Andreone P, Cursaro C, Gasbarrini G
I Patologia Medica, University of Bologna, Policlinico S. Orsola, Italy.
J Hepatol. 1993 Sep;19(2):228-31. doi: 10.1016/s0168-8278(05)80576-8.
Arachidonic acid metabolites seem to play an important role in modulating the post-receptorial activity of interferon-alpha. In this study the effect of interferon-alpha on prostaglandin E2 production was evaluated in cultured liver tissue in 18 patients with chronic active hepatitis related to viral infection (9 hepatitis B virus (HBV) and 9 hepatitis C virus (HCV) positive) and in 7 uninfected patients with various liver diseases. The results show that interferon-alpha induces a significant increase in prostaglandin E2 production in both HBV and HCV chronic active hepatitis. Since the inhibition of the cyclooxygenase pathway increases antiviral protein synthesis and prostaglandin E2 has an immunosuppressive activity, this finding seems to suggest that a combined therapy (interferon-alpha plus non-steroidal anti-inflammatory drugs) should be indicated at least for patients who do not respond to interferon therapy alone.
花生四烯酸代谢产物似乎在调节α干扰素的受体后活性中发挥重要作用。在本研究中,评估了α干扰素对18例与病毒感染相关的慢性活动性肝炎患者(9例乙型肝炎病毒(HBV)阳性和9例丙型肝炎病毒(HCV)阳性)以及7例患有各种肝脏疾病的未感染患者的培养肝组织中前列腺素E2产生的影响。结果表明,α干扰素在HBV和HCV慢性活动性肝炎中均诱导前列腺素E2产生显著增加。由于抑制环氧化酶途径可增加抗病毒蛋白合成,且前列腺素E2具有免疫抑制活性,这一发现似乎表明,至少对于单独使用干扰素治疗无反应的患者,应采用联合治疗(α干扰素加非甾体抗炎药)。