ABSTRACT
<p><b>OBJECTIVE</b>To study the change of TK1 expression level in patients with NHL and its clinical significance.</p><p><b>METHODS</b>A total of 108 NHL patients from July 2013 to January 2016 were chosen, all patients were treated with chemotherapy. The TK1 expression level and TK1 variation rate were compared among CR/PR/PD/DR patients. All patients were followed up, and the relation of TK1 level with OS/PFS was analyzed.</p><p><b>RESULTS</b>After treatment, the TK1 expression level of CR/PR/SD patients decreased significantly (P<0.05). Before treatment, the TK1 expression level of CR patients was 1.49±0.34,that after treatment was 0.45±0.17,the variation rate was (68.12±5.41)%; those of PR patients were respectively 2.89±0.58, 1.43±0.29 and (50.27±4.82)%; those of PD patients were respectively 3.98±0.78, 3.71±0.85 and (5.04±0.31)%; and those of SD patients were respectively 3.49±0.92, 2.45±0.57 and (28.65±3.97)%, the difference had statistic significance(P<0.05). After treatment, TK1 level related significantly with OS and PFS (P<0.05).</p><p><b>CONCLUSION</b>TK1 expression level has suggested implications for the evaluation of tumor loading, and treatment effect as well as prognosis of patients with NHL.</p>
ABSTRACT
OBJECTIVE: To explore the inhibitory effect and its mechanism of platycodin D (PD) on human colonic cancer SW620 cell proliferation. METHODS: The inhibitory effect of PD on SW620 cell proliferation was analyzed by MTT assay, while the effect of PD on cell cycle distribution and apoptosis were evaluated by flow cytometry. The effect of PD on expression of cyclin and ap-optosis associated proteins were detected by Western blot. RESULTS: The cell proliferation of human colonic cancer SW620 cell was inhibited by PD in a dose-dependent manner. After cells were treated with PD(15, 20 μmol · L-1) for 24 h, the proportions of cells in G0/G1 phase were (72.83±5.26)% and (76.82±5.83)% respectively, while the control group cells was (56.78±4.92)%, which suggested PD could block SW620 in the G, phase compared with the control group cells. Furthermore, the expressions of cyclinD1, c-myc and GDK6 were reduced obviously. Compared with the control group cells, the apoptotic rates were increased [(19.5±5.1)%, (35.8±5.3)% and (43.8±4.0)% respectively] after cells were treated by PD (10, 15, 20 μmol · L-1) for 48 h. The expression of procaspase 3 and PARP with proenzyme form were reduced. CONCLUSION: PD could inhibit the growth of colon cancer cell by blocking SW620 in the G, phase through regulating the expression of cyclinD1, c-myc and CDK6 and thus inducing the apoptosis by cell cycle arrest.
ABSTRACT
Objective To assess the impact of tea consumption on the risk of osteoporotic hip fractures.Methods Between January 2008 and June 2012,581 (148 males,433 females) incident cases of hip fractures were enrolled from four hospitals in Guangdong province,with 581 sex-and age-matched (± 3 years) controls from either hospitals or communities.Face-to-face interviews wer conducted to collect data pertaining to tea drinking and various covariates.Results Results from univariate conditional logistic analyses showed that an inverse association was observed in tea drinking and hip fracture risk.Longer time,greater frequency and dosage of tea consumption were dose-dependently associated with lower risk of hip fractures (P-trend ＜0.05).Compared to non drinkers,the odd ratios related to regular tea drinkers,subgroups with different length,frequency,dosage,type of tea consumption were ranged between 0.54 and 0.74 (all P＜0.05).After adjustment for factors as age,daily energy intake,BMI,education levels,passive smoking,calcium supplement and physical activity,the dose-dependent associations among above said factors still remained significant.However,the strength of the association lowered slightly.The beneficial effect of tea was significant only in men but not in women.Similar effects were found in subjects with different education levels.Conclusion Regular tea drinking habit might decrease the risk of osteoporotic hip fractures in the elderly males.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the molecular mechanism of platycodin D showing the inhibitory effect on proliferation and induced apoptosis of humane long cancer cells A549.</p><p><b>METHOD</b>Humane long cancer cells A549 were cultured in vitro, with the final PD concentration of 5-20 micromol x L(-1). PD's inhibitory effect on cell proliferation was examined by MTT assay. Morphological changes in cells were observed with microscope. The cell apoptosis rate was detected by Annexin V-FITC/PI double staining. The change of mitochondrial membrane potential was detected by JC-1. The protein expressing of leaved Caspase-3, cleaved Caspase-9, cleaved PARP, Bcl-2, Bcl-xl, Bak and Bax were detected by Western blot analysis.</p><p><b>RESULT</b>PD could inhibit the proliferation of A549 cells and show stronger effect with the increase of concentration and over time. Compared with the control group, PDs of different concentration showed significant increase in the cell apoptosis rate, decrease in mitochondrial membrane potential after 24 h. Protein electrophoresis inspection showed cut segments in both protein Caspase-3 and Caspase-9 and notable fractures with time. Further study found that PD decreased Bcl-2, Bcl-xl proteins and increased Bax, Bak proteins after processing A549 cells.</p><p><b>CONCLUSION</b>PD shows notable effect on cytotoxicity and can induce A549 cell apoptosis. It causes decrease in mitochondrial membrane potential by regulating Bax, Bak, Bcl-2 and Bcl-xl expressions, and thus activating caspase and finally causing long cancer cell apoptosis.</p>