印度國(guó)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(huì)刺激中樞神經(jīng)系統(tǒng)的白血球攻擊健康細(xì)胞,，進(jìn)而導(dǎo)致大腦急性神經(jīng)損壞,。
由印度國(guó)立腦科研究中心研究員高許與巴蘇合作進(jìn)行的這項(xiàng)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(jiǎn)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(guò)程中會(huì)轉(zhuǎn)變成為致癌物，會(huì)誘發(fā)支氣管上皮細(xì)胞惡化,，導(dǎo)致癮君子罹患肺癌,。
但報(bào)告又指出，NNK同時(shí)會(huì)刺激腦部的免疫細(xì)胞,，即小膠質(zhì)細(xì)胞,，產(chǎn)生過(guò)敏反應(yīng)，使得原來(lái)僅摧毀不健康或受損細(xì)胞的小膠質(zhì)細(xì)胞,，行動(dòng)變得激烈,，進(jìn)而攻擊其它健康的腦細(xì)胞。
巴蘇表示,，研究證實(shí)煙草中的NNK復(fù)合物,，能對(duì)小膠質(zhì)細(xì)胞起到相當(dāng)大程度的活化作用，但也造成對(duì)腦神經(jīng)細(xì)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(bào)告,。
高許則表示，這項(xiàng)研究成果將有助了解癮君子神經(jīng)細(xì)胞經(jīng)常受損的因素,。他表示,，這項(xiàng)研究成果報(bào)告將會(huì)刊登在7月版的美國(guó)《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.
