ABSTRACT
<p><b>OBJECTIVE</b>To establish a model of systemic inflammatory response syndrome (SIRS) in rats.</p><p><b>METHODS</b>SD rats were intraperitoneally injected with different concentrations of zymosan suspension. The general status, temperature, white cell count, tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), interleukin-10 (IL-10) and the pathological changes of main organs were examined.</p><p><b>RESULTS</b>The conditions of rats receiving zymosan doses of 750 mg/kg and 1000 mg/kg were consistent with the criteria of SIRS model; however, the mortality of 1000 mg/kg group was higher than that of 750 mg/kg group.</p><p><b>CONCLUSION</b>The rat model of systemic inflammatory response syndrome has been successfully induced.</p>
Subject(s)
Animals , Female , Male , Rats , Disease Models, Animal , Interleukin-10 , Blood , Interleukin-6 , Blood , Paraffin , Toxicity , Rats, Sprague-Dawley , Systemic Inflammatory Response Syndrome , Blood , Pathology , Tumor Necrosis Factor-alpha , Blood , Viscera , Pathology , Zymosan , ToxicityABSTRACT
<p><b>OBJECTIVE</b>To explore the signal pathway mediating the regulatory effect of Hepatitis B virus X protein (HBX) on c-met gene promoter in HepG2 cells.</p><p><b>METHODS</b>The expression of c-met in HBX-transfected HepG2 cells treated with different signal pathway inhibitors was detected by western blot, the invasion capability of cells was determined by Matrigel invasion assay.</p><p><b>RESULTS</b>ERK inhibitor U0126 inhibited the expression of the c-Met in HBx-transfected HepG2 cells. However, both p38MAPK inhibitor SB203580 and PI-3K inhibitor wortmanin had no effect on expression of the c-Met in HBx-transfected HepG2 cells. Furthermore, the ERK inhibitor U0126 also inhibited the invasiveness of HBX-transfected HepG2 cells.</p><p><b>CONCLUSION</b>HBx induces invasion of HCC via activation of ERK pathway.</p>