allopurinol 英 /,ælə(ʊ)'pjʊərɪnɒl/ 美 /,ælo'pjʊrə,nɔl; ,ælo'pjʊrə,nol; ,ælo'pjʊrə,nɑl/
释 义 n. [药] 别嘌呤醇
例 句 In addition, the decrease in ambulatory BP was directly correlated with allopurinol treatment. 此外，持续测量血压的降低直接与别嘌呤醇治疗相关。
作者： Ahmad Safari Sultan Abad
Oxidative and nitrosative stress, as well as mitochondrial dysfunction, have been identified as key factors in the pathogenesis of neuropathic pain. In addition, it has been recognized that glia (microglia and astroglia) in CNS, not only act as supporting cells but also have function as essential factors in the pathogenesis of neuropathic pain. The purine nucleoside has neuromodulatory effects on pain transmission by actions on sensory nerve terminals and actions within the spinal cord. Immunomodulatory effects of adenosine have been studied through the activation of three subtypes A1, A2, and A3 receptors. Allopurinol and its active metabolite, oxypurinol, are potent inhibitors of xanthine oxidase (XO), the enzyme responsible for catalysing hypoxanthine to xanthine and uric acid. For decades, allopurinol has been used for the management of gout and conditions associated with hyperuricemia. This drug has shown therapeutic effects in some pathological states by decreasing oxidative stress. Allopurinol exhibits good penetration to CNS, and has shown beneficial effects in patients with a recent acute ischemic stroke through lowering inflammatory marker, intercellular adhesion molecule-1 levels. But Dawson et. al. (2009) found no protective effect of allopurinol. In other studies antinociception and adenosine mechanisms have been implicated in its actions. However, current findings in a neuropathic pain model are original. In this study, we evaluated anti-allodynic and anti-hyperalgesic effects of intraperitoneal allopurinol on the chronic constriction injury (CCI) model of neuropathic pain in rats. We sought to investigate possible pathways involved by measuring gene expression levels of inducible nitric oxide synthase (iNOS), an enzyme responsible for nitric oxide (NO) production, as well as programed cell death (apoptosis) regulating factors including bax, bcl2 and caspase 3. Furthermore, glial fibrillary acidic protein (GFAP) and ionized binding protein (Iba1) were measured as the indicators of astroglia and microglia activation, respectively. The role of adenosine receptors was evaluated using the A1 receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX), and non-selective receptor antagonist, theophylline.