Biomedical subjects

Cesônia A Martinusso

Publications and source records attributed to Cesônia A Martinusso.

3 recordsLinked to original sources

PubMed2006

Effects of low molecular weight heparin in obstructed kidneys: decrease of collagen, fibronectin and TGF-beta, and increase of chondroitin/dermatan sulfate proteoglycans and macrophage infiltration.

BACKGROUND: Heparin exerts beneficial effects in different experimental models of nephropathy, as observed by the preservation of the structural morphology of the kidney after heparin therapy. Here we investigate molecular and cellular events involved in the protective effects of heparin in the progression of renal disease after unilateral ureteral obstruction. METHODS: Thirty-six rats were divided into six groups: group C (control) was not subjected to any surgical manipulation; group S (sham) was subjected to surgical manipulation but without ureteral ligation; group UUO was subjected to ureteral obstruction and received no treatment; group UUO + S was subjected to ureteral obstruction and received saline subcutaneously (s.c.) once daily; group UUO + H was subjected to ureteral obstruction and received low molecular weight heparin (LMW-Hep; 4 mg/kg) s.c. once daily; and group C + H was not subjected to any surgical manipulation and received LMW-Hep (4 mg/kg) s.c. once daily. After 14 days, the content of collagen, fibronectin, total glycosaminoglycans (GAGS), chondroitin sulfate/dermatan sulfate proteoglycans (CS/DSPGs), transforming growth factor-beta (TGF-beta) and cellular infiltration were determined in the kidneys by immunohistochemical and biochemical techniques. RESULTS: Collagen, fibronectin, total GAGS, CS/DSPGs, TGF-beta and cellular infiltration increased significantly in group UUO. LMW-Hep treatment reduced collagen, fibronectin and TGF-beta, but induced an increase in the content of total GAGS, CS/DSPGs and macrophage infiltration in group UUO + H when compared with group UUO. CONCLUSIONS: LMW-Hep diminishes fibrosis in obstructed kidneys by downregulating the synthesis of collagen, fibronectin and TGF-beta. The mechanisms underlying the overproduction of CS/DSPGs and the increase in cellular infiltration upon LMW-Hep administration remain to be elucidated.

Animals↗

PubMed2004

Effects of mycophenolate mofetil and lisinopril on collagen deposition in unilateral ureteral obstruction in rats.

BACKGROUND/AIMS: Unilateral ureteral obstruction (UUO) in rats has been used as a model of renal interstitial fibrosis, in which therapeutic trials can be of important clinical relevance. In this study, we investigated the effects of mycophenolate mofetil (MMF), the angiotensin-converting enzyme (ACE) inhibitor lisinopril (L), and the combination of both drugs, given daily for 14 days to UUO rats, on the renal fibrogenic process triggered by UUO. METHODS: Rats underwent surgical UUO, followed by treatment with daily doses of either MMF, lisinopril, or both, and were then sacrificed after 14 days. Kidney fragments were fixed for histopathological examination (hematoxylin-eosin and periodic acid-Schiff reactive) and immunohistochemistry for myofibroblasts (alpha-smooth muscle actin; alpha-SMA) and macrophages (ED-1). Histomorphometrical analysis of collagen was performed with Sirius red staining, and collagen content was assessed by the amount of hydroxyproline. Cortex and medulla were analyzed separately. RESULTS: MMF, lisinopril and MMF+L reduced the density of alpha-SMA- and ED-1-positive cells (p < 0.05), interstitial volume (p < 0.05) and decreased Sirius-red-stained areas by 54.6, 35.6 and 58.0%, and hydroxyproline content by 60.1, 49.7 and 62.7%, respectively. No differences were observed among treated groups. CONCLUSION: MMF and the ACE inhibitor lisinopril attenuated the progression of the fibrogenic process of UUO in an equivalent manner. The combination of both drugs did not add any further improvement in the collagen content.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2003

Effects of ethanol on gut-associated lymphoid tissues in a model of bacterial translocation: a possible role of apoptosis.

Chronic ethanol intake has been shown to be associated with immune suppression and impairment of epithelial barrier function. We investigated the effects of ethanol on intestinal immunity and its relation to bacterial translocation (BT). Male Wistar rats were assigned to one of three groups and received respective diets for 28 days. The ethanol-fed group [(EG); n=11] received a liquid diet containing 5% [volume/volume (vol./vol.)] ethanol; a pair-fed group [(PFG); n=11] received an isocaloric diet without ethanol; and a third (control) group [(CG); n=11] received water and chow ad libitum. On experimental day 29, animals in the EG and the PFG underwent distal ileum ligature and small intestine inoculation of a tetracycline-resistant Escherichia coli strain (TcR E. coli R6), by means of gastric intubation, followed by duodenal ligature. One hour after inoculation, mesenteric lymph nodes, right lobe of liver, spleen, and left kidney were excised for bacterial studies. Sections of jejunum and colon were immunostained, with the use of antibodies against immunoglobulin (Ig) A, T cells, macrophages, and proliferating cell nuclear antigen (PCNA). Apoptosis was determined by the terminal deoxynucleotidyltransferase TdT-mediated dUDP-biotin nick end labeling (TUNEL) method. Bacterial translocation rates were greater in the PFG compared with findings for the EG. Lamina propria of the jejunum of the EG showed a reduction in the densities of IgA+ cells and T cells compared with findings for the PFG and the CG. Colonic lamina propria of the EG showed reduced densities of IgA+ cells and macrophages compared with findings for the PFG and the CG. Apoptotic index was increased in the EG compared with findings for the PFG and the CG, in both jejunum and colon. Proliferation index was not significantly different among groups. Results of the current study show that chronic ethanol ingestion led to a reduction of cellular and humoral components of the intestinal mucosa, possibly by cell loss as a result of ethanol-induced apoptosis. The reduced rates of BT observed after chronic ethanol intake seem to indicate that factors irrespective of immune function might be involved in BT inhibition.

Animals↗