Investigation of the protective effect of anzer propolis in cerebral ischemia-reperfusion injury.

OBJECTIVE: Globally, stroke is the leading cause of disability and death. With the use of thrombolytic therapy, reperfusion injury, and its consequences came to the fore. We aimed to find out how anzer propolis, which can only be obtained in Turkey's Eastern Black Sea region, affected ischemia-reperfusion injury using biochemical and histological techniques. MATERIALS AND METHODS: 32 female Wistar albino rats were divided into 4 groups, including a control group. Three of the groups underwent 30 minutes of induced ischemia via clamping of the common carotid artery, followed by ischemia-reperfusion injury through the release of the clamp. One group received no treatment, another received oral administration of 100 mg/kg of anzer propolis one hour before surgery, and the third group received oral administration of 40 mg/kg of acetylsalicylic acid just before surgery. Histopathological examination assessed apoptosis and tissue necrosis, while serum and brain tissue were evaluated for levels of nerve growth factor (NGF), Interlokin 1ß (IL-1ß), Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), total antioxidant capacity (TAS), and total oxidant capacity (TOS). RESULTS: Anzer propolis and acetylsalicylic acid significantly reduced hyperemia in vessels, vacuolization in neurons, glial cell infiltration, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positivity. The anzer propolis group had the highest NGF levels. The anzer propolis and acetylsalicylic acid groups had lower levels of TNF-a and IL-6 in the brain tissue than the ischemia-reperfusion group, while TAS levels were higher. CONCLUSIONS: The findings obtained in this study suggest that anzer propolis has a neuroprotective effect against ischemia-reperfusion injury and will have beneficial effects on neurodegeneration. We believe our findings will contribute to the clinical treatment of ischemia-reperfusion injury.

Effects of infliximab against carbon tetrachloride-induced intestinal injury via lipid peroxidation and apoptosis.

Carbon tetrachloride (CCL4) is often employed in the production of chlorofluorocarbons, petroleum refining, oil and rubber processing, and laboratory applications. Oral, subcutaneous, and inhalation exposure to CCL4 in animal studies have been shown to be capable of leading to various types of cancer (benign and malignant, liver, breast, and adrenal gland tumors). The present study also evaluated the protective role of infliximab (INF) against the deleterious effects of CCL4 on the intestinal system. Twenty-four male Sprague-Dawley rats were randomly assigned into three groups, control (n = 8), CCL4 (n = 8), and CCL4 + INF (n = 8). The control group received 1 mL isotonic saline solution only via intraperitoneal (i.p.) injection. The CCL4 group received a single i.p. dose of 2 mL/kg CCL4. The CCL4 + INF group received a single i.p. dose of 7 mg/kg INF followed 24 h later by a single dose of 2 mL/kg CCL4. All rats were euthanized 2 days following drug administration. CCL4 group samples also exhibited diffuse loss of enterocytes, vascular congestion, neutrophil infiltration, an extension of the subepithelial space and significant epithelial lifting along the length of the villi with a few denuded villous tips. In addition, CCL4 treatment increased intestinal malondialdehyde (MDA) level and caspase-3 positivity. On the other hand, INF decreased MDA levels, caspase-3 positivity, and loss of villous. Our findings suggest that CCL4 appears to exert a highly deleterious effect on the intestinal mucosa. On the other hand, INF is effective in preventing this CCL4-induced intestinal injury by reducing oxidative stress and apoptosis.