鉈誘導C6 glioma 細胞周期停止及/或凋亡
Effect of thallium acetate on cell cycle arrest and/or apoptosis of C6 glioma cell
中文摘要
鉈曾被發現具有神經毒性，我們利用C6 glioma 細胞研究鉈中毒之分子機制 。 MTT assay 顯示鉈會抑制細胞生長。流式細胞儀分析顯示在 300μM 濃度下，
鉈會引起C6 glioma 細胞之細胞周期停止和凋亡；Bad 蛋白（凋亡促進蛋白）
隨著鉈濃度上升有增加情形，而抗凋亡蛋白（Bcl-XL 及 Bcl-2）則明顯減少。投 予鉈之C6 glioma 細胞，其 p21 蛋白量有顯著增加。這些結果顯示鉈會誘導 p21 蛋白增加，造成 C6 glioma 細胞之細胞周期停止和凋亡，進而抑制其細胞 生長。
英文摘要
Thallium acetate is known to have neurotoxicity. No available study of its molecular mechanism by literature reviewed. We investigate the molecular mechanism of the toxicity of thallium acetate using C6 glioma cell. Inhibition of cell proliferation was shown by MTT assay. The flow cytometry analysis revealed cell cycle arrest and apoptosis of C6 glioma cell upon exposure to thallium acetate at concentration of 300μM. Western blotting analysis demonstrated a dose
dependent increase of pro-apoptotic protein, the bad protein. Decrease of anti- apoptotic proteins, bcl-XL and bcl-2, were also found. The protein level of p21 was increased by treatment with thallium acetate. These results suggest that thallium acetate inhibits the proliferation of C6 glioma cells via cell cycle arrest in
association with induction of p21 and apoptosis.
