ABSTRACT
Background Alkali burn-induced corneal neovascularization(CNV) usually leads to blindness.Recently,study determined that vascular endothelial growth factor(VEGF) and basic fibroblast growth factor(bFGF) were the main regulating factors inducing angiogenesis,and canstatin proteins can inhibit the growth of VEGF and bFGF and thereby inhibit CNV growth.Objective The present study was to investigate the effect of recombinant canstatin protein on mouse CNV induced by alkali burn and its mechanism.Methods CNV models were induced in the right eyes of 40 female BALB/c mice by sticking the 2.0 mm filtering paper with 1 mol/L NaOH at the central cornea for 10 seconds.The animals then were randomized into two groups.Recombinant canstatin protein drops(5 mg/L) was topically administered 4 times daily in the mice of the experimental group,and normal saline solution was used at the same way in the control group.Corneas of the mice were examined under the slit lamp to calculate the CNV area 1 day,3,7,14 days after modeling.The mice were sacrificed at above time points and corneas were obtained.The expressions of VEGF protein and bFGF protein in cornea were detected by Western blot,and the results were analyzed by enhanced chemiluminescence(ECL).The use of the experimental animals complied with the Instructive Notions with Respect to Caring for Laboratory Animals by State Ministry of Science and Technology.Results In 3,7 and 14 days after establishment of models,the area of CNV was (1.98-0.31) mm2,(6.21 ±0.44) mm2 and (9.83±0.72) mm2 in the experimental group,and that in the control group was (2.92 ± 0.41) mm2,(8.04 ± 0.56) mm2 and (11.78 ±0.84) mm2,showing significant reduce in the mice treated with recombinant canstatin protein(t3d =4.332,P=0.005 ;t7 d =11.729,P =0.000 ;t14 d =14.562,P =0.000).Western blot analysis showed that there was significant increase in the gray scale of VEGF protein 1 day,3,7,14 days following alkali burn in the experimental group compared with the control group(t1 d =-3.980,P＜0.001 ;t3d =-10.020,P＜0.001 ;t7d =-4.355,P＜0.001 ;t14 d =-8.156,P＜0.001),and the gray scale of bFGF was significantly ascent at various time points in the the experimental in comparison with the control groups (t1 d =-3.488,P＜0.001 ; t3 d =-2.124,P =0.013; t7 d =-1.977,P =0.028; t14 d =-4.542,P＜0.001).Conclusions Topical application of recombinant canstatin protein drops inhibits CNV growth induced by alkali burn by down-regulating the expressions of VEGF and bFGF proteins.
ABSTRACT
γ-glutamyltranspeptidase was detected from the cultured mycelia of Cordyceps sinensis (CSGT). Km and Vmax of CSGT was 2.54×10-4 mol/L and 0.1808 mol/L·min respectively when L-glutamic acid 5-(4-nitroanilide) (GpNA) and glycyglycine was used as its substrate. CSGT was stable from pH 8.0 to 11.0 and at or below 20℃. It was optimally active at pH 9.0～10.0 and 30℃. A series of reducing reagents could activate CSGT, and metal cations such as Zn2+, Cu2+, Hg2+ , Mn2+ inhibited strongly activity of the enzyme, but K+, Ca2+, Mg2+ and Na+ at high concentrations had no effect on its activity, indicating that its active center could contain -SH.
ABSTRACT
γ-glutamyltranspeptidase was detected from the cultured mycelia of Cordyceps sinensis (CSGT). Km and Vmax of CSGT was 2.54×10-4 mol/L and 0.1808 mol/L·min respectively when L-glutamic acid 5-(4-nitroanilide) (GpNA) and glycyglycine was used as its substrate. CSGT was stable from pH 8.0 to 11.0 and at or below 20℃. It was optimally active at pH 9.0～10.0 and 30℃. A series of reducing reagents could activate CSGT, and metal cations such as Zn2+, Cu2+, Hg2+ , Mn2+ inhibited strongly activity of the enzyme, but K+, Ca2+, Mg2+ and Na+ at high concentrations had no effect on its activity, indicating that its active center could contain -SH.
ABSTRACT
γ-glutamyltranspeptidase was detected from the cultured mycelia of Cordyceps sinensis (CSGT). Km and Vmax of CSGT was 2.54×10-4 mol/L and 0.1808 mol/L·min respectively when L-glutamic acid 5-(4-nitroanilide) (GpNA) and glycyglycine was used as its substrate. CSGT was stable from pH 8.0 to 11.0 and at or below 20℃. It was optimally active at pH 9.0～10.0 and 30℃. A series of reducing reagents could activate CSGT, and metal cations such as Zn2+, Cu2+, Hg2+ , Mn2+ inhibited strongly activity of the enzyme, but K+, Ca2+, Mg2+ and Na+ at high concentrations had no effect on its activity, indicating that its active center could contain -SH.
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Objective To quantify the benefit of primary Pdmor removal in patients with differently presenting incurable coloreetal cancer,while no other therapy combined.Methods One hundred and forty-three consecutive patients were operated for incurable colorectal cancer(91 undergoing resective and 52 non-resective procedures),with the purpose of comparing homogenous populations and of identifying whether the patients got benefit from primary tumor resection.Results In patients with resectable primary tumors,resective procedures were associated with longer median survival than non-resective procedures(10 months vs 3 months),patients with distant spread without neoplastic ascites/implanting metastasis got benefit from primary tumor removal(P＜0.01).The complication of resective procedures was not significantly differ-ent from that of non-resective procedares(P＞0.05).Conclusion Palliative resection of primary colorectal cancer should be pursued in patients with unresectable distant metastasis whenever the primary tumor is technically resectable.
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Genistein is a high specific and noncompetitive inhibitor of epidermal growth factor receptor tyramine kinase domain (EGFR-TK). In the paper, a molecular docking between genistein and EGFR-TK was studied to explore the mechanism of their interaction and antitumor mechanism of genistein by AUTODOCK 3.05 program. The results indicated that genistein located in the active cavity of EGFR-TK by high affinity (deltaG = -31.2 kJ/mol), and genistein inhibited EGFR-TK by interfering with forming of Lys721/Glu738 ion pair. The inhibition belonged to noncompetitive interaction, in which hydrophobic force and hydrogen bond played key roles.
Subject(s)
Catalytic Domain , Genistein , Metabolism , Pharmacology , Models, Molecular , ErbB Receptors , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To study the polymorphism of c-Ha-ras 3' variable number of tandem repeat (VNTR) and its relationship with development of postmolar tumor.</p><p><b>METHODS</b>The cases of hydatidiform mole (HM) were retrospectively analyzed by amplified fragment length polymorphism-polyacrylamide gel electrophoresis. The DNA origin of HM was determined by comparison with the parents' DNA amplified results.</p><p><b>RESULTS</b>Among the samples from 15 cases, DNA from only paternal origin was found in 2 cases. DNA from both parents was in 13 cases, and of these 13 cases, 2 were found to be had balanced DNA origin, 11 had more DNA form paternal origin than DNA from maternal origin.</p><p><b>CONCLUSION</b>The HM which has DNA from both parents origin and predominantly from paternal origin developed to postmolar tumor more frequently.</p>