Zhu L Q, Liao X L, Feng Z K, Fan C K
Zhongguo Yao Li Xue Bao. 1989 Jan;10(1):81-4.
Diethylcarbamazine citrate (DEC) at 180-300 mg/kg ip or 560 mg/kg ig inhibited hind paw swelling induced by sc 0.15 ml of carrageenan in normal and adrenalectomized rats. DEC ip 300 mg/kg also inhibited the same swelling induced by sc 2.5% formaldehyde in rats. The proliferation of granuloma induced by cotton-pellets tended to be inhibited by DEC, although not significantly. It inhibited the swelling of mouse ear induced by xylene and the increased vascular permeability induced by ip 0.7% HAC. DEC neither prolonged the survival time in adrenalectomized rats nor increased the weight of the adrenal or plasma cortisol levels in normal rats. DEC decreased the prostaglandin E content in inflammatory tissue, although less than the extent in the indomethacin group. These results indicate that the anti-inflammatory action of DEC is presumably due to the inhibition of synthesis or the release of prostaglandin E, in addition to a possible action mediated by its leukotriene synthesis inhibitor action.
枸橼酸乙胺嗪(DEC)腹腔注射180 - 300毫克/千克或灌胃560毫克/千克可抑制正常和肾上腺切除大鼠皮下注射0.15毫升角叉菜胶所致的后爪肿胀。腹腔注射300毫克/千克的DEC也可抑制大鼠皮下注射2.5%甲醛所致的同样肿胀。DEC对棉球诱导的肉芽肿增殖有一定抑制作用,但不显著。它可抑制二甲苯诱导的小鼠耳肿胀以及腹腔注射0.7%醋酸所致的血管通透性增加。DEC既未延长肾上腺切除大鼠的存活时间,也未增加正常大鼠肾上腺重量或血浆皮质醇水平。DEC可降低炎症组织中前列腺素E的含量,但其降低程度小于吲哚美辛组。这些结果表明,DEC的抗炎作用可能是由于抑制前列腺素E的合成或释放,此外还可能通过其白三烯合成抑制作用介导。