生物谷報(bào)的：有人喜歡大蒜，有人討厭大蒜，但很少有人會(huì)把大蒜和疼痛扯上關(guān)系,。不過(guò)，研究結(jié)果表明,，痛覺(jué)神經(jīng)會(huì)對(duì)大蒜中的硫基化學(xué)物質(zhì)產(chǎn)生反應(yīng),。新出版的美國(guó)《國(guó)家科學(xué)院學(xué)報(bào)》上刊載的一項(xiàng)研究報(bào)告稱，實(shí)際上,，人體對(duì)大蒜的反應(yīng)機(jī)制與對(duì)辣椒和芥末的反應(yīng)機(jī)制是相同的,。
舊金山加利福尼亞大學(xué)細(xì)胞與分子藥理學(xué)系的戴維·朱利葉斯說(shuō)，他是在對(duì)痛覺(jué)機(jī)制進(jìn)行研究時(shí)得到這一發(fā)現(xiàn)的,。朱利葉斯發(fā)現(xiàn),，當(dāng)實(shí)驗(yàn)鼠的一組痛覺(jué)神經(jīng)元激活一個(gè)名為TRPAI的細(xì)胞膜的通道時(shí)，就會(huì)導(dǎo)致大腦釋放出刺激血管膨脹和紅腫的化學(xué)物質(zhì),。朱利葉斯表示,，了解這些神經(jīng)如何起作用有助于研究人員更好地認(rèn)識(shí)關(guān)節(jié)炎和一些肌肉疾病是怎樣逐漸發(fā)展的。他解釋說(shuō)：“人們能利用這些天然產(chǎn)品導(dǎo)致疼痛的機(jī)制進(jìn)行非常有意思的藥理學(xué)探究,。”
俄亥俄州立大學(xué)的蘇珊·特拉弗斯說(shuō),，對(duì)大蒜化合物有反應(yīng)的神經(jīng)元，只是那些對(duì)辣椒中的辣椒素有反應(yīng)的神經(jīng)的一個(gè)子系統(tǒng),，這是這份研究報(bào)告最有趣的發(fā)現(xiàn),。有些被稱為“發(fā)臭玫瑰”的大蒜是蔥屬植物，所有蔥屬植物都產(chǎn)生硫基化合物,，從而使這些植物具有刺激性,。其中一種名為蒜素的化合物能夠刺激一些痛覺(jué)神經(jīng),，它在大蒜中尤為突出。除了用于烹調(diào)外,，大蒜在民間醫(yī)藥的應(yīng)用也有悠久的歷史,，它一直被用于治療高血壓、膽固醇甚至血栓等疾病,。（科技日?qǐng)?bào)）
生物谷推薦原始出處：
Published online before print August 8, 2007, 10.1073/pnas.0705924104
PNAS | August 14, 2007 | vol. 104 | no. 33 | 13525-13530
OPEN ACCESS ARTICLE
BIOLOGICAL SCIENCES / PHYSIOLOGY
TRPA1 mediates formalin-induced pain
Colleen R. McNamara*, Josh Mandel-Brehm*, Diana M. Bautista, Jan Siemens, Kari L. Deranian*, Michael Zhao*, Neil J. Hayward*, Jayhong A. Chong*, David Julius,, Magdalene M. Moran*,, and Christopher M. Fanger*
*Hydra Biosciences, Inc., 790 Memorial Drive, Cambridge, MA 02139; and Departments of Physiology and Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143
Contributed by David Julius, July 5, 2007 (received for review June 18, 2007)
The formalin model is widely used for evaluating the effects of analgesic compounds in laboratory animals. Injection of formalin into the hind paw induces a biphasic pain response; the first phase is thought to result from direct activation of primary afferent sensory neurons, whereas the second phase has been proposed to reflect the combined effects of afferent input and central sensitization in the dorsal horn. Here we show that formalin excites sensory neurons by directly activating TRPA1, a cation channel that plays an important role in inflammatory pain. Formalin induced robust calcium influx in cells expressing cloned or native TRPA1 channels, and these responses were attenuated by a previously undescribed TRPA1-selective antagonist. Moreover, sensory neurons from TRPA1-deficient mice lacked formalin sensitivity. At the behavioral level, pharmacologic blockade or genetic ablation of TRPA1 produced marked attenuation of the characteristic flinching, licking, and lifting responses resulting from intraplantar injection of formalin. Our results show that TRPA1 is the principal site of formalin's pain-producing action in vivo, and that activation of this excitatory channel underlies the physiological and behavioral responses associated with this model of pain hypersensitivity.
analgesia | inflammation | trp channel | formaldehyde
