The assignment電影:維拉帕米對耐藥的抑制作用

The assignment電影:維拉帕米對耐藥的抑制作用

對於有效的癌癥化療,最大的障礙是多藥耐藥(MDR)。多藥耐藥(multidrug resistance, MDR)往往與滲透性糖蛋白(滲透性糖蛋白,Pgp)上調有關,Pgp是一種atp依賴的外排泵,支持細胞內藥物濃度降低。為了克服多藥耐藥(MDR),已經探索了一系列的方法,包括使用細胞毒性藥物聯合Pgp抑制劑。維拉帕米(Verapamil, VER)是一種鈣通道拮抗劑,已顯示出Pgp的抑制活性。然而,所需的劑量的版本Pgp封鎖(2-6µM)更高的相比,目前臨床治療心律失常和可能產生毒性。

The assignment電影:維拉帕米對耐藥的抑制作用

本實驗觀察到,脂質體給藥可通過降低全身循環中遊離血管濃度來降低其心臟毒性。在K562白血病細胞中觀察到脂質體與阿黴素、維拉帕米(VER)共同產生並與轉移(Tf-L-DOX/VER)混合,並進行了檢測。該制劑以腫瘤細胞為靶點,降低阿黴素和維拉帕米的心臟毒性。除此之外,這種聯合支持克服p -糖蛋白(P-glycoprotein, Pgp)介導的多藥耐藥表型。TfR靶向、多柔比星與維拉帕米聯合包封對K562白血病細胞耐藥有較好的抑制作用。

The assignment電影:維拉帕米對耐藥的抑制作用

For efficient administration of cancer chemotherapy, the greatest obstacle is multidrug resistance (MDR). The multidrug resistance (MDR) is frequently linked with up-regulation of the permeability-glycoprotein (Pgp), which is an ATP-dependent efflux pump and support in decreasing intracellular drug concentration. For overcoming the multidrug resistance (MDR), a range of approaches has been explored, including the usage of cytotoxic drugs combined with Pgp inhibitor. Verapamil (VER) is a calcium channel adversary has been exhibit Pgp inhibitory activity. However, the amount of dose of VER needed for Pgp blockade (2-6µM) is substantially higher in comparison to the present clinical treatment for arrhythmia and possibly induce cardiotoxicity.

The assignment電影:維拉帕米對耐藥的抑制作用

In this matter, it is observed that liposomal delivery of VER can decrease its cardiotoxicity by declining free VER concentration in the systemic circulation. It is observed that liposomes along with doxorubicin and verapamil (VER) and mixed with transferring (Tf-L-DOX/VER) were produced as well as examined in K562 Leukemia Cells. The formulation is to target the tumor cells, decreasing cardiotoxicity of Doxorubicin and Verapamil. Besides this, this combination support in overcoming P-glycoprotein (Pgp) mediated multidrug resistance phenotype. The mixer of TfR targeting, co-encapsulation of doxorubicin and verapamil is shown to be highly efficient for overcoming the drug resistance in the K562 leukemia cell.

 

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