The effects of pioglitazone and rosiglitazone on liver function in hypothyroid rats.

OBJECTIVES: This study aimed to investigate the antioxidant effect of rosiglitazone (ROG) and pioglitazone (POG) on oxidative damage and dysfunction of hepatic tissue in hypothyroid rats. METHODS: The male rats were classified into six groups: (1) Control; (2) Hypothyroid, (3) Hypothyroid-POG 10, (4) Hypothyroid-POG 20, (5) Hypothyroid-ROG 2, and (6) Hypothyroid-ROG 4. To induction hypothyroidism in rats, propylthiouracil (PTU) (0.05 %w/v) was added to drinking water. In groups 2-6, besides PTU, the rats were also intraperitoneal administrated with 10 or 20 mg/kg POG or 2 or 4 mg/kg ROG for six weeks. Finally, after deep anesthesia, the blood was collected to measure the serum biochemical markers and hepatic tissue was separated for biochemical oxidative stress markers. RESULTS: Administration of PTU significantly reduced serum thyroxin concentration, total thiol levels, activity of superoxide dismutase (SOD) and catalase (CAT) enzymes, and increased serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (Alk-P) and malondialdehyde (MDA) in the liver. Additionally, our results showed that prescription of POG or ROG for six weeks to hypothyroid rats resulted in an improvement in liver dysfunction (decrease in serum levels of AST, ALT, and ALK-P) through reducing oxidative damage in hepatic tissue (increase in CAT, SOD, or total thiols and decrease in MDA levels). CONCLUSIONS: The findings of the present study presented that the IP administration of POG and ROG for six weeks improves liver dysfunction induced by hypothyroidism in juvenile rats by reducing oxidative damage.

Distribution of Ebp pili among clinical and fecal isolates of Enterococcus faecalis and evaluation for human platelet activation.

Although Enterococcus faecalis is known as normal flora in colon, it is also amongst the most common causative agents of infective endocarditis (IE). Platelet activation resulting from adherence to platelets is an essential step in the pathogenesis of IE. One of the factors proposed in adhesion is endocarditis- and biofilm- associated pili encoded by ebp operon. The aim of this study was to investigate ebp in isolates from different origins and analyze the potential of isolates to activate human platelets of different donors. The ebp distribution was investigated in E. faecalis from different origin infections (n = 103) and fecal flora (n = 20). Then, selected isolates from blood (n = 5), urine (n = 2), and fecal flora (n = 3) were analyzed by flow cytometry assay for the ability to activate platelets of four different donors. No statistically significant difference was found for the ebp presence between infective and fecal isolates. Also, it was found that the ability for platelet activation is independent of the bacterial origin. However, significant difference was found in platelet activation between different donors. The results suggest that the presence or absence of ebp is not a critical factor for platelet activation by E. faecalis isolates. However, host factors seem to contribute in this activity.

Survey for Correlation between Biofilm Formation and Virulence Determinants in a Collection of Pathogenic and Fecal Enterococcus faecalis Isolates.

BACKGROUND: Enterococcus faecalis is an opportunistic pathogen that causes most of the enterococcal infections. Among the different factors implicated in the pathogenesis of these organisms, biofilm formation and antibiotic resistance are the most important. The ability for biofilm formation has been attributed to the presence of some virulence genes. However, no definite correlation has been found. This study aimed to detect biofilm formation and antibiotic resistance patterns in E. faecalis isolates collected from clinical and fecal samples, and to investigate possible correlation between some virulence genes (esp, cyl, gelE) and biofilm formation. MATERIALS AND METHODS: A collection of 123 E. faecalis isolates were investigated for antibiotic resistance and production of hemolysin, gelatinase, and biofilm using phenotypic methods. The esp, gelE and cyl genes were detected using polymerase chain reaction. RESULTS: Thirty-eight pathogenic isolates (37%) were positive for biofilm formation. Additionally, the gelE, esp, and cyl genes were detected in 74 (71.8%), 79 (76.7%) and 42 (40.8%) isolates, respectively. In the fecal samples, 18 (90%) isolates were biofilm producers and 11 (55%), 17 (85%) and 8 (40%) isolates were positive for gelE, esp, and cyl, respectively. There were significant differences in biofilm production between pathogenic and fecal isolates (P <0.001). Multidrug resistance (MDR) was found among 32% (n = 33) and 15% (n = 3) of the clinical and fecal isolates, respectively. However, no significant difference was seen between MDR and biofilm formation. Five pathogenic and two fecal isolates were negative for all investigated genes while they were they were biofilm producers. In contrast, 22 pathogenic isolates and 1 fecal isolate were positive for the tested genes, but did not form any biofilm. No significant differences were observed between biofilm formation and the presence of the esp, gelE and cyl genes in the pathogenic and fecal isolates (P >0.05). CONCLUSION: The presence of the esp, gelE and cyl genes might not be determining factors for biofilm formation in enterococci and other mechanisms might be involved in this process.