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Analysis of the mechanisms underlying the antinociceptive effect of epicatechin in diabetic rats

机译：表儿茶素抗糖尿病作用的机制研究

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Aims The purpose of this study was to investigate the antinociceptive effect of epicatechin as well as the possible mechanisms of action in diabetic rats. Main methods Rats were injected with streptozotocin to produce hyperglycemia. The formalin test was used to assess the nociceptive activity. Key findings Acute pre-treatment with epicatechin (0.03-30 mg/kg, i.p.) prevented formalin-induced nociception in diabetic rats. Furthermore, daily or every other day treatment for 2 weeks with epicatechin (0.03-30 mg/kg, i.p.) also prevented formalin-induced nociception in diabetic rats. Acute epicatechin-induced antinociception was prevented by l-NAME (N ω-nitro-l-arginine methyl ester hydrochloride, 1-10 mg/kg, non-selective nitric oxide synthesis inhibitor), 7-nitroindazole (0.1-1 mg/kg, selective neuronal nitric oxide synthesis inhibitor), ODQ (1H-(1,2,4)- oxadiazolo(4,2-a)quinoxalin-1-one, 0.2-2 mg/kg, guanylyl cyclase inhibitor) or glibenclamide (1-10 mg/kg, ATP-sensitive K+ channel blocker). Moreover, epicatechin (3 mg/kg)-induced antinociception was fully prevented by methiothepin (0.1-1 mg/kg, serotonergic receptor antagonist), WAY-100635 (0.03-0.3 mg/kg, selective 5-HT1A receptor antagonist) or SB-224289 (0.03-0.3 mg/kg, selective 5-HT1B receptor antagonist). In contrast, BRL-15572 (0.03-0.3 mg/kg, selective 5-HT1D receptor antagonist) only slightly prevented the antinociceptive effect of epicatechin. Naloxone (0.1-1 mg/kg, opioid antagonist) did not modify epicatechin's effect. Significance Data suggest the involvement of the nitric oxide-cyclic GMP-K+ channel pathway as well as activation of 5-HT1A and 5HT1B, and at a lesser extent, 5-HT1D, but not opioid, receptors in the antinociceptive effect of epicatechin in diabetic rats. Our data suggest that acute or chronic treatment with epicatechin may prove to be effective to treat nociceptive hypersensitivity in diabetic patients.
机译：目的本研究的目的是研究表儿茶素的抗伤害感受作用以及在糖尿病大鼠中可能的作用机制。主要方法给大鼠注射链脲佐菌素以产生高血糖。使用福尔马林测试评估伤害感受活性。主要发现用表儿茶素（0.03-30 mg / kg，腹膜内）进行急性预处理可以预防福尔马林对糖尿病大鼠的伤害感受。此外，每天或隔两天用表儿茶素（0.03-30 mg / kg，腹腔注射）治疗也能预防糖尿病大鼠中福尔马林引起的伤害感受。 l-NAME（Nω-硝基-1-精氨酸甲酯盐酸盐，1-10 mg / kg，非选择性一氧化氮合成抑制剂），7-硝基吲唑（0.1-1 mg / kg）可预防急性表儿茶素诱导的抗伤害感受，选择性神经元一氧化氮合成抑制剂），ODQ（1H-（1,2,4）-oxadiazolo（4,2-a）quinoxalin-1-one，0.2-2 mg / kg，胍基环化酶抑制剂）或glibenclamide（1 -10 mg / kg，ATP敏感性K +通道阻滞剂）。此外，美索托平（0.1-1 mg / kg，血清素能受体拮抗剂），WAY-100635（0.03-0.3 mg / kg，选择性5-HT1A受体拮抗剂）或SB完全预防了表儿茶素（3 mg / kg）诱导的镇痛作用。 -224289（0.03-0.3 mg / kg，选择性5-HT1B受体拮抗剂）。相反，BRL-15572（0.03-0.3 mg / kg，选择性5-HT1D受体拮抗剂）仅轻微阻止了表儿茶素的抗伤害感受作用。纳洛酮（0.1-1 mg / kg，阿片类药物拮抗剂）未改变表儿茶素的作用。重要数据表明，一氧化氮-环GMP-K +通道途径以及5-HT1A和5HT1B的激活以及5-HT1D（但不是阿片类）受体的激活参与了表儿茶素在糖尿病中的抗伤害感受作用大鼠。我们的数据表明，表儿茶素的急性或慢性治疗可能被证明可有效治疗糖尿病患者的伤害性超敏反应。

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