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Chinese journal of integrative medicine ; (12): 17-21, 2015.
Article in English | WPRIM | ID: wpr-262653

ABSTRACT

<p><b>OBJECTIVE</b>To analyze the clinical evaluation of Parkinson's disease (PD) patients receiving integrated Chinese and Western medicine therapy.</p><p><b>METHODS</b>One hundred and twenty patients were enrolled and randomly allocated to a control group or treatment group. Patients in the two groups received placebo and Bushen Huoxue Granule (, BHG), respectively. Both groups received baseline levodopa and benserazide (Madopar). The effects of treatment were assessed monthly during the 9-month treatment. Means of evaluation included Unified PD Rating Scale (UPDRS) scores (II and III), sleep scale score, 10 m turn back test (getting up time, 10 m×2 times, and turning time), timing motor test (TMT)-left and TMT-right, which were treated as the dependent variables; and age, sex, duration of PD, Hoehn and Yahr (H-Y) stage and Madopar dosage of admitted PD patients were as the independent variables. Multiple linear regression was used to analyze these factors.</p><p><b>RESULTS</b>H-Y stage significantly affected UPDRS II score, UPDRS III score, and getting up time (P<0.01). Madopar dosage and H-Y stage significantly affected the 10 m×2 times (P<0.05 or <0.01). Madopar dosage significantly affected the sleep scale score (P<0.05). There were also significant correlations between age and TMT-left or TMT-right (P<0.01), and duration of PD and TMT-right (P<0.05).</p><p><b>CONCLUSIONS</b>The six assessed means of clinical evaluation (including UPDRS II and UPDRS III scores, sleep scale score, getting up time, 10 m×2 times, and turning time) are sensitive indexes in all PD patients. H-Y stage and Madopar dosage are the major factors influencing means of clinical assessment of PD treatment.</p>


Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Integrative Medicine , Medicine, Chinese Traditional , Parkinson Disease , Therapeutics , Sleep , Time Factors , Treatment Outcome
2.
Chinese Journal of Oncology ; (12): 4-9, 2010.
Article in Chinese | WPRIM | ID: wpr-295194

ABSTRACT

<p><b>OBJECTIVE</b>To study the effects of genistein on the proliferation, apoptosis induction and expression of related gene proteins of human colon cancer cells in vitro and in vivo, and its mechanisms of action.</p><p><b>METHODS</b>MTT colorimetric assay was used to detect the effects of genistein on the proliferation of human colon adenocarcinoma SW480 cells. Light and transmission electron microscopy were used to study the histological and ultrastructural changes. Flow cytometry was used to determine the effects of genistein on cell cycle and apoptosis. Flow cytometry and immunohistochemistry were used to determine the effects of genistein on apoptosis induction and expression of related gene proteins of colon cancer cells.</p><p><b>RESULTS</b>The MTT colorimetric assay showed that genistein inhibited the proliferation of SW480 cells in a dose-dependent and time-dependent manner, and the highest inhibition rate was 60.2% after 80 microg/ml genistein treatment for 72 h. The light microscopy revealed that many genistein-treated cancer cells were shrunken, disrupted, or showing cytoplasmic vacuolization. The electron microscopic examination showed cell shrinkage, nuclear fragmentation and pronounced chromatin condensation, sometimes formed crescent chromatin condensation attached to the nuclear membrane. The results of flow cytometry showed that: after SW480 cells were treated with 0, 20, 40, 80 microg/ml genistein for 48 h, the FI values of PCNA were 1.49 +/- 0.02, 1.28 +/- 0.04, 1.14 +/- 0.03, and 0.93 +/- 0.08; the FI values of VEGF were 1.75 +/- 0.02, 1.34 +/- 0.06, 1.32 +/- 0.04, and 1.23 +/- 0.04; the fluorescence index (FI) values of p21 were 1.26 +/- 0.05, 1.36 +/- 0.06, 1.61 +/- 0.03, and 1.73 +/- 0.03, respectively. There were statistically significant differences between the control group and each treatment group (P < 0.05 or P < 0.01). The scores of immunohistochemical staining of PCNA and VEGF proteins were decreased, while p21 increased. There were statistically significant differences between the control group and each treatment group (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Genistein can inhibit the growth of colon cancer cells via apoptosis induction and cell cycle arrest at G(2)/M phase. The anti-tumor mechanisms of genistein may be related with the down-regulation of expression of VEGF and PCNA, and up-regulation of the expression of p21.</p>


Subject(s)
Animals , Humans , Male , Mice , Adenocarcinoma , Metabolism , Pathology , Anticarcinogenic Agents , Pharmacology , Apoptosis , Cell Cycle , Cell Line, Tumor , Cell Proliferation , Colonic Neoplasms , Metabolism , Pathology , Cyclin-Dependent Kinase Inhibitor p21 , Metabolism , Dose-Response Relationship, Drug , Gene Expression Regulation, Neoplastic , Genistein , Pharmacology , Mice, Inbred BALB C , Neoplasm Transplantation , Proliferating Cell Nuclear Antigen , Metabolism , Vascular Endothelial Growth Factor A , Metabolism
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