RESUMO
<p><b>OBJECTIVE</b>To investigate the effect of Ganfukang (GFK) on connective tissue growth factor (CTGF) and focal adhesion kinase (FAK)/protein kinase B (PKB or Akt) signal pathway in a hepatic fibrosis rat model and to explore the underlying therapeutic molecular mechanisms of GFK.</p><p><b>METHODS</b>Fifty SD rats were randomly divided into five groups as follows: the control group, the model group (repeated subcutaneous injection of CCl4), and the three GFK treatment groups (31.25, 312.5, and 3125 mg/kg, intragastric administration). Reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemistry were used to examine the expression of CTGF, integrin α5, integrin β1, FAK/Akt signal pathway, cyclinD1, and collagen in the different-treated rats.</p><p><b>RESULTS</b>GFK attenuated the up-regulation of CTGF, integrin α5, and integrin β1 in hepatic fibrosis rats and suppressed both the phosphorylation of FAK and the phosphorylation of Akt simultaneously (P<0.01). At the same time, the expression of cyclinD1, collagen I, and collagen III was decreased by GFK significantly (P<0.01).</p><p><b>CONCLUSIONS</b>CTGF and FAK/Akt signal pathway were activated in the CCl4-induced hepatic fibrosis rats, which contribute to increased expression of cyclinD1 and collagen genes. The mechanisms of the anti-fibrosis activity of GFK may be due to its effects against CTGF and FAk/Akt signal pathway.</p>
Assuntos
Animais , Feminino , Masculino , Colágeno , Genética , Metabolismo , Fator de Crescimento do Tecido Conjuntivo , Genética , Metabolismo , Ciclina D1 , Genética , Metabolismo , Medicamentos de Ervas Chinesas , Farmacologia , Usos Terapêuticos , Proteína-Tirosina Quinases de Adesão Focal , Metabolismo , Regulação da Expressão Gênica , Integrina alfa5 , Genética , Metabolismo , Integrina beta1 , Genética , Metabolismo , Fígado , Patologia , Cirrose Hepática , Tratamento Farmacológico , Genética , Patologia , Fosforilação , Proteínas Proto-Oncogênicas c-akt , Metabolismo , Ratos Sprague-Dawley , Transdução de SinaisRESUMO
<p><b>OBJECTIVE</b>To investigate the effect of Lipoplus on postoperative nutritional status and inflammatory response in patients with gastrointestinal malignancies.</p><p><b>METHODS</b>Sixty-four patients with gastrointestinal malignancies were randomized using random digit table to receive isonitrogenous, isocaloric total parenteral nutrition for 5 days including either Lipoplus or Lipofundin with 32 patients in each group. Blood samples were obtained before the surgery, postoperative days 1, 2, 3, and 6 to evaluate the nutritional status(prealbumin, retinol binding protein, and nitrogen balance) and inflammatory response [C-reaction protein(CRP), and leukotriene(LTB) 5, LTB4]. The incidence of postoperative systemic inflammatory response syndrome(SIRS), infection, postoperative complications, mortality, APACHEII score, length of hospital stay and other clinical indicators were recorded.</p><p><b>RESULTS</b>On postoperative day 1, prealbumin and retinol binding protein were significantly lower as compared to preoperative levels. These parameters increased significantly(P<0.05) on postoperative day 6 and the nitrogen balance was positive. On postoperative day 6, CRP was significantly lower in both groups as compared to postoperative day 3 (P<0.05), and the decrease was more prominent in Lipoplus than Lipofundin(P<0.05). There was a significant increase in LTB5/LTB4 as compared to postoperative day 1(P<0.05) in the Lipoplus group, however the increase was not statistically significant in the Lipofundin group(P>0.05). The incidence of postoperative infection was significantly lower in the Lipoplus group(3.1% vs. 6.3%, P<0.05), as was that of SIRS(9.4% vs. 15.6%, P<0.05). The APACHEII score was higher in the Lipoplus group but the difference was not statistically significant(3.6±2.0 vs. 3.3±2.1, P>0.05). The length of hospital stay was significantly shorter in Lipoplus group[(6.4±1.1) d vs. (8.2±1.3) d, P<0.05].</p><p><b>CONCLUSION</b>Lipoplus can improve the postoperative nutritional status and minimize the inflammatory response in patients with gastrointestinal malignancies.</p>