丹参素对大鼠肝星状细胞氨基末端蛋白激酶信号转导的影响

Objective To investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1 β. Methods The proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expres-sion and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen Ⅰ were detected by the quantitative immunocytochemical assay and ELISA. Results Danshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-115 (P < 0.05). Synthesis and secretion of Type β collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1 β was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu. Conelutions Danshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type β collagen, possibly via the repression of the JNK signal transduction.     

丹参素对大鼠肝星状细胞氨基末端蛋白激酶信号转导的影响

Objective To investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1 β. Methods The proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expres-sion and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen Ⅰ were detected by the quantitative immunocytochemical assay and ELISA. Results Danshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-115 (P < 0.05). Synthesis and secretion of Type β collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1 β was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu. Conelutions Danshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type β collagen, possibly via the repression of the JNK signal transduction.     

丹参素对大鼠肝星状细胞氨基末端蛋白激酶信号转导的影响

Objective To investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1 β. Methods The proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expres-sion and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen Ⅰ were detected by the quantitative immunocytochemical assay and ELISA. Results Danshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-115 (P < 0.05). Synthesis and secretion of Type β collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1 β was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu. Conelutions Danshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type β collagen, possibly via the repression of the JNK signal transduction.     

丹参素对大鼠肝星状细胞氨基末端蛋白激酶信号转导的影响

Objective To investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1 β. Methods The proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expres-sion and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen Ⅰ were detected by the quantitative immunocytochemical assay and ELISA. Results Danshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-115 (P < 0.05). Synthesis and secretion of Type β collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1 β was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu. Conelutions Danshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type β collagen, possibly via the repression of the JNK signal transduction.     

丹参素对大鼠肝星状细胞氨基末端蛋白激酶信号转导的影响

Objective To investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1 β. Methods The proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expres-sion and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen Ⅰ were detected by the quantitative immunocytochemical assay and ELISA. Results Danshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-115 (P < 0.05). Synthesis and secretion of Type β collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1 β was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu. Conelutions Danshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type β collagen, possibly via the repression of the JNK signal transduction.     

丹参素对大鼠肝星状细胞氨基末端蛋白激酶信号转导的影响

Objective To investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1 β. Methods The proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expres-sion and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen Ⅰ were detected by the quantitative immunocytochemical assay and ELISA. Results Danshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-115 (P < 0.05). Synthesis and secretion of Type β collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1 β was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu. Conelutions Danshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type β collagen, possibly via the repression of the JNK signal transduction.     

丹参素对大鼠肝星状细胞氨基末端蛋白激酶信号转导的影响

Objective To investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1 β. Methods The proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expres-sion and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen Ⅰ were detected by the quantitative immunocytochemical assay and ELISA. Results Danshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-115 (P < 0.05). Synthesis and secretion of Type β collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1 β was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu. Conelutions Danshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type β collagen, possibly via the repression of the JNK signal transduction.     

丹参素对大鼠肝星状细胞氨基末端蛋白激酶信号转导的影响

Objective To investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1 β. Methods The proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expres-sion and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen Ⅰ were detected by the quantitative immunocytochemical assay and ELISA. Results Danshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-115 (P < 0.05). Synthesis and secretion of Type β collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1 β was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu. Conelutions Danshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type β collagen, possibly via the repression of the JNK signal transduction.     

丹参素对大鼠肝星状细胞氨基末端蛋白激酶信号转导的影响

Objective To investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1 β. Methods The proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expres-sion and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen Ⅰ were detected by the quantitative immunocytochemical assay and ELISA. Results Danshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-115 (P < 0.05). Synthesis and secretion of Type β collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1 β was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu. Conelutions Danshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type β collagen, possibly via the repression of the JNK signal transduction.     

Metformin attenuates motility,contraction,and fibrogenic response of hepatic stellate cells in vivo and in vitro by activating AMP-activated protein kinase

AIM To investigate the effect of metformin on activated hepatic stellate cells(HSCs) and the possible signaling pathways involved. METHODS A fibrotic mouse model was generated by intraperitoneal injection of carbon tetrachloride(CCl_4) and subsequent treatment with or without metformin. The level of fibrosis was detected by hematoxylin-eosin staining, Sirius Red staining, and immunohistochemistry. The HSC cell line LX-2 was used for in vitro studies. The effect of metformin on cell proliferation(CCK8 assay),motility(scratch test and Transwell assay), contraction(collagen gel contraction assay), extracellular matrix(ECM) secretion(Western blot), and angiogenesis(ELISA and tube formation assay) was investigated. We also analyzed the possible signaling pathways involved by Western blot analysis.RESULTS Mice developed marked liver fibrosis after intraperitoneal injection with CCl_4 for 6 wk. Metformin decreased the activation of HSCs, reduced the deposition of ECM, and inhibited angiogenesis in CCl_4-treated mice. Platelet-derived growth factor(PDGF) promoted the fibrogenic response of HSCs in vitro, while metformin inhibited the activation, proliferation, migration, and contraction of HSCs, and reduced the secretion of ECM. Metformin decreased the expression of vascular endothelial growth factor(VEGF) in HSCs through inhibition of hypoxia inducible factor(HIF)-1α in both PDGF-BB treatment and hypoxic conditions, and it down-regulated VEGF secretion by HSCs and inhibited HSC-based angiogenesis in hypoxic conditions in vitro. The inhibitory effects of metformin on activated HSCs were mediated by inhibiting the Akt/mammalian target of rapamycin(m TOR) and extracellular signal-regulated kinase(ERK) pathways via the activation of adenosine monophosphate-activated protein kinase(AMPK).CONCLUSION Metformin attenuates the fibrogenic response of HSCs in vivo and in vitro, and may therefore be useful for the treatment of chronic liver diseases.     

State of knowledge of helminth fauna of freshwater fishes of Poland

A total 89 fish and lamprey species has been recorded from Polish freshwater habitats. Twenty-seven of them (30.3%) have not been surveyed for parasitic helminthes. Some of the latter fishes are either rare or not easily accessible. Other live only in specific habitats in scattered localities. An important obstacle for studying parasite faunas of some fishes may be their status on an endangered species. Among the non-surveyed fishes, are those which have been relatively recently introduced to Poland or migrated there on their own. The present paper attempts to review all hitherto not studied helminthologically fish species, their habitats, localities and current protection status.     

高血压降压治疗目标的再认识

根据传统的高血压水平的定义,1993年WHO高血压治疗指南提出血压控制目标为<140/90mm Hg(1mm Hg=0.133kPa),但是并非所有患者都必须将血压降至同一水平,而应根据患者情况进行个体化治疗。Framingham进行的一项长达10～12年的心血管事件研究发现,第5年后,正常上限血压[收缩压(SBP     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.