ABSTRACT
This study was carried out to investigate the ulcero–protective activity of methanolic extract of Acacia ataxacantha leaves (MEAAL) against indomethacin and stress induced gastric ulcer in experimental rats. Study Design: Administration of MEAAL at the dose of 100mg/kg body weight and 200mg/kg body weight and evaluation of its ulcero-protective activity. Place and Duration of Study: The experiments were conducted at the Department of Biochemistry, University of Ilorin between September 2012 to May 2013. Methodology: Acacia ataxacantha leaves were extracted with 95% methanol. MEAAL at the dose of 100 and 200mg/kg body weights were administered to male albino rats 30 minutes before the administration of indomethacin and subjecting to stress. Ranitidine was used as a standard antiulcer drug. Animals were then sacrificed and various gastric parameters assessed were gastric ulcer indices, gastric pH levels, gastric ulcer percentage inhibition, which were done in order to explore the ulcero-protective potential of the plant. Results: Induction of ulcer by the intraperitoneal administration of indomethacin and forcing rats to undergo stress by swimming resulted in increased ulcer index and decreased pH. Rats pretreated with MEAAL (100 and 200mg/kg body weights) showed significant reduction in ulcer index to indomethacin and stress induced ulcer models in a dose dependent manner when compared to the negative control group. Also, the significant decrease in the gastric pH levels of both ulcer models, were normalized by MEAAL. The various percentages of gastric ulcers inhibition were statistically significant (P<.05) in the groups pretreated with MEAAL. The overall effect of the extract was comparable to that of the standard drug (ranitidine) used. Conclusion: These findings validated the potentials of Acacia ataxacantha leaves as an ulcero-protective agent and provides a scientific rationale for the use of Acacia ataxacantha in Senegalese folk medicine.
ABSTRACT
Background: The cerebellum, also called the little brain is an organ concerned with regulation of movement and other associated motor functions. It is believed to be phylogenetically one of the oldest parts of the brain. It accounts for one tenth of the brain volume and contains approximately 50% of the total brain neuron. Damage to the cerebellum is major factor involved in the progression of movement disorders. Aim: To investigate possibility of selective neuronal vulnerability in neurotoxicity and the etiology of neurodegenerative diseases especially those involving movement disorders originating from the cerebellum. Method: F1 Generation adult Wistar rats were treated with 20 and 10 mg/Kg BW of potassium cyanide (KCN), the cerebellar cortex was harvested and processed for immunohistochemistry of cell cycle markers (anti-p53 and anti-Bax) and the neuronal glycolytic pathway marker; Neuron Specific Enolase (anti-NSE). Antigen retrieval method was used specifically as peroxidase anti peroxidase reaction (PAP). The reaction was developed using a polymer 3’3’Diaminobenzidine tetrachloride (DAB), intensified in Methenamine Silver and counterstained in Hematoxylin. Results: Cyanide toxicity induced apoptosis in the cerebellum via a pathway involving Bax in mitochondria dysregulation (mitochondria apoptotic signaling) and a cytoplasmic pathway involving p53 (a nucleolase). The NSE expression level also indicates associated metabolic dysregulation with alteration in expression of cell cycle proteins. Conclusion: Cyanide toxicity induced cell death in the cerebellar cortex by metabolic alteration (NSE) and ROS formation. The expression of Bax and p53 showed that apoptosis was triggered via a mitochondria/Bax dependent, p53 related apoptotic pathway.