原生态的困境——以哈尼族哭嫁歌为例

从哈尼族哭嫁歌形成的历史语境出发,概括了迁徙民族哭嫁民俗产生的社会性冲突因素,归纳了学术界对这一民俗艺术现象的社会性分析路径。通过它的原生性、场域、语境的渐消性分析,得出哭嫁歌的原生性决定了它对哭嫁的具体场域、情景和婚俗仪式的依赖。脱离了真实的环境和情景的哭嫁歌,内容构成了一种外在性与娱乐表演,使它不再具备独立存在的艺术样式。从民族文化传承的角度看,哭嫁歌已经失去了生存的土壤,民俗的内涵流失殆尽,演出形态的存在只是一种失去灵魂的表象。

Influence of paeonol on expression of COX-2 and p27 in HT-29 cells

AIM： To investigate the effect of paeonol on controlling the proliferation of colorectal cancer cell line HT-29 and to discuss its possible mechanism. METHODS： The inhibitory effect of paeonol on proliferation of HT-29 cells was detected by M-I-I- assay. The results of apoptosis were measured by flow cytometry. Immunocytochemical staining was performed to detect the expression of cyclooxygenase-2 （COX-2） and protein p27 in HT-29 cells treated with paeonol at different concentrations. Reverse transcription-polymerase chain reaction （RT- PCR） was used for mRNA analysis. RESULTS： From the data of both MTT and flow cytometry, we observed that cell proliferation was inhibited by different concentrations of paeonol. By immunocytochemical staining, we found that HT-29 cells treated with paeonol （0.024-1.504 mmol/L） reflected reduced expression of COX-2 and increased expression of p27 in a dose-dependent manner. RT-PCR showed that paeonol down-regulated COX-2 and up-regulated p27 in a dose- and time-dependent manner in HT-29 cells. CONCLUSION： One of the apoptotic mechanisms of paeonol is down-regulation of COX-2. p27 is upregulated simultaneously and plays an important part in controlling cell proliferation and is a crucial factor in the Fas/FasL apoptosis pathway.

Effect of aspirin alone or combined with cisplatin on human cervical carcinoma HeLa cells

Objective： To study the effect and mechanism of aspirin alone or combined with cisplatin （DDP） on human cervical carcinoma HeLa cells. Methods： HeLa cells were treated by different concentrations of aspirin, DDP alone or both. The inhibitory effect on cell growth was analyzed by MTT and colony-forming assay. Cell apoptosis was measured with flow cytometry. The mRNA levels ofBcl-2, Bax and NF-κB（P65） were studied by RT-PCR. Results： MTT assay showed that aspirin inhibited HeLa cell proliferation in a time-and dose-dependant maoner. Aspirin decreased clone numbers in colony formation assay. Aspirin also induced apoptosis of HeLa cells in a dose- and time-dependent manner as detected by flow cytometry. The inhibition effects on proliferation, colony formation and apoptosis were significantly enhanced when cells were treated with both aspirin and DDP. RT-PCR demonstrated that aspirin decreased the transcription of Bcl-2 and NF-κB, and increased expression of Bax gene. Conclusion： Aspirin can induce apoptosis in HeLa cells. Combination of aspirin and DDP displays a synergistic effect. The possible mechanism might be that aspirin downregulates the mRNA levels of Bcl-2 and NF-κB gene and upregulates the expression of Bax.

The impact of beta-elemene on beta-tubulin of human hepatoma hepg2 cells

Objective: The aim of this study was to investigate the impact of beta-elemene injection on the growth and beta-tubulin of human hepatocarcinoma HepG2 cells. Methods: Cell proliferation was assessed by MTT assay. Cell cycle distribution was detected by flow cytometry(FCM). The mRNA expression of beta-tubulin was measured by RT-PCR. Western blot analysis was used to determine protein expression of beta-tubulin and the polymerization of beta-tubulin. Results: Beta-elemene injection inhibited HepG2 cells proliferation in a dose- and time-dependent manner; FCM analysis indicated beta-elemene injection induced cell cycle arrested at S phase. RT-PCR and western-blot analysis showed that beta-elemene injection down-regulated beta-tubulin expression at both mRNA and protein levels, presenting a dose-dependent manner. Moreover, beta-elemene injection reduced the polymerization of microtubules in a dose-dependent manner. Conclusion: Beta-elemene injection can inhibit the proliferation of hepatoma HepG2 cells, the mechanism might be partly related to the down-regulation of beta-tubulin and inhibition of microtubular polymerization.