Effects of interferon-alpha combined with saikosaponin on serum T lymphocyte subgroups and hepatic cytokines in mice with immune hepatic injury / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To observe the effects of interferon-alpha combined with saikosaponin on serum T lymphocyte subgroups and hepatic cytokines in mice with immune hepatic injury.</p><p><b>METHODS</b>The mice were randomly divided into five groups, i. e., the normal control group, the model group, the interferon group, the saikosaponin group, and the interferon combined saikosaponin group. Corresponding medication was given to mice in respective groups for two days. Peripheral blood was collected 8 and 24 h after concanavalin A (Con A) was injected. Serum lymphocyte subgroups, tumor necrosis factor alpha (TNF-alpha), levels of interleukin 18 (IL-18) and IL-10, activities of alanine aminotransferase (ALT) and aspartate transaminase (AST) were detected. Pathological changes of the liver tissue were observed.</p><p><b>RESULTS</b>(1) Compared with the normal control group, serious inflammation and necrosis was significant in the liver tissue of the model group. The serum levels of ALT and AST obviously increased. Meanwhile, the 24-h peripheral blood CD4+ T cell and CD8+ T cell ratios and the hepatic IL-10 level obviously decreased (P < 0.01). The levels of IL-18 and TNF-alpha significantly increased (P < 0.05, P < 0.01). (2) Compared with the model group, dot and lamellar necrosis was dispersedly seen in the liver tissue in the three medication groups. The serum activities of ALT and AST significantly decreased (P < 0.01). Meanwhile, the peripheral blood CD4+ T cell and CD8+ T cell ratios, as well as the hepatic IL-10 level obviously increased (P < 0.01, P < 0.05). The levels of IL-18 and TNF-alpha significantly decreased (P < 0.05, P < 0.01). (3) In the interferon combined saikosaponin group, the 24-h peripheral blood CD4+ T cell and CD8+ T cell ratios increased more obviously than those of the interferon group. The 8- and 24-h IL-18 levels were obviously lower than those of the interferon group, while the 24-h TNF-alpha level significantly decreased more than that of the interferon group (P < 0.05).</p><p><b>CONCLUSION</b>Interferon-alpha combined saikosaponin could effectively play a role in fighting against the immune hepatic injury.</p>

Effects of salvianolic acid B on signal transduction induced by transforming growth factor-beta1 and platelet-derived growth factor- BB in hepatic stellate cells of rats / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To explore the anti-hepatic fibrosis mechanisms of salvianolic acid B (SA-B).</p><p><b>METHODS</b>Hepatic stellate cells (HSCs) isolated from rats were primarily cultured in uncoated plastic culture dish for 7 days, then were incubated with 10(-6) mmol/L SA-B and stimulated with 10 ng/ml transforming growth factor-beta1 (TGF-beta1) or platelet-derived growth factor-BB (PDGF-BB). Expressions of extracellular-regulated kinase (ERK) and its phosphorylation in HSC, and expressions of TGF beta1, receptor I (TbetaR I) and II (TbetaR II) and PDGF receptor beta (PDGFR-beta) on the surface of HSC induced by TGF-beta1 or PDGF-BB were detected with Western blot assay.</p><p><b>RESULTS</b>SA-B inhibited the phosphorylation of ERK1/2 in HSC primary normally cultivated for 9 days stimulated or un-stimulated by TGF-beta1, but could not affect the expressions of TbetaR I and TbetaR II on the HSC surface; it down-regulated the expression of PDGFR-beta, but had no obvious effect on the phosphorylation of ERK1/2 in those HSC stimulated or un-stimulated by PDGF-BB.</p><p><b>CONCLUSION</b>SA-B inhibits the ERK signal transduction induced by TGF-beta1 in HSC, which is independent of the expressions of TbetaR on HSC surface and also free from the ERK signal transduction stimulated by PDGF-BB. And its inhibition on PDGF-BB signal transduction in HSC is by way of restraining the expression of PDGFR in HSC.</p>

Expression of survivin mRNA of sputum and pleural effusions in human lung cancer / 中南大学学报(医学版)

OBJECTIVE@#To determine the diagnostic value of the expression of survivin mRNA in sputum samples and pleural effusions in lung cancer.@*METHODS@#The sputum samples of 104 patients with lung cancer and 30 patients with chronic obstructive pulmonary disease (COPD), and the pleural effusion of 56 patients with lung cancer and 30 patients with tuberculosis pleural effusions were detected.Reverse transcription-polymerase chain reaction (RT-PCR) was performed to detect the survivin mRNA expression in the specimens. The results were compared with their cytological examinations.@*RESULTS@#The sensitivity of the cytological examinations combined with the detection of survivin mRNA in sputum samples was higher than that of either cytological examination or survivin mRNA detection of sputum samples alone (P<0.01). The sensitivity of the diagnosis for lung cancer increased from 37.5% (sputum cytology alone) to 78.8% (sputum survivin mRNA detection combined with sputum cytology) (P<0.01), and the negative predictive value increased from 31.6% (sputum cytology alone) to 43.5% (sputum survivin mRNA detection combined with sputum cytology) (P<0.01). The sensitivity of the cytological examinations combined with the detection of survivin mRNA in pleural effusion samples was higher than that of cytological examination of pleural effusion samples alone (P<0.01). The sensitivity of the diagnosis for lung cancer increased from 42.9% (pleural effusion cytology alone) to 80.4% (pleural effusion survivin mRNA detection combined with cytology) (P<0.01), and the negative predictive value increased from 48.4% (pleural effusion cytology alone) to 77.8% (pleural effusion survivin mRNA detection combined with cytology) (P<0.01).@*CONCLUSION@#The detection of survivin mRNA from sputum samples and pleural effusions samples is a new diagnostic method for lung cancer.

Salianic-acid B inhibits MAPK signaling in activated rat hepatic stellate cells / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the inhibiting effect of salianic-acid B (SA-B) on mitogen-activated protein kinase (MAPK) Signaling in activated rat hepatic stellate cells (HSCs).</p><p><b>METHODS</b>HSCs were isolated from normal rat by in situ perfusion and Nycodenz density-gradient centrifugation method. HSCs were primarily cultured on uncoated plastic for 7 days. Then cells were stimulated with 10ng/ml transforming growth factor-beta1 (TGF-beta1) after incubated with 10-6 M/L SA-B. The effects of SA-B on Extracellular-regulated kinase (ERK) expression and its phosphorylation. Transforming growth factor beta1 receptor I (TbetaR I) and transforming growth factor beta1 receptor II (TbetaR II) on HSCs, type I collagen expression in HSC Induced by TGF-beta1 were detected with western blot assay. Quantity of Type I collagen in the medium of HSCs was detected by ELISA. Matrix metalloproteinase 2, 9, 13 (MMP-2, MMP-9 and MMP-13) in the medium of HSCs was tested by Zymography.</p><p><b>RESULTS</b>The phosphorylation of ERK1/2 in HSCs with or without TGF-beta1 was inhibited by SA-B. The expression of TbetaR I and TbetaR II on HSCs can not be affected by SA-B. The synthesization of Type I collagen in HSCs was decreased by SA-B; The synthesization and secretion of type I collagen in HSCs with TGF-beta1 were reduced by SA-B too. SA-B had no effect on the activity of MMP-2 and MMP-13, but induced the activity of MMP-13.</p><p><b>CONCLUSION</b>SA-B inhibits ERK signaling induced by TGF-b1 in HSC. This inhibition has no association with the expression of TbetaR I and TbetaR II on HSCs. SA-B reduces the synthesization and secretion of Type I collagen in HSC by means of inhibiting TGF-beta1 signaling, which might be not related to the degrading activities of MMPs.</p>