Liang Jiexian, Bi Hua, Ji Wenjin
Division of Anesthesiology, Department of Cardiovascular Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, PR China.
Neuroreport. 2010 Feb 17;21(3):201-5. doi: 10.1097/WNR.0b013e328335b3c5.
Transient receptor potential ankyrin subfamily member 1 (TRPA1) is a nonselective cation channel known as a noxious cold-activated ion channel. Recent findings implicated its involvement in acute and chronic cold nociception processes. Here, we investigated whether TRPA1 is involved in endothelin-1 (ET-1)-induced spontaneous pain-like behavior in C57BL/6J mice. We found that TRPA1 antagonists, HC-030031 and AP18, significantly reduced the pain-like behavior caused by ET-1. AP18 also significantly reduced the pain caused by cinnamaldehyde, an agonist of TRPA-1. However, AP18 did not alleviate the pain caused by capsaicin. The pain-like behavior caused by ET-1 was inhibited by phospholipase C inhibitor, but not by protein kinase C inhibitor. Low dose of ET-1 could potentiate cinnamaldehyde-induced nociception. Our results suggested that TRPA1 is involved in ET-1-induced spontaneous pain-like behavior in mice.
瞬时受体电位锚蛋白亚家族成员1（TRPA1）是一种非选择性阳离子通道，被认为是一种有害冷激活离子通道。最近的研究结果表明它参与了急性和慢性冷痛觉感受过程。在此，我们研究了TRPA1是否参与内皮素-1（ET-1）诱导的C57BL/6J小鼠自发性疼痛样行为。我们发现TRPA1拮抗剂HC-030031和AP18显著降低了ET-1引起的疼痛样行为。AP18也显著减轻了由TRPA-1激动剂肉桂醛引起的疼痛。然而，AP18并未减轻辣椒素引起的疼痛。ET-1引起的疼痛样行为被磷脂酶C抑制剂抑制，但未被蛋白激酶C抑制剂抑制。低剂量的ET-1可增强肉桂醛诱导的伤害感受。我们的结果表明，TRPA1参与了ET-1诱导的小鼠自发性疼痛样行为。
