Endoh T, Matsuura H, Tajima A, Izumimoto N, Tajima C, Suzuki T, Saitoh A, Suzuki T, Narita M, Tseng L, Nagase H
Basic Research Laboratories, Toray Industries, Inc., Kanagawa, Japan.
Life Sci. 1999;65(16):1685-94. doi: 10.1016/s0024-3205(99)00417-8.
TRK-820, a new type of 4,5-epoxymorphinan derivative, was investigated in vivo for antinociceptive activities and its selectivity on various opioid receptors in mice. TRK-820 given s.c. or p.o. was found to be 351- and 796-fold more potent than U50,488H with acetic acid-induced abdominal constriction test. The duration of the antinociceptive effect produced by TRK-820 was longer than that produced by mu-opioid receptor agonist morphine or other kappa-opioid receptor agonists. In addition, with four other antinociceptive assays, low temperature hot plate (51 degrees C), thermal tail flick, mechanical tail pressure and tail pinch tests, TRK-820 was also found to be 68- to 328-fold more potent than U-50488H, and 41- to 349-fold more potent than morphine in producing antinociception, as comparing the weight of the different compound. However, TRK-820 was less active in inhibiting the high temperature (55 degrees C) hot plate response. The antinociceptive effects produced by TRK-820 were inhibited by nor-BNI, but not by naloxone or naltrindole (NTI) with the abdominal constriction test, indicating that the antinociception is selectively mediated by the stimulation of kappa-, but not mu- or delta-opioid receptors. Co-administration of TRK-820 with morphine slightly enhanced the antinociception induced by morphine in the mouse hot plate test. On the other hand, pentazocine significantly reduced the morphine-induced antinociception. TRK-820 produced sedation at doses, which are much higher than the doses for producing antinociception. These results indicate that the potent antinociception induced by TRK-820 is mediated via the stimulation of kappa-, but not mu- or delta-opiod receptors.
TRK - 820是一种新型的4,5 - 环氧吗啡喃衍生物,在小鼠体内研究了其镇痛活性及其对各种阿片受体的选择性。通过醋酸诱导的腹部收缩试验发现,皮下或口服给予TRK - 820的效力分别比U50,488H高351倍和796倍。TRK - 820产生的镇痛作用持续时间比μ - 阿片受体激动剂吗啡或其他κ - 阿片受体激动剂产生的持续时间更长。此外,在其他四种镇痛试验中,即低温热板(51℃)、热尾甩、机械性尾压和尾夹试验中,与不同化合物的重量相比,TRK - 820产生镇痛作用的效力也比U - 50488H高68至328倍,比吗啡高41至349倍。然而,TRK - 820在抑制高温(55℃)热板反应方面活性较低。在腹部收缩试验中,TRK - 820产生的镇痛作用被去甲 - BNI抑制,但不被纳洛酮或纳曲吲哚(NTI)抑制,这表明镇痛作用是由κ - 阿片受体的刺激选择性介导的,而非μ - 或δ - 阿片受体。在小鼠热板试验中,TRK - 820与吗啡联合给药略微增强了吗啡诱导的镇痛作用。另一方面,喷他佐辛显著降低了吗啡诱导的镇痛作用。TRK - 820在远高于产生镇痛作用的剂量下产生镇静作用。这些结果表明,TRK - 820诱导的强效镇痛作用是通过刺激κ - 阿片受体介导的,而非μ - 或δ - 阿片受体。