5 research outputs found
ウズラ卵白オボムコイドのラット脂質代謝に及ぼす影響
It is well known that trypsin inhibitors(TIs)alter exocrine pancreatic function. We found that dietary TIs decreased serum triglyceride levels in Wistar rats in a previous investigation. In this study,we tried to confirm the effect of TIs on lipid metabolism of Sprague-Dawley(SD)rats with Japanese quail ovomucoid(OM)as a TI. Five-week-old male SD rats were fed a 20% casein control diet or OM diets containing 0.1% OM,0.2% OM or 0.4% OM for 4 weeks. Rats had no change in food intake and growth rate between the control and OM fed groups. An OM fed group(0.4% OM)had lower serum triglyceride levels and no change in serum cholesterol levels. OM led to increased pancreatic protein content and trypsin and chymotrypsin activities in a dose dependent manner,but no difference in amylase activity. Liver fatty acid synthetase activity significantly decreased in OM fed groups. Therefore,we suggested that dietary OM caused increased pancreatic protein synthesis,which resulted in increased energy expenditure and decreased serum triglyceride level
Role of Plasma Proteins in Pharmacokinetics of Micafungin, an Antifungal Antibiotic, in Analbuminemic Rats ▿
There were no significant differences in the pharmacokinetics of micafungin and expression of hepatic multidrug resistance-associated protein 2 (ABCC2/Mrp2) between analbuminemic and Sprague-Dawley rats. Micafungin bound strongly to high-density lipoprotein (HDL) and moderately to gamma globulin. These results suggest that HDL and gamma globulin contribute to the pharmacokinetics of micafungin
Mouse-Passaged Severe Acute Respiratory Syndrome-Associated Coronavirus Leads to Lethal Pulmonary Edema and Diffuse Alveolar Damage in Adult but Not Young Mice
Advanced age is a risk factor of severe acute respiratory syndrome (SARS) in humans. To understand its pathogenesis, we developed an animal model using BALB/c mice and the mouse-passaged Frankfurt 1 isolate of SARS coronavirus (SARS-CoV). We examined the immune responses to SARS-CoV in both young and adult mice. SARS-CoV induced severe respiratory illness in all adult, but not young, mice on day 2 after inoculation with a mortality rate of 30 to 50%. Moribund adult mice showed severe pulmonary edema and diffuse alveolar damage accompanied by virus replication. Adult murine lungs, which had significantly higher interleukin (IL)-4 and lower IL-10 and IL-13 levels before infection than young murine lungs, rapidly produced high levels of proinflammatory chemokines and cytokines known to induce macrophage and neutrophil infiltration and activation (eg, tumor necrosis factor-α). On day 2 after inoculation, young murine lungs produced not only proinflammatory cytokines but also IL-2, interferon-γ, IL-10, and IL-13. Adult mice showed early and acute excessive proinflammatory responses (ie, cytokine storm) in the lungs after SARS-CoV infection, which led to severe pulmonary edema and diffuse alveolar damage. Intravenous injection with anti-tumor necrosis factor-α antibody 3 hours after infection had no effect on SARS-CoV infection. However, intraperitoneal interferon-γ injection protected adult mice from the lethal respiratory illness. The experimental model described here may be useful for elucidating the pathophysiology of SARS and for evaluating therapies to treat SARS-CoV infection