Caffeic acid phenethyl ester decreases the level of S-100B protein after middle cerebral artery [correction for after] occlusion in rabbits.

Effects of caffeic acid phenethyl ester (CAPE) on the serum S-100B levels were studied as an index for brain damage after permanent middle cerebral artery (MCA) occlusion in rabbits. Twenty rabbits were divided into four groups (n=5): control, sham, non-treatment and CAPE. The right MCA was occluded using a microsurgical procedure with bipolar coagulation and was then transected in non-treatment and CAPE groups. The rabbits in the sham group underwent a surgical procedure but the MCA was not occluded. No surgery was performed in the control group. CAPE was administered after MCA occlusion at the dose of 10 microg/kg, once a day intraperitoneally for 7 days in the CAPE group. Serum S-100B levels were determined on days 1, 2, 4 and 7. Serum S-100B level was significantly increased following permanent MCA occlusion. Posttreatment of CAPE significantly reduced the serum S-100B level. This study demonstrated that CAPE is capable of attenuating increased serum S-100B level induced by MCA occlusion in rabbits. CAPE may be useful as a neuroprotective agent.

Caffeic acid phenethyl ester protects rabbit brains against permanent focal ischemia by antioxidant action: a biochemical and planimetric study.

The present study was conducted to investigate whether caffeic acid phenethyl ester (CAPE), an active component of propolis extract, has a protective effect on brain injury after focal permanent cerebral ischemia, and to determine the possible antioxidant mechanisms. Cerebral infarction in adult male New Zealand rabbits was induced by microsurgical procedures producing right focal permanent middle cerebral artery occlusion (pMCAO). CAPE was administered to the treatment group after pMCAO at a dose of 10 micromol kg(-1) once a day intraperitoneally for 7 days. Neurological deficits were evaluated, using a modified six-point scale. Spectrophotometric assay was used to determine the contents of malondialdehyde (MDA), glutathione (GSH), catalase (CAT), nitric oxide (NO) and xanthine oxidase (XO). In the ipsilateral hemisphere, the infarct volume of the brain was assessed in brain slices stained with heamatoxylen and eosin. The results showed that treatment with CAPE significantly reduced the percentage of infarction in the ipsilateral hemisphere compared with the ischemia group. CAPE treatment significantly attenuated the elevation of plasma MDA, CAT and XO content (p<0.05), whereas it significantly increased the levels of plasma GSH and NO (p<0.05). Therefore, subacute CAPE administration plays a protective role in focal pMCAO due to attenuation of lipid peroxidation and its antioxidant activity. All of these findings suggest that CAPE provides neuroprotection against cerebral ischemia injury through its antioxidant action.

The protective effect of erythropoietin and dimethylsulfoxide on ischemia-reperfusion injury in rat ovary.

OBJECTIVES: The aim of this study was to investigate the effects of erythropoietin and dimethylsulfoxide in the recovery from ischemia-reperfusion injury in an experimental rat adnexal torsion model. STUDY DESIGN: Thirty-six Wistar-albino rats were divided into six groups. Except for the sham operation group, all groups were subjected to left unilateral adnexal torsion for 3h. Erythropoietin and dimethylsulfoxide were intraperitoneally administered 30min before the detorsion operation. Malondialdehyde and nitric oxide levels were detected from both the plasma and the tissue samples. The sections of the tissues were evaluated histologically. The results were analyzed by a one-way analysis of the variance (ANOVA) followed by the Duncan test for multiple comparisons using computer software, SPSS Version 15.0 for Windows. RESULTS: This study demonstrated that dimethylsulfoxide and erythropoietin pretreatment attenuated ischemia-reperfusion-induced lipid peroxidation, prevented post-ischemic ovarian injury and helped to maintain the ovarian morphology. Malondialdehyde levels of plasma and ovary were higher in the torsion and detorsion groups than the sham group. This showed that ischemia-reperfusion had caused lipid peroxidation of the ovarian tissue, thus leading to oxidative damage. One of the major findings of this study is that malondialdehyde was significantly decreased in the plasma of rats who were pre-treated with dimethylsulfoxide and erythropoietin before detorsion. This suggests that dimethylsulfoxide and erythropoietin might prevent oxidative damage in ovarian ischemia-reperfusion injury. Histological examination confirmed that reperfusion caused more detrimental effects than only ischemia, which could be at least partially prevented by dimethylsulfoxide and erythropoietin administration prior to detorsion. CONCLUSION: Erythropoietin and dimethylsulfoxide may have beneficial effects in ischemia-reperfusion injury in ovarian torsion.

Effects of trimetazidine on crush injury of the sciatic nerve in rats: a biochemical and stereological study.

Trimetazidine (TMZ) is an anti-ischemic agent which has been used for years as an effective anti-anginal agent in cardiac patients. The aim of the study was to investigate the effect of TMZ on the level of malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH), catalase (CAT), histopathological changes and the number of myelinated axons in a crush injury model of sciatic nerve in rats. In this study, 50 Wistar albino rats were used and the right sciatic nerves of all animals were injured. They were randomly divided into two groups equal in number, called treatment and non-treatment groups. The animals were subdivided into four subgroups, non-injury/non-treatment (left sciatic nerves of non-treatment animals, NI-NT) and non-injury/treatment (left sciatic nerves of treatment animals, NI-T) and injury/non-treatment (right sciatic nerves of non-treatment animals, I-NT) and injury/treatment (right sciatic nerves of treatment animals, I-T). At the end of the experiment, the bilateral sciatic nerves and blood samples collected from these animals were analyzed using histological, stereological and biochemical methods. There was a progressive increase in the serum level of GSH and progressive decrease in serum MDA levels in the treatment group. Progressive decrease in serum NO levels was observed in the treatment groups and it was statistically significant on day 14 (p<0.05) compared to the non-treatment group. The activities of CAT were low in the treatment groups on days 21 (p<0.05) and 42 (p<0.05). In the NI-NT group, some unimportant degenerative changes such as irregularity in myelin sheets were observed. Many pathologic changes in the I-NT group and some minimal degeneration in the I-T group were observed. TMZ treatment resulted in increases in the myelinated axon numbers by a range of 223 to 604 in the I-NT group compared to the I-T. In conclusion, TMZ appears to be beneficial for induction of axonal regeneration and myelination in healthy nerves as well as injured nerves.

Orchiectomy or testosterone receptor blockade reduces intestinal mucosal damage caused by ischemia-reperfusion insult.

The aim of the present study was to investigate whether orchiectomy or administration of flutamide an antagonist of the testosterone receptor can reduce oxidative stress and histologic damage in the rat small bowel subjected to mesenteric ischemia/reperfusion (I/R) injury. A total of 32 Sprague-Dawley rats were divided into four groups. Group 1 was control (sham), group 2 was I/R, group 3 was I/R plus orchiectomy (orchiectomy was performed 14 days before I/R), group 4 was I/R plus flutamide (flutamide was given throughout 14 days before mesenteric IR). Rats were subjected to 45 min of mesenteric ischemia followed by 3 h of reperfusion. The levels of ileal malondialdehyde (MDA) and nitric oxide (NO) were found to be significantly lower in orchiectomy and flutamide treatment groups compared with I/R group (P < 0.05). The histopathological injury scores were consistent with the MDA and NO levels. These results suggest that castration or testosterone receptor blockade decreases the level of intestinal I/R injury in male rats and it is an another example for disease variations based on gender differences.

The protective effect of darbepoetin alfa on experimental testicular torsion and detorsion injury.

AIM: Testicular torsion is a serious urological emergency, usually involving newborns, children, and adolescents which can lead to subfertility and infertility. Prevention of testicular damage caused by torsion is still a clinical and experimental problem. So far many chemicals and drugs have been investigated for decreasing ischemia/reperfusion (I/R) injury in experimental animals. The possible protective effect of darbepoetin alfa, a novel erythropoietic protein, on testicular tissue after I/R injury was examined in this study. METHODS: Thirty rats were divided into three groups: sham operation, torsion/detorsion, and torsion/detorsion plus darbepoetin alfa groups. After torsion (2 hours) and detorsion (4 hours), bilateral orchiectomy was performed. Malondialdehyde, nitric oxide and glutathione levels were determined in testicular tissue. RESULTS: Administration of darbepoetin alfa caused a decrease of malondialdehyde and nitric oxide levels and an increase in glutathione levels compared with the torsion/detorsion group. In addition, histological injury scores were significantly decreased in the treatment group more than the torsion/detorsion group. CONCLUSION: The results suggest that darbepoetin alfa may be a potential protective agent for preventing testicular injury caused by testis torsion.