印度國立腦科研究中心科學(xué)家日前表示,，吸煙產(chǎn)生的前致癌原亞硝胺NNK會刺激中樞神經(jīng)系統(tǒng)的白血球攻擊健康細胞,，進而導(dǎo)致大腦急性神經(jīng)損壞。
由印度國立腦科研究中心研究員高許與巴蘇合作進行的這項最新研究指出,，吸煙或嚼食煙草甚或吸二手煙,，都與大腦受損有直接關(guān)系。
高許與巴蘇在發(fā)表的研究簡介中表示,，煙草中常見的化學(xué)復(fù)合成分亞硝胺NNK在人體代謝過程中會轉(zhuǎn)變成為致癌物,，會誘發(fā)支氣管上皮細胞惡化，導(dǎo)致癮君子罹患肺癌,。
但報告又指出,，NNK同時會刺激腦部的免疫細胞，即小膠質(zhì)細胞,，產(chǎn)生過敏反應(yīng),，使得原來僅摧毀不健康或受損細胞的小膠質(zhì)細胞，行動變得激烈,，進而攻擊其它健康的腦細胞,。
巴蘇表示，研究證實煙草中的NNK復(fù)合物,，能對小膠質(zhì)細胞起到相當大程度的活化作用,，但也造成對腦神經(jīng)細胞的傷害。巴蘇去年曾經(jīng)發(fā)表一篇破解乙腦病毒的研究報告。
高許則表示,，這項研究成果將有助了解癮君子神經(jīng)細胞經(jīng)常受損的因素,。他表示，這項研究成果報告將會刊登在7月版的美國《神經(jīng)化學(xué)雜志》,。（生物谷Bioon.com）
生物谷推薦原始出處：
Journal of Neurochemistry DOI:10.1111/j.1471-4159.2009.06203.x
Tobacco carcinogen induces microglial activation and subsequent neuronal damage
1 Debapriya Ghosh, Manoj Kumar Mishra, Sulagna Das, Deepak Kumar Kaushik and Anirban Basu
2 National Brain Research Centre, Manesar, Haryana, India
4-Methylnitrosamino-1-(3-pyridyl)-1-butanone (NNK) is a tobacco-specific procarcinogen. We have investigated whether NNK causes inflammatory upheaval in the brain by activation of resident microglia and astrocyte and result in bystander neuronal damage. We have carried out the work in both in vitro and in vivo models. We have found that treatment with NNK causes significant activation of mouse microglial (BV2) cell line as evident by increase in reactive oxygen species and nitric oxide level. Western blot analysis has showed increase in proinflammatory signaling proteins, proinflammatory effector proteins, and other stress-related proteins. Interestingly, increased levels of proinflammatory cytokines like interleukin (IL)-6, tumor necrosis factor-α, monocyte chemoattractant protein 1 (MCP1), and IL-12p70 are also detected. Work from our in vivo studies has demonstrated similar increase in proinflammatory signaling and effector molecules along with the proinflammatory cytokine levels, following NNK treatment. Immunohistochemical staining of the brain sections of NNK-treated mice reveals massive microglial and astrocyte activation along with distinct foci of neuronal damage. Both in vitro and in vivo results provide strong indication that NNK causes significant upheaval of the inflammatory condition of brain and inflicts subsequent neuronal damage.
