ABSTRACT
The pathogenesis of chronic obstructive pulmonary disease is the dysfunction of qi-blood-body fluid.By the analysis of the pathogenesis of different stages of COPD,qi deficiency,phlegm,blood stasis is the key to COPD.According to the pathogenesis of syndrome differentiation,a good curative effect can be achieved by the selection of different treatment methods like tonifying qi,eliminating phlegm and removing blood stasis.
ABSTRACT
Objective To observe the curative effect of treating CHD angina pectoris with the therapy of clearing away heat and detoxification. Methods Sixty patients with angina pectoris were randomly recurited into two groups, a trial group and a control group. The trial group was treated by Chinese medicine which has the efficacy of clearing away heat and detoxification (Qingre-Jiedu decoction) and conventional therapy of Isosorbide Mononitrate tablets as same as the control group. The period of treatment was 4 weeks. Compare the curative effect and the change of ECG between the two groups after the treatment. Results After the treatment,the curative effect and the change of ECG of the trial group were both better than the control group with significant difference (P< 0.05). Conclusion It was better to treat coronary heart disease with the management of clearing away heat and detoxification and western medicine than that with western medicine only.
ABSTRACT
With IL-6R as target, a new compound 2460A was identified from fungus using HTS screening model. The taxonomics of the produced strain was confirmed to be Trichoderma hazianum rifai after sequencing analysis of rDNA-ITS (internal transcribed spacer). Results showed that this compound has a binding activity on IL-6R competed with IL-6, thus it is a new ligand of IL-6R originating from microbe. With MTT assay, the anti-tumor activities of 2460A were demonstrated on CM126 and HT-29 cell lines separately, the IC50 are 2.17 x 10(-5) mol x L(-1) and 1.8 x 10(-5) mol x L(-1) respectively. The compound affected lightly the HT-29 cell cycle at S phase. Studies for the anti-tumor activity of 2460A in vivo are in progress in our lab.
ABSTRACT
Cellular senescence is one of the important steps against tumor. This study was to observe the characteristics of boningmycin induced senescence of human tumor cells. MIT method and clone formation assay were used to detect the growth-inhibitory effect. Cellular senescence was detected with senescence-associated beta-galactosidase staining. Cell cycle distribution and accumulation of intracellular reactive oxygen species (ROS) were analyzed with flow cytometry. Protein expression was detected by Western blotting. The results showed that the growth-inhibitory effect of boningmycin was obviously stronger on human oral epithelial carcinoma KB cells than that on non-small cell lung cancer A549 cells. Comparison to the similar action of doxorubicin, that boningmycin induced the features of cellular senescence in both cell lines, its due to the arrest at G2/M phase and an increase of ROS level. The molecular senescence marker P21 increased significantly after boningmycin treatment at a dosage of 0.1 micromol x L(-1), whereas a higher concentration of it induced apoptosis. The results indicated that cellular senescence induced by boningmycin was one of its mechanisms in tumor suppression.
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AIM To study the features of cell death induced by the anticancer antibiotic lidamycin (LDM) in human hepatoma BEL-7402 cells. METHODS Chromatin condensation was observed by co-staining with fluorescent dyes, hoechst 33342 and propidium iodide. “G1 sub-peak” was detected by flow cytometry and DNA ladder was observed using agarose gel electrophoresis. The caspase-3, 6 activities were measured with kits specific for them. RESULTS Typical apoptotic chromatin condensations appeared when the BEL-7402 cells were treated with the conventional antitumor agent mitomycin C 30 μmol.L-1 for 12 h. However, an abnormal type of chromatin condensation occurred when the cells were treated with LDM 1 μmol.L-1 for 6 h, which was characterized with keeping the completeness of nuclear membrane and not forming apoptotic bodies. The DNA ladder patterns were observed using agarose gel electrophoresis. The “G1 sub-peak” occurred only in the cells treated with LDM for 24 h, though chromatin condensation was earlier detected in treatment with LDM for 6 h. The caspase-3, 6 activities were increased about 5 and 4 folds, after the cells were treated with LDM 1 μmol.L-1 for 6 h, as did mitomycin C. The time of initiating chromatin condensation was earlier than that of the high peak activities of caspase-6. CONCLUSION The characterization of cell death induced by lidamycin in the human hepatoma BEL-7402 cells differs from typical apoptosis. The results make it helpful to explain the molecular mechanism of the highly potent cytotoxicities of lidamycin toward tumor cells.