| The innate immune system plays a crucial role in protecting the host gainst infectious microorganisms. An inappropriate control of this system may have profound consequences such as SIRS (systemic inflammatory response syndrome) and MODS (multiple organ dysfunction syndrome) because of the maintained production of specific proinflammatory molecules. Monoclonal antibody or binding protein of some cytokines failed to imorove the survival or may place the host at increased risk of infectious complications. There are not yet any effective therapy in clinical practice. Therefore in China, many herbs are universaly adnministered on patients to sustain the balance of immune responses. Astragalus has a long history of medicinal use within the traditional Chinese system. Astragalus has demonstrated a wide range of immunopotentiating effects. In this study, a SIRS model of acute murine toxoplasmosis were established to access the efficacy of Astraglus on sustaining the balance of immune responses. Previous researches have suggested that Astraglus had the function of modulating some cytokine during the development of SIRS, but the resultes failed to describe the immune status of hosts. In our model of acute murine toxoplasmosis, the efficacy of Astraglus can be quantified by the survival of mice which is a consequence of delebrate regulation of immune response. In our study, mice were intraperitoneally infected with different doses of tachyzoites, and the effecacy of Astraglus were observed. Serum levels of ALT, IFN-r, IL-18, iNOS prodece in liver, apoptosis of spleen were assayed at intervals to study the mechanism.-4-MethodsICR Mice respectedly infected with 10 10 10 tachyzoites of RH strain, Toxoplasma Gondii were orally treated with Astraglus memberane and Azithromycin from 1st day post infection.Control groups were infected with same dose of tachyzoites and given water. The dose of infection with which Astragli demonstrated best effectiveness was decided as the one to establish the target model. Mice treated with Astraglus and water were killed at intervals to collect sera and tissues. Parasites loads were deterimined with quantitative fluorescence Poly merase Chain Reaction (PCR). Serum enzyme levels of alanine aminotransferase (ALT) were quantified using a commercial kit. Serum levels of IFN-r, IL-18 were assayed using two-site ELISA sets. Paraffin sections of tissues were stained with H&E. Frozen sections were stained by the method of nicotinamide adenosine dinudeotide phosphate diaphorase to quantitate iNOS. Splenocytes were stained by annexin V before being analyzed on a FACScan to evaluate the apoptosis rates.ResultsNo mice but 20% of those who were infected with low dose of tachyzoites (10) and treated with Astragli survived 10 days or above.As to the average survival time post infection, mice receiving Astragli demonstrated no benefit comparing control groups when infected with middle (10) or high (10) dose of tachyzoites. But when infected with low dose of tachyzoites (10), mice receiving Astragli survived 8.74d that was significant longer than the control(7.63d) (p<0.05) .The following results were obtained from the murine model infected with low dose of tachyzoites (10). Parasite loads in live and lung detected at 4dpi and 8dpi were common between Astrgli group and control group.The ALT levels in-5-sera of both groups kept elevating. ALT level was observed increasing to 87.20u at 4dpi in Astrgali group,while it remained low(34.44u) in control group. But at 7dpi, ALT level in Astragli group(172.5u) were significant lower than that in control group(225.69u)(P<0.05). Serum levels of IL-18 increased until death, whereas IFN- Y levels peaked and then decreased IFN- y levels of Astragli group were higher than that of control group at 4dpi and 8dpi (P0.05) . IL-18 levels of Astragli group were lower than that of control group at 8dpi (P<0.05) .Control groups demonstrated low levels of iNOS expression until death,while Astragli induced higher levels of iNOS and more extensive expression from 4 dpi. Apl... |
PDF Full Text Request