//kg once daily for 7 days. The injection of MTX induced a significant increase in the activities of ADA and XO, and NO levels in renal tissue of rats (p < 0.0001). Co-treatment with CAPE caused a significantly decrease activities of ADA and XO, and the levels of NO in renal tissue (p < 0.0001). The results of this study revealed that NO, XO and ADA may play an important role in the pathogenesis of MTX-induced oxidative renal damage. CAPE may have protective potential in this process and it will become a promising drug in the prevention of this undesired side effect of MTX.

Melatonin and caffeic acid phenethyl ester (CAPE), a component of honeybee propolis, were recently found to be potent free radical scavengers and antioxidants. There are a number of reports on the effects induced by electromagnetic radiation (EMR) in various cellular systems. Mechanisms of adverse effects of EMR indicate that reactive oxygen species may play a role in the biological effects of this radiation. The present study was carried out to compare the protective effects of melatonin and CAPE against 900 MHz EMR emitted mobile phone-induced renal tubular injury. Melatonin was administered whereas CAPE was given for 10 days before the exposure. Urinary N-acetyl-beta-D-glucosaminidase (NAG, a marker of renal tubular injury) and malondialdehyde (MDA, an index of lipid peroxidation), were used as markers of oxidative stress-induced renal impairment in rats exposed to EMR. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status in renal tissue. Urinary NAG and renal MDA were increased in EMR exposed rats while both melatonin and CAPE caused a significant reduction in the levels of these parameters. Likewise, renal SOD and GSH-Px activities were decreased in EMR exposed animals while melatonin caused a significant increase in the activities of these antioxidant enzymes but CAPE did not. Melatonin caused a significant decrease in urinary NAG activity and MDA levels which were increased because of EMR exposure. CAPE also reduced elevated MDA levels in EMR exposed renal tissue, but the effect of melatonin was more potent than that of CAPE. Furthermore, treatment of EMR exposed rats with melatonin increased activities of SOD and GSH-Px to higher levels than those of control rats. In conclusion, melatonin and CAPE prevent renal tubular injury by reducing oxidative stress and protect the kidney from oxidative damage induced by 900 MHz mobile phone. Nevertheless, melatonin seems to be a more potent antioxidant compared with CAPE in kidney., ((Mol Cell Biochem 276: 31-37, 2005).)

The aim of this experimental study was to investigate the effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, on cisplatin-induced hepatotoxicity through adenosine deaminase (AD), xanthine oxidase (XO), catalase (CAT), superoxide dismutase (SOD) activities and malondialdehyde (MDA) and nitric oxide (NO) levels in liver tissue of rats. Wistar albino rats were divided into three groups: control group (n = 6), cisplatin group (n = 9) and CAPE + cisplatin group (n = 8). All the chemicals used were applied intraperitoneally. Spectrophotometric methods were used to determine the activities of the above-mentioned enzymes in the liver tissue. NO level and XO activity were found to be increased in the cisplatin group compared to the control group. NO level was found to be decreased in the cisplatin + CAPE group in comparison with the cisplatin group. There was no significant change in the activity of XO between the cisplatin and cisplatin + CAPE groups. The activity of SOD was lower in the cisplatin group than both the control and cisplatin + CAPE groups. There was no significant change in the activity of CAT between the control and cisplatin groups. CAT activity was increased in the cisplatin + CAPE group compared to the cisplatin group. The AD activity and MDA level remained unchanged in all groups. The results obtained suggested that CAPE significantly attenuated the hepatotoxicity as an indirect target of cisplatin in an animal model of cisplatin-induced nephrotoxicity.

Objectives: The risk for cardiovascular disease is significantly high in diabetes mellitus. Experimental evidence suggests that oxidative stress plays a dominant role in the pathogenesis of diabetes mellitus. Caffeic acid phenethyl ester (CAPE), an active component of propolis, has several biological and pharmacological properties, including antioxidant, anti-inflammatory, anti-carcinogenic, antiviral, and immunomodulatory activities. In light of the antioxidant ability of CAPE, the effects of CAPE on the antioxidative status of cardiac tissue were investigated in streptozotocin (STZ)-induced diabetic rats., Design and Methods: Twenty-six rats were randomly divided into three groups: group I, control, nondiabetic rats (n = 9); group II, STZ-induced, untreated diabetic rats (n = 7); and group III, STZ-induced, CAPE-treated diabetic rats (n = 10). In groups II and III, diabetes developed 3 days after intraperitoneal (ip) administration of a single 35 mg kg(-1) dose of STZ. Thereafter, while the rats in group II received no treatment, the rats in group III began to receive a 10 mumol kg(-1) ip dose of CAPE per day. After 8 weeks, the levels of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in the cardiac tissues of all groups were analyzed., Results: In untreated diabetic rats, MDA markedly increased in the cardiac tissue compared with the control rats (P < 0.05). However, MDA levels were reduced to the control level by CAPE. The activities of SOD and CAT in the untreated diabetic group and the CAPE-treated diabetic group were higher than those of the control group (P < 0.05). Rats in the CAPE-treated diabetic group had reduced activities of SOD and CAT in comparison with the rats in the untreated diabetic group (P < 0.05). There were no significant differences in the activity of GSH-Px between the rats in the untreated diabetic group and the control group. However, the activity of GSH-Px was increased in CAPE-treated diabetic rats compared with the control and untreated diabetic rats (P < 0.05)., Conclusion: These results reveal that diabetes mellitus increases oxidative stress in cardiac tissue and CAPE has an ameliorating effect on the oxidative stress via its antioxidant property.

The aim of this study was to examine the effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation (LPO) and the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in the liver of streptozotocin (STZ)-induced diabetic rats. Twenty-seven rats were randomly divided into three groups: group I, control non-diabetic rats (n = 9); group II, STZ-induced, untreated diabetic rats (n = 8); group III, STZ-induced, CAPE-treated diabetic rats (n = 10), which were intraperitoneally injected with CAPE (10 microM kg(-1) day(-1)) after 3 days followed by STZ treatment. The liver was excised after 8 weeks of CAPE treatment, the levels of malondialdehyde (MDA) and the activities of SOD, CAT, and GSH-Px in the hepatic tissues of all groups were analyzed. In the untreated diabetic rats, MDA markedly increased in the hepatic tissue compared with the control rats (p < 0.0001). However, MDA levels were reduced to the control level by CAPE. The activities of SOD, CAT, and GSH-Px in the untreated diabetic group were higher than that in the control group (p < 0.0001). The activities of SOD and GSH-Px in the CAPE-treated diabetic group were higher than that in the control group (respectively, p < 0.0001, p < 0.035). There were no significant differences in the activity of CAT between the rats of CAPE-treated diabetic and control groups. Rats in the CAPE-treated diabetic group had reduced activities of SOD and CAT in comparison with the rats of untreated diabetic group (p < 0.0001). There were no significant differences in the activity of GSH-Px between the rats of untreated diabetic and CAPE-treated groups. It is likely that STZ-induced diabetes caused liver damage. In addition, LPO may be one of the molecular mechanisms involved in STZ-induced diabetic damage. CAPE can reduce LPO caused by STZ-induced diabetes.

Testicular artery occlusion causes an enhanced formation of reactive oxygen species, which contributes to the pathophysiology of tissue damage. Here, we have investigated the effects of caffeic acid phenethyl ester (CAPE), a new antioxidant and antiinflammatory agent, in rats subjected to testicular torsion/detorsion (T/D). Thirty-five male rats were divided into four groups: sham operation group ( n=8), torsion group ( n=9), T/D+saline group ( n=9) and T/D+CAPE group ( n=9). Rats, except the sham operation group, were subjected to left unilateral torsion (720 degrees rotation in the clockwise direction) without including the epididymis. After torsion (2 h) and detorsion (4 h) periods, rats were sacrificed and bilateral orchidectomy was performed. Testis tissues were washed with cold saline solution, cut into small pieces with scissors, placed into glass bottles and homogenised in four volumes of ice-cold Tris-HCl buffer. Clear supernatant fluid was used for biochemical analyses. Treating rats with CAPE (applied at 10 micro mol/kg, 30 min prior to T/D) attenuated the testicular injury, as well as the increase in the tissue levels of myeloperoxidase and thiobarbituric acid-reactant substances (TBARS) caused by T/D in the testis. Testis tissues showed a significant increase in glutathione peroxidase (GSH-Px) activity compared to the torsion group when CAPE was applied. Taken together, our results clearly demonstrate that CAPE treatment exerts a protective effect on testicular T/D, and part of this effect may be due to inhibiting the neutrophil-mediated cellular injury.

Nitric oxide (NO) plays an important role in modulating blood flow in normal and in several pathological conditions, and its levels seem to change with ischemia-reperfusion injuries. Caffeic acid phenethyl ester (CAPE), an active component of propolis, exhibits antioxidant properties. This experimental study was designed to determine the changes in NO levels and the effect of CAPE on NO levels after testicular torsion/ detorsion in rats. Thirty-five adult male albino rats were divided into four groups: sham operation (n = 8), torsion (n = 9), saline/detorsion (n = 9), and CAPE/detorsion (n = 9). Rats in the sham operation group were killed after the testes were handled without torsion. Rats in the torsion group were killed after 720 degrees clockwise testicular torsion for 2 h. CAPE was administered 30 min before detorsion in the CAPE/detorsion group and saline was administered in the saline/detorsion group. After 4 h of testicular detorsion in both of these groups, the rats were killed and bilateral orchiectomy was performed to determine the tissue levels of NO. The level of NO in the torsion group (113.77 +/- 33.18 nmol/g protein) was significantly higher than that of the sham operation group (64.53 +/- 29.64 nmol/g protein). In the saline/detorsion group, the NO level (31.26 +/- 12.58 nmol/g protein) was significantly lower than in the torsion and sham operation groups. CAPE administration in the CAPE/detorsion group seemed to raise the NO level (72.63 +/- 23.87 nmol/g protein) above the level of the sham operation group. Contralateral testes were not affected by the torsion/detorsion processes performed on the ipsilateral testes. These results show that NO levels increase with torsion and decrease with detorsion. CAPE administration seems to increase tissue NO levels and this may be important for protecting the testes from torsion/detorsion injuries.

Background/purpose: Ischemia-reperfusion injury is encountered frequently in conditions that diminish intestinal blood flow. Caffeic acid phenethyl ester (CAPE), which is a specific component of the honeybee hive product propolis, exhibits potential antioxidant properties. This experimental study was designed to determine the effect of CAPE on ischemia-reperfusion injury in rat intestine., Methods: Fifty rats were divided into 5 groups; sham (SH), saline ischemia (SI), saline reperfusion (SR), CAPE ischemia (CI), and CAPE reperfusion (CR). Either CAPE, 10 micromol/kg, or saline was administered intraperitoneally 30 minutes before ischemia. Intestinal ischemia for 30 minutes and reperfusion for 60 minutes were applied. Ileum specimens were obtained to determine the tissue levels of malondialdehyde, superoxide dismutase, catalase, and histological changes., Results: Malondialdehyde levels in the CR group did not increase after reperfusion when compared with the CI group. However, statistically significant differences were observed between the SR and SI groups. Additional mucosal injury in the CR group when compared with the CI group was not observed. Whereas, there was a statistically significant increase in mucosal injury in the SR group. Reperfusion did not cause further injuries through both biochemical and histological parameters in the CR group., Conclusions: Results of this study showed that prophylactic administration of CAPE in ischemic condition prevents reperfusion injuries by eliminating oxygen radicals and inhibiting polymorphonuclear leukocyte infiltration. CAPE may be useful in combating the diseases of oxidative stress.

Objective: Oxygen-derived free radicals have been implicated in the pathogenesis of spinal cord neuronal injury after both trauma and ischemia-reperfusion. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant properties. This experimental study was designed to determine the effect of CAPE on ischemia-reperfusion of spinal cord in rabbits., Methods: Forty-one New Zealand white rabbits were used in the study. The animals undergone aortic occlusion were divided into three groups each consisting of 11 rabbits: methylprednisolone (MP), CAPE, and control. CAPE 10 micromol/kg, methyl prednisolone (MP) 30 mg/kg or similar dose saline were injected intraperitoneally before surgical intervention. Animals were subjected to 21 min of cross-clamp time. At the end of occlusion time, the clamps were removed and restoration of the blood flow was verified visually. Animals in sham group (n = 8) underwent a surgical procedure similar to the other groups but the aorta was not occluded. Neurological status was scored by assessment of hindlimb motor function deficit., Results: The scores in CAPE group was different from control groups at 48 h (3.91+/-0.5 vs. 2.91+/-0.7; P = 0.0013). Spinal cord specimens were obtained to determine the tissue levels of malondialdehyde, superoxide dismutase, catalase, and histological changes. Malondialdehyde levels in control group were increased significantly when compared to sham group (124.22+/-24.36 and 41.92+/-10.08 nmol/g wet tissue, P = 0.0003). MDA levels in the CAPE group were lower than MP group and differences between the two groups were statistically significant (56.77+/-15.265 and 107.74+/-19.31 nmol/g wet tissue, P = 0.0001). We did not observe additional tissue injury in CAPE group when compared to control group. SOD and CAT activities were not concordant in all the groups., Conclusions: These results suggest that CAPE may be an available agent to protect the spinal cord from ischemia-reperfusion injury.