ABSTRACT
Ulcerative colitis is a disease of undetermined etiology and treatment. It affects the colon and rectum and typically involves the mucosa, manifesting as continuous areas of inflammation and ulceration. Aloe gel contains more than a hundred potentially active constituents of different classes. This study investigated the effect of aloe gel on experimentally-induced ulcerative colitis. Male Wistar rats were randomly allocated into groups A to F of six rats each. Ulcerative colitis was induced to rats in groups B to F by single intra-colonic administration of 2 mL of 4% acetic acid with a size 6F pediatrics catheter. In contrast, group A received an equivalent volume of normal saline by the same route. Twenty-four hours after induction, rats in groups B and C received normal saline and 1 mg/kg b. wt. daily dose of dexamethasone, respectively. In contrast, those in groups D, E, and F received 20, 40, and 60 mg/kg b. wt. doses of aloe gel, respectively, for 14 days. They were sacrificed 24 h after the last administration. We assessed disease progression by determining the clinical activity index, gross inflammation, histological alterations, the intensity of DNA in colon cells, and tissue level of nitric oxide. All the parameters but one increased significantly in group B rats. The quantitative distribution of DNA in colon cells reduced significantly in this group. Aloe gel doses significantly reversed these changes in a dose-dependent manner. Dexamethasone showed lesser efficacy relative to 60 mg dose of the Aloe gel extract. We conclude that Aloe vera gel has therapeutic potential in the treatment and management of ulcerative colitis. The most significant effects were observed in the groups treated with the highest dose of Aloe gel (60 mg/kg b. wt.). It is also worth noting that the remediated potential of aloe gel in acetic acid-induced UC surpasses that of dexamethasone.
ABSTRACT
The germinal epithelium is the delicate epithelial lining of the seminiferous tubule lying on the blood-testes barrier; formed by the sustenacular cells of Sertoli and the adjoining basement epithelium this study addresses the effect of lead (Pb) toxicity on the epithelium and the proliferative effect of Zinc (Zn) and Selenium (Se) administered in trace concentration. Sixty F1 generation adult male Wistar rats were divided into four groups of 15 animals each. Group 1 received normal saline, group 2: 100 mg kg(-1) of lead acetate, group 3: 100 mg kg(-1) of lead acetate then 2.25 mg kg(-1) each of Zinc (Chelated zinc) and Selenium (Sodium Selenium) and group 4: 2.25 mg kg(-1) of zinc and selenium (Se+Zn). The duration of treatment was 56 days following which the animals were sacrificed on the 57th day and the testes harvested and fixed in Bouin's fluid. Pb induced toxicity can follow a mitochondria pathway involving Cathepsin D (CAD) or a cytoplasmic pathway involving p53 (protein 53; a 53 KDa nucleolase), the most predominant form of cell death is apoptosis which can result from both pathways. Se+Zn treatment improves proliferation and counters Pb toxicity by substitution, activation of enzymes (radical scavengers and vitamins), growth factors, activation of endothelial factors and activation of oxygen radical scavengers.
