Chronic treatment with resveratrol, a natural polyphenol found in grapes, alleviates oxidative stress and apoptotic cell death in ovariectomized female rats subjected to chronic cerebral hypoperfusion.

OBJECTIVES: Resveratrol appears to have neuroprotective potential in various animal models of brain disorders including cerebral ischemia and neurodegenerative diseases. Chronic cerebral hypoperfusion is a well-known pathological condition contributing to the neurodegenerative diseases such as vascular dementia. Purpose of the present study is to evaluate the possible therapeutic potential of resveratrol in a model of vascular dementia of ovariectomized female rats. Assessment of the potential was based on the determination of brain oxidative status, caspase-3 level, glial fibrillary acidic protein (GFAP), and neuronal damage on hippocampus and cerebral cortex. METHODS: For creating the model of chronic cerebral hypoperfusion, ovariectomized female Wistar rats were subjected to the modified two vessel occlusion method, with the right common carotid artery being occluded first and the left one a week later. RESULTS: At the 15th day following the ligation, neuronal damage was accompanied by the increased immunoreactivities of both GFAP and caspase-3, and significant neurodegeneration was evident in the hippocampus and cortex, all of which were significantly alleviated with resveratrol treatment (10 mg/kg). Biochemical analysis revealed that the resveratrol treatment decreased lipid peroxidation and restored reduced glutathione level as well. DISCUSSION: The collected data of the present study suggest that the administration of resveratrol may provide a remarkable therapeutic benefit for vascular dementia, which is most likely related to the prevention of both apoptotic cell death and oxidative stress. We believe that therapeutic efficacy of resveratrol deserves to be tested for potential clinical application in postmenopausal elderly women suffering from vascular dementia.

Does intraabdominal use of Ankaferd Blood Stopper cause increased intraperitoneal adhesions?

BACKGROUND: The aim of this study was to investigate whether intraabdominal Ankaferd Blood Stopper (ABS) causes increased intraabdominal adhesion formation and to determine any side effects of ABS in vivo. METHODS: The present experimental study was designed to examine the effects of Ankaferd solution on peritoneal adhesion formation in a rat model of cecal abrasion. Intraperitoneal adhesions were assessed macroscopically and histopathologically on the 10th postoperative day. The possible adverse affects of ABS on liver and lung tissues were analyzed histopathologically, and blood chemistry was also evaluated. RESULTS: Our study revealed that ABS reduced intraperitoneal adhesion formation in an experimental rat model. The blood chemistry was not disturbed due to ABS administration. Intraperitoneal administration of ABS led to some minor changes in the lungs and serosal surfaces of the intestines, with minor architectural changes in the liver that were not considered as toxic. Further studies with various application doses and routes with more detailed cellular analysis are thus warranted to clarify the possible pleiotropic and adverse effects of this new agent away from hemostasis. CONCLUSION: There was less intraperitoneal adhesion formation in the ABS group than in the control group and saline group. Intraperitoneal administration of ABS has no toxic effects on blood chemistry or the lungs, kidneys and the liver, but it has some minor adverse effects.