The,pharmacological,mechanism, health The pharmacological mechanism of paclitaxel
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Vitroexperiments show that paclitaxel has significant radiosensitizing effect, maybe suspending the cells in G2 and M phase of radiotherapy sensitive. Paclitaxelbelongs to mitotic inhibitors or spindle toxins, have a different mechanism ofaction with currently used chemotherapy drugs, it is the assembly to induce andpromote microtubule. Taxol has polymerization and stabilizing microtubule role,resulting in rapidly dividing tumor cells firmly fixed during mitosis phase,make the cancer cells replication was blocking and death. Microtubulesare a component of the eukaryotic cell, which is composed of two similarpolypeptides (a and p) microtubule subunits dimer. Under normal circumstances,microtubules and tubulin dimer exists dynamic balance. Paclitaxel is a kind of pharmaceutical rawmaterials can make them lose thisdynamic balance, induce and promote tubulin polymerization, preventingdepolymerization, stable microtubules. These effects lead to cells duringmitosis cannot form a spindle and spindle fibers, inhibit cell division andproliferation, thus play an anti-tumor effect. Invitro studies shown that paclitaxel concentration was dependent, reversiblybound to microtubules, in particular binding to N-terminal the P- tubulinsubunits, this effect reduces the microtubule protein concentration ofpolymerization required, make the dynamic equilibrium towards the direction ofmicrotubule assembly, increasing the rate of microtubule polymerization andyield. Paclitaxel-induced microtubule formation is shorter, and about ten timeslarger than not use paclitaxels normal buckling microtubules. Paclitaxel inthe ratio of 1:1 binding to microtubules, indicated that drugs in microtubuleonly have one binding site. In addition, the microtubule network required bypaclitaxel inhibited mitosis normal dynamic regeneration, preventing the normalmitotic spindle formation, resulting in chromosome breakage, and inhibitingcell replication. Paclitaxel and cholesterol and A2780 ovarian cancer celllines incubated 24h, 99% cell death, of which 57% cells enter division stage,and occurs a wide range of nuclear damage. Taxolchanges cells mitosis process, make the mitotic duration from 0.5h to 15h, andinhibit cytokinesis, leading to form multinucleate cells. These multinucleatecells continue to revert to division stage, and then tried to divide again, butthere are not arresting cells, in many cells also observed micronuclei. Inhibitspindle forming seems related to this abnormal mitosis. Low concentrations ofpaclitaxel in vitro (less than 8.5pg/L) block metaphase transitions to anaphasein cell cycle, prevent cell proliferation, without increasing the amount ofmicrotubule multimer or form microtubule spindle. Paclitaxel inhibits cell proliferationand block cell metaphase degree parallel. Higher concentration paclitaxel(greater than 8.5fig/L) increased microtubule polymer amount, in 282pg/L, it is500% higher than the control level, resulting in forming large spindle ofmicrotubules. Leukemia cells and 85pg/L or greater concentrations paclitaxelincubated for 24h, 40% of the cell contraction, chromosome concentrated. ArticleSource:http://www.cospcn.com
The,pharmacological,mechanism,