美國科學家最新試驗發(fā)現(xiàn):在“納米蜂”幫助下,,蜂毒可以在不損害健康細胞前提下有效摧毀癌細胞,。
這一研究結果發(fā)表在11日出版的美國《臨床檢查雜志》上。
華盛頓大學醫(yī)學院塞特曼癌癥中心教授塞繆爾·威克萊恩和他的團隊組織這次研究,。
他們給一組老鼠植入黑色素腫瘤,,也就是皮膚癌細胞,在另一組老鼠體內植入人類乳腺癌細胞,。隨后,,研究人員把蜂毒中的主要活性物質——蜂毒肽附著在“納米蜂”上注射進老鼠體內。
經(jīng)過4,、5次注射后,,他們發(fā)現(xiàn),與沒接受注射的老鼠相比,,癌癥老鼠體內乳腺癌腫瘤縮小四分之一,,黑色素腫瘤更是縮小至原來的約十分之一。
“這些‘納米蜂’降落在細胞表面,,它們‘卸載’下來的蜂毒肽會迅速融入目標細胞,”研究領頭人威克萊恩說,。
此外,,當蜂毒肽‘卸載’在細胞上后,“納米蜂”就會溶解并在肺部蒸發(fā),。
研究人員解釋說,,蜂毒肽之所以能夠摧毀癌細胞,,是因為它們接觸細胞表面后可以撕裂細胞膜,破壞細胞內部組織,。“(蜂毒肽)濃度足夠高時,,可以破壞任何接觸到的細胞,”論文另一名作者保羅·施萊辛格說,。
如果將蜂毒肽直接注射進血液,,那么在殺死癌細胞的同時也會導致血液細胞大量“犧牲”,因此科學家設計讓“納米蜂”來充當蜂毒載體,。
“納米蜂”并非真蜂,,而是由全氟碳構成的微粒。它體積大小適中,,既可以運送上千的活性化合物,,也可以在血管里靈巧地游動去接觸細胞膜。
一旦進入體內,,“納米蜂”就會聚集在腫瘤組織處,。此外,為了提高“準確度”,,科學家還在“納米蜂”上加載了特殊化合物來引導它們接近癌細胞,。
試驗顯示,老鼠接受治療時均沒有發(fā)生“附帶損害”:它們的血細胞計數(shù)正常,,也沒有器官受損征兆,。這意味著,蜂毒肽附著“納米蜂”進入血液后不僅可以有效破壞癌細胞還可以避免傷害到健康細胞,。
研究人員說,,蜂毒治療相比化學療法副作用較小,在特定癌癥治療上很有可能取代傳統(tǒng)治療方法,,有可能開啟人類抗癌治療的新篇章,。
參與研究的科學家認為“納米蜂”具有很大潛力,它不僅可能“干掉”已形成的腫瘤組織,,還有可能成功遏制早期癌癥的發(fā)展,。
“我們正在吸收越來越多的腫瘤生物學知識,這可以讓我們從‘納米蜂’入手,,盡快為特定腫瘤造出特定的納米運載物,,”施萊辛格博士說。(生物谷Bioon.com)
生物谷推薦原始出處:
J. Clin. Invest. doi:10.1172/JCI38842.
Molecularly targeted nanocarriers deliver the cytolytic peptide melittin specifically to tumor cells in mice, reducing tumor growth
Neelesh R. Soman1, Steven L. Baldwin2, Grace Hu2, Jon N. Marsh2, Gregory M. Lanza1,2, John E. Heuser3, Jeffrey M. Arbeit4, Samuel A. Wickline1,2,3 and Paul H. Schlesinger3
1Department of Biomedical Engineering,
2Department of Medicine,
3Department of Cell Biology and Physiology, and
4Department of Surgery, Washington University School of Medicine, St. Louis, Missouri, USA.
The in vivo application of cytolytic peptides for cancer therapeutics is hampered by toxicity, nonspecificity, and degradation. We previously developed a specific strategy to synthesize a nanoscale delivery vehicle for cytolytic peptides by incorporating the nonspecific amphipathic cytolytic peptide melittin into the outer lipid monolayer of a perfluorocarbon nanoparticle. Here, we have demonstrated that the favorable pharmacokinetics of this nanocarrier allows accumulation of melittin in murine tumors in vivo and a dramatic reduction in tumor growth without any apparent signs of toxicity. Furthermore, direct assays demonstrated that molecularly targeted nanocarriers selectively delivered melittin to multiple tumor targets, including endothelial and cancer cells, through a hemifusion mechanism. In cells, this hemifusion and transfer process did not disrupt the surface membrane but did trigger apoptosis and in animals caused regression of precancerous dysplastic lesions. Collectively, these data suggest that the ability to restrain the wide-spectrum lytic potential of a potent cytolytic peptide in a nanovehicle, combined with the flexibility of passive or active molecular targeting, represents an innovative molecular design for chemotherapy with broad-spectrum cytolytic peptides for the treatment of cancer at multiple stages.