Background: Piroxicam is one of the nonsteroidal anti-inflammatory drugs used as antipyretic, analgesic and anti-inflammatory drug often used for the relief of nonspecific fever condition and in arthritis. This study investigated the protective potential of tannin-rich extract of Chasmanthera dependens (TRECDS) against piroxicam-induced hepatotoxicity in male Wistar rats.Materials and Methods: Thirty two rats were divided into four groups. Group 1 received normal saline and served as the control group, group 2 were given 20 mg/kg piroxicam only, while groups 3 and 4 were given 20 mg/kg piroxicam with the addition of 200 and 400 mg/kg of tannin-rich extract of Chasmanthera dependens, respectively. All rats were treated orally once daily for ten days.Results: Administration of piroxicam caused liver atrophy demonstrated by significant rise in serum alanine aminotransferase (ALT), alkaline phosphatase (ALP), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), glucose-6-phosphate dehydrogenase (G6PDH) levels of albumin (ALB), bilirubin (BIL), total cholesterol (TCHOL), triglyceride (TRIGS) and low-density lipoprotein (LDL). Piroxicam also decreased high-density lipoprotein (HDL) level, enzymatic and nonenzymatic antioxidant levels significantly (p>0.05) with attendant increase in oxidative stress indices in the liver of rats compared with control group. Histological assessment reveled severe damaged to the liver of rats. However, co-administration with TRECDS reversed these observations as evidenced in the histological results.Conclusion: The findings of this study showed that exposure of rats to piroxicam provoked damage to the liver via oxidative damage and TRECDS has the potential of ameliorating the damage.Keywords: hepatotoxicity, piroxicam, Chasmanthera dependens, oxidative stress

No abstract

No abstract

Aim: Manganese (Mn) is an essential trace element in many cellular processes. However, there is dearth of literature on its influence on indomethacin-induced hepatorenal damage. Therefore, this study was conducted to investigate the effect of manganese on indomethacin-induced hepatorenal damage in rats. Methods: Rats were divided into four groups of eight rats consisting of control group, indomethacin (IND) alone (20 mg/kg), Mn alone (10 mg/kg) and co-treated group that were treated orally for 14 consecutive days. Twenty four hours after treatment, under pentobarbital anesthesia, blood was collected and liver was excised to prepare homogenate and histology staining. Liver and kidney function tests aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), lactate dehydrogenase (LDH), malate dehydrogenase (MDH), glutamine dehydrogenase (GLDH), sorbitol dehydrogenase (SDH), glucose-6-phosphate dehydrogenase (G6PD), bilirubin (BIL), urea, creatinine, cholesterol (CHOL), triglycerides (TG), low and high density lipoprotein (LDL and HDL), electrolytes and oxidative stress superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and lipid peroxidation (LPO) biomarkers were assessed. Results: The results showed that indomethacin caused hepatorenal damage in rats manifested with increase in serum hepatic and renal function biomarkers. But co-administration of IND with Mn significantly (p < 0.05) decreased the level of hepatorenal biomarkers. Additionally, co-administration of IND with Mn improved the antioxidant status with concomitant reduction of LPO and restored the integrity of the liver and kidney histologically. Conclusion: The results of this study emphasize that co-administration of IND with Mn to rats alleviated IND-induced hepatorenal toxicities and oxidative stress in rats.

This study was designed to evaluate the therapeutic potentials and neuroprotective effects of methanol extract of Buchholzia coriacea (BC) seeds on sodium azide (NaN3) induced neurotoxicity of the prefrontal cortex in male Wistar rats. Neurotoxicity occurs as a result of exposure to neurotoxins in the environment, of which NaN3 is a potent neurotoxin. Thirty male Wistar rats were were randomly divided into 5 groups. Group A were administered with distilled water. Group B was administered with NaN3 for 28 days. Group C was administered with NaN3 for 28 days and thereafter B. coriacea for 21 days. Group D was administered with B. coriacea for 21 days and then NaN3 for 28 days. Group E was administered with only B. coriacea for 21 days. After treatment, neurobehavioral assessment was carried out after which the rats were sacrificed, and the prefrontal cortex excised. The prefrontal cortex was then processed for histological and biochemical analysis (SOD, MDA, GSH, and CAT). Pre-treatment and post-treatment with Buchholzia coriacea revitalized the cells of the Prefrontal cortex which were damaged by NaN3 exposure. Oxidative stress levels also decreased as a result of B. coriacea treatment, suggesting neuroprotective effects of Buchholzia Coriacea.Keywords: Buchholzia coriacea, Sodium Azide, Neurodegeration, Prefrontal cortex