Phosphorylation of GST-c-Jun was then visualized by SDS-PAGE and autoradiography imaging

rat after injection of OSE were greater than IC50. Hence, the data demonstrated sufficient inhibition of influenza viruses in the fetus when the injection dose was 10 mg/kg. OSE is an ester prodrug which will be catalyzed by carboxylesterase, human carboxylesterase to the antiviral active metabolite OCA. A cell viability test demonstrated by Shi et al. suggested that OCA is more toxic than OSE. In the case of pregnant woman concern in 2009, the OSE could hurt her baby. Our data demonstrate that only 1.9% of the more toxic metabolite OCA penetrated through the blood-placenta barrier into the fetus. In conclusion, a sensitive, accurate and precise HPLC-MS/MS analytical method for the simultaneous quantification of OSE and OCA has been demonstrated. This assay system can be used for pharmacokinetics of OSE and OCA in rat plasma, amniotic fluid, placenta, and fetus. It presents no order Triptolide endogenous interference which would hinder the separation of analytes and it is sufficiently sensitive for the determination of analytes in biological samples. Values represent the means 6 tandard deviation. P,0.05, compared with the same parameters in rat maternal plasma. Transplacental Transfer of Oseltamivir much higher than that of OCA. The results show that rapid conversion to OCA occurred in maternal plasma after OSE administration and that the presence of OCA was observed immediately in maternal plasma. However, the OCA level in the fetus is about 1/50 of that presented in material plasma. Such difference is attributed to the absence of OSE metabolic enzyme in the fetus. These pharmacokinetic results provide a constructive contribution to better understand the placental transfer of OSE and OCA to support clinical application. A novel small non-coding RNA species known as microRNAs is involved in biological control at multiple levels. They regulate gene expression essential for cell development and function through mRNA degradation or translational inhibition. Evidences indicated that miRNAs played important roles in immune system. In T lymphocytes, conditional deletion of Dicer, a RNase III enzyme which is critical for the generation of mature miRNAs, resulted in impaired thymic development and diminished T helper cell differentiation. And Dicer deficiency in B lymphocytes showed a block in B lymphocytes development. Subsequent reports revealed the roles of individual miRNAs in immune system. MiR-181 induced B lymphocytes differentiation from hematopoietic stem cells. MiR-146a negatively regulated innate immune response by interfering Toll-like receptor signaling pathway. MiR-155 has been found apparently up-regulated in several activated immune cells, including T lymphocytes, B lymphocytes, macrophages and dendritic cells. It is up-regulated by a broad range of inflammatory mediators during innate immune response. Thai et al. demonstrated that bic/miR-1552/2 mice showed diminished geminal center response. While Rodriguez et al. found that bic/miR-1552/2 CD4+ T cells were intrinsically biased toward Th2 cell differentiation rather than Th1 cell. These studies indicated that miR-155 involved in both innate and adaptive immune responses. CD4+ CD25+ regulatory T and Th17 cells are novel Th cell subsets distincted from Th1 and Th2 cells. Treg is a suppressive Th cell subset. It functions in maintenance of selftolerance and preventing the development of various inflammatory diseases by directly contacting effective immune cells and secreting anti-inflammator