ABSTRACT
INTRODUCTION: Lipopolysaccharide is a bacterial endotoxin that induces acute lung injury in experimental animals, which is similar to acute respiratory distress syndrome in humans. The induced tissue trauma ends in fibrosis. Understanding the pathogenesis is important in the prevention and treatment of the complications. This study was assigned to investigate the long-term lipopolysaccharide-induced lung injury and the postulated protective effect of ascorbic acid on these changes. MATERIALS AND METHODS: Twenty-four adult male albino rats were divided into three groups. Group I was the controls, group II received lipopolysaccharide and group III received lipopolysaccharide and ascorbic acid. After 30 days of starting treatment, lung tissue samples were obtained. RESULTS: Group II lung tissues showed marked thickening of the alveolar septa with collapsed alveolar sacs, detached bronchial epithelium, inflammatory cell infiltration and excessive deposition of collagen. Group III showed mild thickening of the alveolar walls, scanty inflammatory cell infiltration, mild parabronchial fibrosis and less marked collagen deposition. α-Smooth muscle actin staining of group II showed marked expression of the actin-positive cells. Less potential expression of the dye was found in group III. Ultrastructural examination of group II showed evident structural changes in pneumocytes with capillary basement membrane irregularity and interruption compared to uniform basement membrane in group III with less prominent intracellular changes in pneumocytes. CONCLUSION: Ascorbic acid attenuated the inflammatory response and fibrosis in the lungs of rats treated with lipopolysaccharide as evidenced by the histological, immunohistochemical and ultrastructural studies.
ABSTRACT
This study was conducted to investigate how far dietary zinc (Zn) modifies the histomorphological alterations induced by diabetes in rat kidneys. The animals were divided into negative control group (10 rats). Diabetes was induced in thirty animals by streptozotocin. After confirming diabetes, the animals were divided into three groups (n = 10). Group II served as the positive control group (fed on standard diet), group III was fed on Zn deficient diet, and group IV was fed on Zn supplemented diet. Caspase-3 immune staining was used to estimate the caspase activity. Stereological procedures were used to measure the quantity of the immune stain and the surface area of the Bowman's space. The renal cortices of group II rats revealed apparent widening of Bowman's spaces with few apoptotic figures. The filtration barrier showed thickening of the basement membrane. The proximal convoluted tubules showed patchy loss of the apical microvilli with swollen mitochondria. The distal convoluted tubules revealed area of irregular basal enfolding. The picture was aggravated by Zn deficiency in group III besides areas of cortical interstitial fibrosis. The histopathological alterations were minimal in the cortices of group IV. A significant increase of the Bowman's space surface area in group II and IV while decrease in group III compared with group I. The expression of Caspase-3 density was significantly increased in group II and III compared with group I while in group IV was non significant. In conclusion, dietary Zn modulated renal cortical changes caused by diabetes in rats.
