Veterinary Physiology Biochemistry & Pharmacology
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Item Cobalt chloride-induced hepatic and intestinal damage in rats: protection by ethyl acetate and chloroform fractions of Ocimum gratissimum(Informatics Publishing Limited, 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Nwozuzu, V. C.Cobalt chloride is known to produce symptoms of diarrhea, vomiting and other gastrointestinal disturbances. We investigated the potential roles of the ethyl acetate and chloroform fractions of Ocimum gratissimum (OG), traditionally used to treat diarrhea and other gastrointestinal disorders in protection against cobalt chloride (CoCl2)-induced liver and intestinal damage. Wistar albino rats were given CoCl2 (350 ppm) in drinking water for 7 days, alone or concurrently with either fractions of OG at 100 and 200mg/kg each. Gallic acid (120 mg/kg) was administered to a group of rats as a standard flavonoid. Biochemical indices of oxidative stress, antioxidant enzyme activities, the levels of pro-inflammatory cytokines (Interleukin 1β; IL-1β and Tumor necrosis factor, TNF-α) were evaluated and the histological appearance of the liver and intestinal mucosa was investigated. CoCl2 produced significant elevations (p<0.05) in hydrogen peroxide (H2O2), malondialdehyde (MDA), IL-1β, alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP). This was accompanied with significant reductions (p<0.05) in reduced glutathione (GSH), glutathione peroxidase (GPX) and glutathione S-transferase (GST) activities. Liver sections of rats exposed to CoCl2 had poor architecture and areas of necrosis with several dead hepatocytes, while some appeared with hyperchromic nuclei. Intestinal mucosa showed significant loss of absorptive epithelial cells with CoCl2 exposure. Treatment with the fractions from OG produced reduction in H2O2, MDA and IL-1β levels; reduced serum activities of ALT, AST and ALP; restoration of GSH levels and improved activities of GPX and GST. The fractions significantly preserved the hepatic and intestinal architecture.Our results indicate that the fractions of OG exhibited considerable hepatic and intestinal protection by reduction in levels of oxidants and pro-inflammatory cytokines, enhancement of antioxidant enzyme activities and preservation of tissue integrity and might thus be very useful agents in protecting the liver and intestines during concurrent exposure to Cobalt chloride.Item Alterations in blood pressure, antioxidant status and caspase 8expression in cobalt chloride-induced cardio-renal dysfunction arereversed by Ocimum gratissimum and gallic acid in Wistar rats(Elsevier B.V., 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Ajibade, T. O.The protective abilities of the chloroform extract of Ocimum gratissimum (COG) and gallic acid againstcobalt chloride (CoCl2) − induced cardiac and renal toxicity were evaluated. Rats were exposed to CoCl2(350 ppm) for 7 days, either alone, or in combination with COG (100 and 200 mg/kg) or gallic acid(120 mg/kg). CoCl2given alone, caused significant increases (p < 0.05) in oxidative stress parameters(hydrogen peroxide, H2O2and malondialdehyde, MDA) and increased expression of the apoptotic initia-tor caspase 8 in the heart and kidneys. There was significant reduction (p < 0.05) in reduced glutathione(GSH) in cardiac and renal tissues; reduction in superoxide dismutase (SOD) activity in the kidneys andadaptive increases in Glutathione S-transferase (GST) and catalase (CAT). CoCl2also produced signifi-cant reduction (p < 0.05) in systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures. OralCOG and gallic acid treatment significantly reduced (p < 0.05) the levels of H2O2and MDA; with reducedexpression of caspase 8 and restoration of GSH levels, GPx, SOD and CAT activities, howbeit, to varyingdegrees in the heart and kidneys. COG (200 mg/kg) was most effective in restoring the blood pressures inthe rats to near control levels. CoCl2-induced histopathological lesions including myocardial infarctionand inflammation and renal tubular necrosis and inflammation were effectively ameliorated by the treat-ments administered. This study provides evidence for the protective roles of O. gratissimum and gallicacid by modulation of CoCl2-induced alterations in blood pressure, antioxidant status and pro-apoptoticcaspase 8 in Wistar rats.Item Ameliorative effect of gallic acid on doxorubicin-induced cardiac dysfunction in rats(De Gruyter, 2017) Omobowale, T. O.; Oyagbemi, A. A.; Folasire, A. F.; Ajibade, T. O.; Asentiga, E. R.; Adejumobi, O. A.; Ola-Davies, O. E.; Oyetola, O.; James, G.; Adedapo, A. A.; Yakubu, M. A.Background: The use of doxorubicin (DOX) as an antineoplastic agent has been greatly limited because of the myriad of toxic sequelae associated with it. The aim of this study was to assess the protective effects of gallic acid (GA) on DOX-induced cardiac toxicity in rats. Methods: Sixty male rats (Wistar strain) were used in this study. They were divided into six groups (A–F) each containing 10 animals. Group A was the control. Rats in Groups B, C, and D were treated with DOX at the dosage of 15 mg/kg body weight i.p. Prior to this treatment, rats in Groups C and D had been treated orally with GA for 7 days at the dosage of 60 and 120 mg/kg, respectively. Animals from Groups E and F received only 60 and 120 mg/kg GA, respectively, which were administered orally for 7 days. Results: The exposure of rats to DOX led to a significant (p 0.05) decrease in the cardiac antioxidant defence system and elevation of creatine kinase myocardial band and lactate dehydrogenase. The electrocardiography results showed a significant decrease in heart rate, QRS, and QT-segment prolongation. GA alone improved the antioxidant defence system. Conclusions: The GA pretreatment significantly alleviated GA-associated ECG abnormalities, restored the antioxidant status and prevented cardiac damage.Item Ameliorative effect of gallic acid in doxorubicin-induced hepatotoxicity in wistar rats through antioxidant defense system(Taylor & Francis, 2017-07) Omobowale, T. O.; Oyagbemi, A. A.; Ajufo, U. E.; Adejumobi, A. O.; Ola-Davies, O. E.; Adedapo, A. A.; Yakubu, M. A.Hepatotoxicity has been found to be one of the main side effects associated with doxorubicin (Dox) administration in cancer therapy. The aim of the present study was to examine the ameliorative effect of gallic acid (GA) in Dox-induced hepatotoxicity. Sixty male Wistar rats of 10 rats per group were used in this study and were randomly divided into 6 experimental groups (A–F). Rats in Group A served as the control group and received distilled water orally for 7 days; Group B was given Dox at 15 mg/kg bodyweight intraperitoneally (IP) on Day 8. Group Cwas given GA at 60 mg/kg body weight orally for 7 days + Dox at 15 mg/kg IP on Day 8. Group D was given GA at 120 mg/kg body weight orally for 7 days +Dox at 15 mg/kg IP on day 8. Rats in Groups E and F were administered GA alone at 60 and 120 mg/kg bodyweight orally for 7 days, respectively. Dox administration led to a significant reduction in hepatic reduced glutathione and nonprotein thiol (NPT) together with significant increase in hepatic malondialdehyde, hydrogen peroxide generation, superoxide dismutase, and catalase activity; hepatic glutathione peroxidase and glutathione-S-transferase activity were significantly inhibited in Dox-treated rats. The serum alanine aminotransferase (ALT), alkaline phosphatase, and total bilirubin concentrations were significantly elevated following Dox administration. Pretreatment with GA ameliorated Dox-induced hepatotoxicity and oxidative stress. The results suggest that GA may offer protection against hepatic damage in Dox cancer chemotherapy.