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首頁 > 美迪醫(yī)訊 > 可防止細(xì)胞受輻射影響的藥物 |
可防止細(xì)胞受輻射影響的藥物 【?2007-06-05 發(fā)布?】 美迪醫(yī)訊
科學(xué)家最近開發(fā)了一種新藥可以防止細(xì)胞照射后的致死效應(yīng)。無論細(xì)胞暴露于輻射前還是輻射后。 目前還沒有有效的藥物保護(hù)受高水平輻射后對(duì)大眾產(chǎn)生的影響,典型的例子是核爆破后產(chǎn)生的破壞力。這種劑量的照射幾周內(nèi)可導(dǎo)致人類死亡,因?yàn)檩椛淦茐牧搜杭?xì)胞,使其喪失了止血和抵抗感染的能力,并且使干細(xì)胞跟不上機(jī)體的更新。 在小鼠身上使用這種藥物,來自華盛頓大學(xué)的學(xué)者發(fā)現(xiàn)這種藥物主要通過保護(hù)那些迅速分裂的細(xì)胞從而防止了輻射的影響,而輻射對(duì)這些正處于分裂期的細(xì)胞產(chǎn)生的影響最大。 最近對(duì)嚴(yán)重輻射暴露的治療,也稱為急性輻射綜合癥,受限于藥物的增強(qiáng)作用,因?yàn)檫@些藥物主要是增加血液細(xì)胞和血小板的合成,而這種療法在干細(xì)胞也被殺絕的情況下是失效的。另外,現(xiàn)在還沒有可行的方法限制輻射后細(xì)胞的破壞。 一種稱為Bcl-xL的蛋白,已知這種蛋白可以阻斷細(xì)胞的死亡過程,科學(xué)家將這種蛋白的一部分連接于HIV病毒蛋白TAT上,通過這種方法可將藥物進(jìn)入細(xì)胞內(nèi)。小鼠經(jīng)過5-Gy照射后在皮下注入這種藥物。對(duì)于人類來說,這種劑量的照射可導(dǎo)致血液細(xì)胞的明顯減少,導(dǎo)致個(gè)體感染和出血的風(fēng)險(xiǎn)增加。 研究表明這種療法可以保護(hù)脾臟中迅速分裂的T細(xì)胞和B細(xì)胞,這些免疫系統(tǒng)的細(xì)胞更傾向于受到輻射的破壞。研究過程中,把小鼠分為兩組,分別在受輻射前后注射這種藥物。 后續(xù)研究表明,這種TAT-BH4藥物在照射后1小時(shí)后使用仍然有效,科學(xué)家并試圖了解這種藥物預(yù)防輻射-誘導(dǎo)細(xì)胞調(diào)亡的持續(xù)時(shí)間。 最近幾年,美國聯(lián)邦政府試圖尋找對(duì)付化學(xué)、生化、輻射、或核威脅給公眾帶來災(zāi)難的方法。TAT-BH4某天可能成為一種有效防止輻射破壞的藥物。可制造成藥丸的形式并且儲(chǔ)備大量這種藥物。以備高水平輻射對(duì)公眾產(chǎn)生的威脅。 來源:medinews.com Agent Protects Cells from Radiation Effects Even if Given After Exposure Scientists have developed a compound that protects cells from the deadly effects of radiation, regardless of whether it is given before or after exposure. No agents yet exist to protect the public from the high levels of radiation that could be released by a 揹irty?bomb or nuclear explosion. Such excessive exposure typically causes death within weeks as the radiation destroys blood cells crucial to clotting and fighting infection, along with the stem cells needed to replenish their supply. Using this agent in mice, the investigators from Washington University School of Medicine in St. Louis (MO, USA) found that the treatment helped protect rapidly dividing cells that are most susceptible to radiation-induced death, providing proof in principle that it is possible to fend off radiation damage, according to a study published in the April 6, 2007, issue of the journal Biochemical and Biophysical Research Communications. Current treatments for severe radiation exposure, also called acute radiation syndrome, are limited to drugs that enhance the production of blood cells and platelets, but this approach is useless if underlying stem cells are also killed off. Furthermore, there are no available treatments that can be given after exposure to limit damage to cells. The investigators developed the agent by attaching a portion of the Bcl-xL protein already known to block cell death--a snippet called BH4--to the HIV protein TAT, which can deftly carry other molecules into cells. They gave the agent intravenously to mice exposed to 5-Gy radiation. In humans, this degree of exposure would cause a sharp decrease in blood cells, leaving individuals with an increased risk of infection and bleeding. The researchers discovered that the treatment helped protect rapidly dividing T cells and B cells in the spleen--immune system cells that are prone to radiation damage--whether it was given 30 minutes before radiation exposure or 30 minutes afterward. Follow-up data suggest that TAT-BH4 is still effective when it is given to irradiated mice one hour after exposure, and the researchers plan additional research to determine how long after exposure the agent can prevent radiation-induced apoptosis. In the past several years, the U.S. federal government has devoted increasing resources to the development of countermeasures that protect the public from chemical, biologic, radiologic, or nuclear attack. TAT-BH4 may one day be a viable candidate because hypothetically it could be given after radiation exposure, administered in pill form, and synthesized and stored in large quantities--all characteristics that would be beneficial for treating large groups of individuals exposed to high levels of radiation, according to Dr. Hotchkiss. 《美迪醫(yī)訊》歡迎您參與新聞投稿,業(yè)務(wù)咨詢: 美迪醫(yī)療網(wǎng)業(yè)務(wù)咨詢
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