The protein expression profiles induced by trimethyltin chloride in Vero cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the biomarkers and mechanism of kidney toxicity induced by trimethyltin chloride (TMT-Cl) through analyzing the differences of protein expression profiles between vero cells and vero cells exposed to TMT-Cl.</p><p><b>METHODS</b>The differences of protein expression levels of three paired samples of vero cells and vero cells exposed to TMT-Cl were compared by two-dimensional gel electrophoresis (2-DE) and liquid chromatography-electrospray ionization-linear trap quadrupole (LC-ESI-LTQ). The differences of expression levels of Annexin A1 and α-Tubulin proteins were validated with western blot assay, and the differences of mRNA expression levels of Annexin A1 and α-Tubulin genes were detected with quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR).</p><p><b>RESULTS</b>Fifteen spots of differential expression in protein profiles between vero cells and vero cells exposed to TMT-Cl were found, and 9 of these spots were identified by LC-ESI-LTQ. The expression levels of 3 proteins (Annexin A1,similar to RAN protein and a hypothetical protein) increased and the expression levels of 6 proteins(growth factor receptor-bound protein 10, tubulin alpha 6, heterogeneous nuclear ribonucleoprotein, similar to elongation factor SIII p15 subunit, S-adenosylhomocysteine hydrolase and a hypothetical protein) reduced. The expression levels of α-Tubulin protein and mRNA significantly decreased in vero cells exposed to TMT-Cl, as compared with vero cells (P < 0.01). The expression of Annexin A1 protein in all exposure groups was significantly up-regulated, the expression of Annexin A1 mRNA in the groups exposed to 25 and 50 µmol/L TMT-Cl was significantly down-regulated, and The expression of Annexin A1 mRNA in the group exposed to 100 µmol/L TMT-Cl was significantly up-regulated (P < 0.01).</p><p><b>CONCLUSIONS</b>The results of present study suggest that 9 proteins with differential expression detected by LC-ESI-LTQ may be related to the kidney toxicity induced by TMT-Cl, which can serve as the biomarkers of early diagnosis and therapeutic effect for the kidney toxicity induced by TMT-Cl.</p>

The influence of postburn administration of rhGH on the host inflammatory response / 中华烧伤杂志

<p><b>OBJECTIVE</b>To investigate the changes in the systemic inflammatory response and T cell induced immunity after systemic administration of recombinant human growth hormone (rhGH) during early postburn stage.</p><p><b>METHODS</b>Forty Sprague-Dawley (SD) rats were randomly divided into three groups for the study. The rats in control group (C, n = 6) were only used for the determination of plasma levels of the cytokines, such as TNFalpha, IL-2, IL-6 and CD4(+) and CD8(+) cells. The SD rats in burn with rhGH treatment group (BT, n = 18) and burn without treatment group (B, n = 18) were inflicted with III degree scalding injury on the back. rhGH was injected subcutaneously on the abdomen of the rats in a dose of 6 IU/kg for 10 days in BT group. The blood samples were harvested from the rats in the two groups for the evaluation of the above indices.</p><p><b>RESULTS</b>The plasma levels of TNFalpha, IL-2, IL-6 and CD4(+) and CD8(+) cells were increased on the 3(rd) postburn day (PBD) and decreased on the 6(th) PBD in B group, while the CD4(+) and CD8(+) cells were increased significantly and the plasma levels of TNFalpha, IL-2, IL-6 decreased obviously on the 3(rd) PBD in BT group. And the plasma levels of IL-2 and IL-6 in BT group on the 6(th) PBD showed no difference from those in C group. But the plasma TNFalpha level in BT group was evidently higher than that in B and C group on the 6(th) PBD. Furthermore, the plasma levels of TNFalpha, IL-2 and IL-6 in BT group were still increased gradually on the 10(th) PBD, while the IL-2 and IL-6 levels were decreased obviously in B group, but the TNFalpha level was increased.</p><p><b>CONCLUSION</b>Systemic administration of rhGH during different states of stress exerted different effects on T cell induced immunity and systemic inflammatory response.</p>