生物谷报的：有人喜欢大蒜，有人讨厌大蒜，但很少有人会把大蒜和疼痛扯上关系。不过，研究结果表明，痛觉神经会对大蒜中的硫基化学物质产生反应。新出版的美国《国家科学院学报》上刊载的一项研究报告称，实际上，人体对大蒜的反应机制与对辣椒和芥末的反应机制是相同的。
旧金山加利福尼亚大学细胞与分子药理学系的戴维·朱利叶斯说，他是在对痛觉机制进行研究时得到这一发现的。朱利叶斯发现，当实验鼠的一组痛觉神经元激活一个名为TRPAI的细胞膜的通道时，就会导致大脑释放出刺激血管膨胀和红肿的化学物质。朱利叶斯表示，了解这些神经如何起作用有助于研究人员更好地认识关节炎和一些肌肉疾病是怎样逐渐发展的。他解释说：“人们能利用这些天然产品导致疼痛的机制进行非常有意思的药理学探究。”
俄亥俄州立大学的苏珊·特拉弗斯说，对大蒜化合物有反应的神经元，只是那些对辣椒中的辣椒素有反应的神经的一个子系统，这是这份研究报告最有趣的发现。有些被称为“发臭玫瑰”的大蒜是葱属植物，所有葱属植物都产生硫基化合物，从而使这些植物具有刺激性。其中一种名为蒜素的化合物能够刺激一些痛觉神经，它在大蒜中尤为突出。除了用于烹调外，大蒜在民间医药的应用也有悠久的历史，它一直被用于治疗高血压、胆固醇甚至血栓等疾病。（科技日报）
生物谷推荐原始出处：
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
