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Objective To observe the curative effect of mouse nerve growth factor and its influence on levels of BDNF,IGF-1,and IL-33 in patients with acute cerebral infarction.Methods Totally 106 cases of patients with acute cerebral infarction were chosen as the research objects between October 2015 and February 2017 in Fourth People's Hospital of Langfang City.According to digital list method,the patients were randomly divided into treatment group and control group,53 cases in each group.The patients in two groups were treated with conventional medicine of acute cerebral infarction,and the patients in treatment group were added to mNGF on the basis of conventional drugs,im injection,18 μg each time,once daily.The patients in control group were not added to NGF treatment,and the patients in two groups were treated for 14 d.Before and after treatment,the degrees of neural function defect in two groups were scored according to NIH Stroke Scale (NIHSS),serum levels of brain-derived neurotrophic factor (BDNF),insulin-like growth factor-1 (IGF-1) and interleukin-33 (IL-33) were determinated using enzyme-linked immunosorbent method.Results Compared with those before treatment,NIHSS scores decreased (P ＜ 0.05) after 14 d of treatment in two groups,but the reduced value in treatment group was obviously higher than that in control group (P ＜ 0.05).After treatment,the total effective rate (93.4％) of treatment group was better than that of control group (46.6％),and the difference was statistically significant (P ＜ 0.05).Compared with before treatment,serum levels of BDNF and IGF-1 rised (P ＜ 0.05),IL-33 decreased (P ＜ 0.05) after 14 d of treatment in two groups,but the changes in treatment group were significantly greater than those in control group (P ＜ 0.05).Conclusion mNGF can effectively reduce the severity of nervous functional defects,and effectively increase expression levels of BDNF and IGF 1 and decreasedexpression level ofIL-33.
ABSTRACT
Objective To observe the curative effect of mouse nerve growth factor and its influence on levels of BDNF,IGF-1,and IL-33 in patients with acute cerebral infarction.Methods Totally 106 cases of patients with acute cerebral infarction were chosen as the research objects between October 2015 and February 2017 in Fourth People's Hospital of Langfang City.According to digital list method,the patients were randomly divided into treatment group and control group,53 cases in each group.The patients in two groups were treated with conventional medicine of acute cerebral infarction,and the patients in treatment group were added to mNGF on the basis of conventional drugs,im injection,18 μg each time,once daily.The patients in control group were not added to NGF treatment,and the patients in two groups were treated for 14 d.Before and after treatment,the degrees of neural function defect in two groups were scored according to NIH Stroke Scale (NIHSS),serum levels of brain-derived neurotrophic factor (BDNF),insulin-like growth factor-1 (IGF-1) and interleukin-33 (IL-33) were determinated using enzyme-linked immunosorbent method.Results Compared with those before treatment,NIHSS scores decreased (P ＜ 0.05) after 14 d of treatment in two groups,but the reduced value in treatment group was obviously higher than that in control group (P ＜ 0.05).After treatment,the total effective rate (93.4％) of treatment group was better than that of control group (46.6％),and the difference was statistically significant (P ＜ 0.05).Compared with before treatment,serum levels of BDNF and IGF-1 rised (P ＜ 0.05),IL-33 decreased (P ＜ 0.05) after 14 d of treatment in two groups,but the changes in treatment group were significantly greater than those in control group (P ＜ 0.05).Conclusion mNGF can effectively reduce the severity of nervous functional defects,and effectively increase expression levels of BDNF and IGF 1 and decreasedexpression level ofIL-33.
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<p><b>OBJECTIVE</b>To explore the expression of ezrin protein in human non-small cell lung cancer (NSCLC) tissues and lung cancer cell lines, and the association between the expression of ezrin protein and the expression of E-cadherin and CD44V6 proteins.</p><p><b>METHODS</b>The expression of ezrin protein and mRNA in lung cancer cell lines was detected by RT-PCR and Western blotting. Ezrin, E-cadherin and CD44V6 were detected by immunohistochemical SP staining in tumor tissues from 150 lung cancer cases and in adjacent normal lung tissues from 30 patients. Furthermore, the expression of ezrin in 30 freshly-taken NSCLC tissues was also detected by Western blot.</p><p><b>RESULTS</b>The expression of ezrin protein and mRNA was up-regulated in highly metastatic human lung cancer. The positive rate of ezrin, E-cadherin and CD44V6 expression in the lung cancer was 61.3%, 54.0% and 58.7%, respectively. The up-regulation of ezrin expression was significantly correlated with lymph node metastasis, but not correlated with age, sex, tumor size, histological type, clinical TNM system and pathological grade. Western blot analysis showed that the level of ezrin in the NSCLC tissues was significantly higher than that in the normal tissues (t = 5.013, P < 0.01). Survival analysis showed that the 5-year survival rate of patients with negative ezrin expression was 29.3%, significantly higher than that of patients with positive ezrin expression (15.2%, χ(2) = 4.128, P = 0.042). Multivariate Cox regression analysis showed that ezrin expression (RR = 3.012, P = 0.047) and lymph node metastasis (RR = 4.827, P = 0.035) were significantly independent prognostic factors for patients with lung cancer. Furthermore, a negative correlation was observed between the expressions of ezrin and E-cadherin in lung cancer, and a positive correlation between the expressions of ezrin and CD44V6 in lung cancer.</p><p><b>CONCLUSIONS</b>Ezrin, E-cadherin and CD44V6 play an important role in the regulation of growth and meastasis of lung cancer. Combined detection of ezrin, E-cadherin and CD44V6 expression is helpful in evaluating the metastasis and prognosis of non-small cell lung cancer.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Cadherins , Metabolism , Carcinoma, Non-Small-Cell Lung , Metabolism , Pathology , Cell Line, Tumor , Cytoskeletal Proteins , Genetics , Metabolism , Hyaluronan Receptors , Metabolism , Lung Neoplasms , Metabolism , Pathology , Lymphatic Metastasis , RNA, Messenger , Metabolism , Survival Rate , Up-RegulationABSTRACT
<p><b>OBJECTIVE</b>To explore the expression of III β-tubulin and MDR1 protein in patients with non-small cell lung cancer (NSCLC), and to clarify its clinical significance.</p><p><b>METHODS</b>Paraffin embedded tissues from 158 primary non-small cell lung cancers and para-cancerous lung tissues were investigated for the expression of III β-tubulin and MDR1 protein by immunohistochemistry, as well as in freshly-taken NSCLC tissues by Western blot. The relationship between the expression of III β-tubulin and MDR1 and the biological features of lung cancer was analyzed.</p><p><b>RESULTS</b>The positive rate of III β-tubulin and MDR1 protein expression in lung cancer tissues was 65.19% and 51.27%, respectively. Western blot analysis showed that the level of of III β-tubulin and MDR1 protein in NSCLC tissues was remarkably higher than that in normal tissues (P < 0.01). The expression of III β-tubulin in stage III-IV cases was significantly higher than that in stage I-II cases (P < 0.05), while the expression of MDR1 protein showed no significant difference (P > 0.05). The positive rate of III β-tubulin expression in well-moderate pathological grades was lower than that in poor ones. The positive rate of MDR1 expression in adenocarcinoma was higher than that in squamous cell carcinoma and large cell undifferentiated cancers (P < 0.01). The positive rate of expression of MDR1 protein and III β-tubulin was not correlated with sex, age, tumor size and lymph node metastasis (P > 0.05).</p><p><b>CONCLUSION</b>The expression of III β-tubulin and MDR1 may play an important role in the development and progression of human non-small cell lung cancer, and could be looked as an important index for judging the prognosis of lung cancer.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , ATP Binding Cassette Transporter, Subfamily B , ATP Binding Cassette Transporter, Subfamily B, Member 1 , Metabolism , Adenocarcinoma , Metabolism , Pathology , Carcinoma, Large Cell , Metabolism , Pathology , Carcinoma, Non-Small-Cell Lung , Metabolism , Pathology , Carcinoma, Squamous Cell , Metabolism , Pathology , Lung Neoplasms , Metabolism , Pathology , Lymphatic Metastasis , Neoplasm Staging , Prognosis , Tubulin , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To detect the expression of alpha-tubulin and MDR1 in human non-small cell lung carcinoma (NSCLC), and to clarify their clinical significance.</p><p><b>METHODS</b>Paraffin embedded tissues from 158 primary non-small lung carcinomas and 30 paracancerous lung tissues were examined for expression of alpha-tubulin and MDR1 by immunohistochemistry (SP method). 30 freshly taken NSCLC tissues were examined by Western blot analysis. The relationship between alpha-tubulin and MDR1 expression and the biological features of lung carcinoma was analyzed.</p><p><b>RESULTS</b>The positive rate of alpha-tubulin and MDR1 expressions in the lung carcinomas was 65.2% and 51.3%, respectively. There was no expression of either of them in 30 paracancerous lung tissues. Western blot analysis showed that the level of alpha-tubulin and MDR1 expressions in NSCLC tissues were 0.49 +/- 0.06 and 0.56 +/- 0.04, respectively, significantly higher than that in paracancerous tissues (0.07 +/- 0.01) (t = 3.693 and t = 6.769, P < 0.01). The positive rate of alpha-tubulin expression was gradually increased with tumor progression, significantly higher in III-IV stage cancers and in poorly differentiated carcinomas (both P < 0.01). There was a distinct statistically significant difference between stage I, stage II and III, and stage IV. The positive rate of alpha-tubulin in well-moderately differentiated carcinomas was lower than that in poorly differentiated ones. There was no significant correlation with age, sex, tumor size, histological type, clinical TNM system and lymph node metastasis. The positive rate of MDR1 was not correlated with sex, age, tumor size, pathological grading, clinical TNM stages and lymph node metastasis. But the positive rate of MDR1 in adenocarcinoma was significantly higher than that in squamous carcinoma and undifferentiated large cell carcinomas (P < 0.01). alpha-tubulin and MDR1 expression had no impact on the outcome of chemotherapy (chi(2) = 0.69 and 1.30, P > 0.05, respectively). Univariate analysis showed that the 5-year survival rate of patients with negative alpha-tubulin and MDR1 expression was 30.7% and 28.5%, respectively, significantly higher than that of patients with positive alpha-tubulin and MDR1 expression (13.5% and 11.8%, respectively) (chi(2) = 20.69 and 15.52, P < 0.01, respectively), and multivariate Cox regression analysis showed that alpha-tubulin (RR = 3.287, P = 0.006) and clinical TNM stage (RR = 1.954, P = 0.025) were significantly independent predictive factor for patients with lung cancer, MDR1 and other factors could not be used as an independent predicitive factors. However, there was no significant correlation between the expression of alpha-tubulin and MDR1 in lung carcinoma(r = 0.093, P > 0.05).</p><p><b>CONCLUSION</b>The expression of alpha-tubulin and MDR1 may play an important role in the development and progression of human non-small cell lung carcinoma. Combined detection could be considered as an important index for predicting prognosis of lung carcinoma.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , ATP Binding Cassette Transporter, Subfamily B , ATP Binding Cassette Transporter, Subfamily B, Member 1 , Metabolism , Adenocarcinoma , Metabolism , Pathology , Carcinoma, Non-Small-Cell Lung , Metabolism , Pathology , Carcinoma, Squamous Cell , Metabolism , Pathology , Gene Expression Regulation, Neoplastic , Lung Neoplasms , Metabolism , Pathology , Lymphatic Metastasis , Neoplasm Staging , Paraffin Embedding , Precancerous Conditions , Metabolism , Pathology , Proportional Hazards Models , Survival Rate , Tubulin , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To study the expression of epithelial-cadherin (E-cad), CD44v6 and Cx43 in hepatocellular carcinoma (HCC) and its relationship with sex and age of patients, as well as tumor histopathologic grades.</p><p><b>METHODS</b>Double immunofluorescent staining and laser scanning confocal microscopy was used to study the expression of E-cad, CD44v6 and Cx43 in 30 cases of normal liver tissue, 25 cases of benign hepatic lesions and 38 cases of HCC. In the HCC group, correlation of antigen expression with sex and age of patients and tumor histopathologic grades was studied by T-test.</p><p><b>RESULTS</b>Significant decrease in expression of E-cad and Cx43 was noted in HCC group, as compared to normal liver tissue and benign hepatic lesion (P<0.05). On the other hand, CD44v6 expression was higher in HCC group than in the other two groups (P<0.05). In HCC group, the expression of E-cad and Cx43 did not correlate with sex, age and histopathologic grades (P>0.05). However, CD44v6 expression positively correlated with higher tumor histopathologic grades (P<0.05) but not sex and age of patients (P>0.05). In HCC group, the expression of E-cad positively correlated with that of Cx43, while the expression of CD44v6 negatively correlated with that of E-cad and Cx43.</p><p><b>CONCLUSIONS</b>Tumor immunophenotype alters during development and progression of HCC. Low expression of E-cad and Cx43 and high expression of CD44v6 may be related to aggressive clinical behavior of HCC, moreover, high expression of CD44v6 correlated with high tumor grades. Detection of E-cad, CD44v6 and Cx43 expression may thus be useful in predicting prognosis of HCC.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Cadherins , Metabolism , Carcinoma, Hepatocellular , Metabolism , Pathology , Connexin 43 , Metabolism , Fluorescent Antibody Technique , Hyaluronan Receptors , Metabolism , Liver , Metabolism , Pathology , Liver Neoplasms , Metabolism , Pathology , Microscopy, Confocal , PrognosisABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of exogenous wild PTEN gene stably transfection on growth of breast cancer cells in vitro.</p><p><b>METHODS</b>At first, a recombinant eukaryotic expression plasmid pcDNA3.1-PTEN was constructed. Human breast cancer cell line MDA468 was transfected with pcDNA3.1-PTEN or mock transfected plasmid pcDNA3.1(-) with lipofectamine. RT-PCR, immunohistochemical staining and Western blot were used to determine target gene expression. Cell viability was tested by MTT assay. Apoptosis was determined by flow cytometry with a double-staining method using FITC-conjugated annexin V and PI.</p><p><b>RESULTS</b>The PTEN stably transfected cells demonstrated the integration of the exogenous target gene and corresponding mRNA and protein over-expression. There was a significant decline in cell viability of pcDNA3.1-PTEN transfected MDA468 cells in comparison with the mock-transfected ones (P < 0.01). The PTEN-trasfected MDA468 cells also showed an increase in the rate of apoptosis, compared with parental and mock-trasfected cells (P < 0.001).</p><p><b>CONCLUSION</b>Stable expression of exogenous PTEN can suppress the malignant phenotypes of the human breast cancer cell line MDA468.</p>
Subject(s)
Humans , Breast Neoplasms , Metabolism , Pathology , Cell Line, Tumor , Eukaryotic Cells , Metabolism , PTEN Phosphohydrolase , Genetics , Phenotype , Plasmids , Genetics , Recombinant Proteins , Genetics , TransfectionABSTRACT
<p><b>OBJECTIVE</b>To investigate the apoptosis inducing effect of tea polyphenols (TPP) on human lung cancer cell (LCC) and its associative mechanism.</p><p><b>METHODS</b>The apoptosis inducing effect of TPP on LCC in vitro, and its influence on expression of the related gene were determined by MTT assay, laser scanning confocal microscopy and flow cytometry.</p><p><b>RESULTS</b>TPP in different concentration (50,100,200 and 400 microg/ml) had dose-dependent inhibitory effect on LCC, the inhibitory rate was 28.69+/-1.27% ,46. 19+/-1.79% ,64.61+/-1.29%, 75.90+/-1.96%, respectively. The inhibited LCC were blocked in (G0/G1 phase, and could not transferred to S and G2/ M phase of cell cycle. Meanwhile, TPP could induce apoptosis of LCC, the apoptotic rate being 4.76+/-0.11 %, 5.78+/-0.38 %, 10.06+/-0.67 %, 24.44+/-0.44 %, respectively. Morphologic changes of cells were seen in laser scanning confocal microscopy observation. Compared to the control group, intracellular Ca2+ concentration, Annexin V expression, phospatase and tensin homologe deleted on chromosome ten (PTEN) protein and expression gradually increased, while Cyclin D1 protein expression gradually decreased in the TPP treated groups along with the increasing of TPS concentration.</p><p><b>CONCLUSION</b>TTP can induce LCC apoptosis, the mechanism is related to the change of intracellular Ca2+ concentration, PTEN protein and Cyclin D1 protein expression.</p>