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Objective:To investigate the effect of modified Si Junzitang on the expression of fibrous protein-5（Fibulin-5）， phosphorylated protein kinase B（p-Akt ）in hippocampus of rats after cerebral ischemia-reperfusion （I/R） injury and the anoikis of nerve cells. Method:The 60 male SD rats of SPF grade were randomly divided into sham operation group， model group， Edaravone group （3.2 mg·kg-1）and modified Si Junzitang high， medium and low-dose groups（19.08，9.54，4.77 g·kg-1）.The middle cerebral artery occlusion （MCAO） model was established by suture method，the rats were killed 7 days later，neurological deficit score was evaluated before the death，histopathological observation was performed by hematoxylin eosin staining， apoptosis index of nerve cells was detected by TdT-mediated dUTP nick end labeling（TUNEL）staining， the expression of Fibulin-5， p-Akt and protein in ischemic hippocampus were detected by immunohistochemistry and Western blot. Result:The neurological deficit score showed that，compared with the sham operation group， the neurological deficit score of the model group was significantly increased （P<0.01）， compared with model group， the neurological deficit score of Edaravone group，the high， medium， low dose groups of modified Si Junzitang were decreased （P<0.05，P<0.01）. Immunohistochemical results showed that，compared with the sham operation group， the expression of Fibulin-5， p-Akt protein and the apoptosis index of nerve cells in the model group were significantly increased （P<0.05，P<0.01）， compared with model group， the protein expressions of Fibulin-5 and p-Akt in Edaravone group， high， medium and low-dose groups of modified Si Junzitang were significantly increased （P<0.05，P<0.01）， and the apoptosis index of nerve cells was obvious，there was a significant decrease （P<0.05，P<0.01）. Western blot results showed that，compared with the sham operation group， the relative expression of Fibulin-5 and p-Akt protein in the model group was significantly down-regulated （P<0.01）， compared with model group， the protein expressions of Fibulin-5 and p-Akt in the Edaravone group， the high， medium and low-dose groups of modified Si Junzitang were significantly up-regulated （P<0.05，P<0.01）. Conclusion:The modified Si Junzitang may stabilize the extracellular matrix （ECM） Fibulin-5， increase the adhesion of ECM to cells and promote the expression of p-Akt protein， thus inhibiting neuronal apoptosis and protecting cerebral ischemia injury.
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Objective To investigate effects of mouse nerve growth factor on serum brain-derived neurotrophic factor, Fibulin-5 and intracranial blood flow in patients with acute cerebral infarction.Methods 98 patients with acute cerebral infarction in our hospital from September 2015 to September 2016 were selected as the research object, divided into observation group and control group, 49 cases in each group.The control group was treated with conventional treatment of acute cerebral infarction, patients in the observation group on the basis of conventional treatment combined with mouse nerve growth factor, Enzyme-linked immunosorbent assay was used to detect serum brain-derived neurotrophic factor, Fibulin-5, Intracranial ultrasonography was used to detect intracranial blood flow, the brain-derived neurotrophic factor, Fibulin-5, cerebral blood flow were compared between the two groups before and after treatment.Results Before treatment, two groups of patients with brain-derived neurotrophic factor (BDNF), Fibulin-5 and hemodynamics, the difference was not statistically significant.After treatment, the levels of BDNF and Fibulin-5 in the observation group were (5.63 ±1.34), (156.63 ±12.79), significantly higher than the control group (4.26 ±1.54), (115.52 ±15.66), the difference was statistically significant ( P<0.05 ) , the observation group of patients with cerebral hemodynamics index , average blood flow ( Qmean ) , the average blood flow velocity (Vmean), dynamic impedance (DR), cerebral vascular characteristic impedance (ZCV), cerebral vascular peripheral resistance (R) were significantly better than the control group, the difference was statistically significant (P<0.05), the prognosis of the observation group was better than that of the control group, the difference was statistically significant ( P<0.05 ) .Conclusion Clinical effect of mouse nerve growth factor on acute cerebral infarction is helpful to promote the growth of nerve function inhibition, improve cerebral blood flow, better prognosis.
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Objective To study the expression of Fibulin-5 in gastric cancer and its correlation with the prognosis of gastric cancer.Methods Tissue chips from 90 gastric cancer cases were used to study the expression of Fibulin-5 protein in cancer tissue and para-carcinoma tissue by immunohistochemistry,and analyze the correlation of Fibulin-5 expression and clinical pathological characteristics.Results The expression of Fibulin-5 in gastric cancer tissue was higher than that of para-carcinoma tissue [cytoplasm:(6.2±4.2) vs.(5.1 ±3.7);nucleus:(7.2 ±3.8) vs.(4.9 ±2.5),all P＜0.05],which was positively related with patient's age (r =0.213,P =0.044) in the cytoplasm of cancerous tissue.The expression of Fibulin-5 in the cytoplasm of cancerous tissue was negatively related with patient's overall survival (25％ vs.56％,P =0.027),which was an independent predictor (P =0.037).Conclusion Fibulin-5 is an independent prognostic factor of gastric cancer,its expression might be related with shortend patient's survival time.
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Objective To analyse the effect of dual antiplatelet drugs on fibulin-5, vWF and P-selection in serum of patients with acute cerebral infarction.Methods Diagnosed 60 patients with acute cerebral infarction in our hospital and collected. All patients were randomly divided into experimental group and control group, 30 cases in each group.The control group was treated with conventional treatment and aspirin, and the experimental group was treated with clopidogrel on the basis of control group.After treatment, the serum levels of Fibulin-5, vWF, P-selection and adverse reactions were detected in all patients.ResuIts After treatment, compared with control group, the serum Fibulin-5 level was significantly lower in experimental group ( P<0.05 );the serum vWF level in experimental group was significantly lower ( P<0.05 );the serum P-selectin level in experimental group was significantly lower (P<0.05);there was no significant difference in the incidence of adverse reactions between two groups. ConcIusion Dual antiplatelet drugs can reduce serum vWF, P-selectin and fibulin-5 in serum of patients with acute cerebral infarction, adverse reactions do not significantly increase, have guiding significance to clinical application.
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OBJECTIVES@#To explore the effect of Fibulin-5 expression on cell proliferation and invasion in human gastric cancer patients.@*METHODS@#Fibulin-5 expression was detected in 56 samples of surgically resected gastric cancer and paired noncancerous tissues using qRT-PCR and immunoblotting. Fibulin-5 was knocked down by Fibulin-5 shRNA in MGC-803 cells, then BrdU cell proliferation and transwell invasion assays were used to determine cell proliferation and invasion.@*RESULTS@#The level of Fibulin-5 mRNA in gastric cancer tissues was significantly higher as compared with that in normal tumor-adjacent tissues (P<0.05). Otherwise, the level of Fibulin-5 protein in cancer and noncancerous tissues was consistent with mRNA expression (P<0.05). Fibulin-5 protein expression in tumor tissues with poorly differentiated, lymph node metastasis and advanced TNM tumor stage was significantly higher (P<0.05, respectively). Fibulin-5 was obviously knocked down by Fibulin-5 shRNA (P<0.05), and Fibulin-5 knockdown significantly inhibited cell proliferation and invasion in MGC-803 cells (P<0.05, respectively).@*CONCLUSIONS@#The high-expression of Fibulin-5 is associated with the malignant clinicopathologic parameters in gastric cancer and Fibulin-5 knockdown inhibits cell proliferation and invasion in MGC-803 cells, suggesting Fibulin-5 may act as a key factor in the progression of gastric cancer.
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Objective To study the role of fibulin-5 in urothelial carcinoma of bladder. Methods Fibulin-5 expression was detected in bladder cancer tissues (13 cases of G_1 and G_2, 7 cases of G_3) and normal bladder mucosa samples by Western blotting assay. Fibulin-5 cDNA was amplified by PCR and cloned into pMD-19T simple vector. The pMD-19T-Fibulin-5 vector was digested by restriction endonucleases XhoI and EcoRI to generate a XhoI-Fibulin5-EcoRI fragment that was then ligated into the identical sites in p-EGFP-Nl plasmid to synthesize p-EGFP-Fibulin-5 plasmid. The p-EGFP-Fibulin-5 plasmid was finally transfected into bladder cancer cell line 5637. The migration and invasion of untransfected, vector-transfected and fibulin-5-transfected bladder cancer cells were measured by Boyden chamber assay. Results Compared to 1. 16 ±0. 28 in the normal control, the expression of fibulin-5 protein in low grade and high grade tumors were 0. 57±0. 32 and 0. 44±0. 42(P<0. 01, respectively). However, the difference between low grade and high grade tumors was not statistically significant (P>0. 05). The successfully transfected bladder cancer cells demonstrated green fluorescent light. The migrated cell number of fibulin-5-transfected cells was 127. 6 ± 3. 1 compared with 139. 3±7. 7 for vector-transfected cells and 136. 9±5. 7 for untransfected cells (P>0. 05, respectively). In contrast, the invaded cell number of fibulin-5-transfected cells was 8. 0±3. 1 compared with 31. 5±4. 8 for vector-transfected cells and 31. 7±4. 7 for untransfected cells (P<0. 01, respectively). Conclusion Fibulin-5 is down-regulated in urothelial carcinoma of bladder and acts as a tumor suppressor gene by inhibiting the invasion of bladder cancer cells.