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- WI-38細胞株WI-38 cells(CCL-75)
- 威斯塔研究院38細胞株WI-38 cells; Wistar Institute 38 cells; Wistar's Insitute 38 cell
- 細胞cell
- SWO-38細胞SWO -38 cells
- 細胞株cell strain
- 人膠質(zhì)瘤SWO-38細胞glioma
- 人淋巴因子激活的殺傷細胞對肝癌細胞株凋謝作用的觀(guān)察A Observaion of Apoptoisi of Liver Cancer Cells Induced by Human LAK Cells
- 人參皂苷Rg1可能通過(guò)激活端粒酶活性和減少端粒長(cháng)度縮短而發(fā)揮其抗t BHP誘導的WI 38細胞衰老作用。Activation of telomerase and prolonging of RTF length might be involved in t he process of ginsenoside Rg1 protection against t-BHP-induced senescence in W I-38 cells.
- T24細胞株T24 Cell lines
- 然后，將WI-38細胞隨機分為4組，用不同劑量人參皂甙Rg1預處理，觀(guān)察其對t-BHP誘導的細胞衰老的影響。After four stresses of t-BHP, we compared cells in three aspects above.
- NB4細胞株NB4 cell line
- 1 .t一BHP可誘導Wl一38細胞衰老，可用于建立體外細胞衰老模型。Conclusion: t-BHP can be used to induce WI-38 cells senescence and to establish a model of premature senescence.
- 肝細胞株hepatocyte lines
- Rgl預處理可明顯減弱t-BHP對WI-38細胞衰老的誘導作用,同時(shí)p21表達水平明顯降低,cyclin E和CDK2表達水平增加。Pretreatment with Rgl significantly attenuated t-BHP-induced senescence in WI-38 cells. Simultaneously, compared with cells treated with t-BHP alone, Rgl pretreatment markedly decreased the level of p21 protein and increased the levels of CDK2 and cyclin E.
- A20細胞株A20 cell line
- B9細胞株B9 cell line
- 方法 :將WI 38細胞隨機分為 4組 ,用不同劑量Rg1預處理。 從 30代開(kāi)始 ,隔代用t BHP作用 ,每次 1h ,共 4次 ,誘導細胞衰老。METHODS: WI 38 cells were divided into 4 groups and randomly added with different concentrations of Rg1. From 30 population doubling (PD), WI 38 cells were exposed to t BHP for 1 h at every two PDs.
- CEM細胞株CEM cell line
- CHO細胞株CHO cell
- CNE細胞株CNE
