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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Role of ATP-sensitive K + channels in the antinociception induced by non-steroidal anti-inflammatory drugs in streptozotocin-diabetic and non-diabetic rats
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Role of ATP-sensitive K + channels in the antinociception induced by non-steroidal anti-inflammatory drugs in streptozotocin-diabetic and non-diabetic rats

机译：ATP敏感的K +通道在链脲佐菌素和非糖尿病大鼠非甾体类抗炎药诱导的抗伤害感受中的作用

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There is evidence that systemic sulfonylureas block diclofenac-induced antinociception in normal rat, suggesting that diclofenac activates ATP-sensitive K + channels. However, there is no evidence for the systemic interaction between different non-steroidal anti-inflammatory drugs (NSAIDs) and sulfonylureas in streptozotocin (STZ)-diabetic rats. Therefore, this work was undertaken to determine whether two sulfonylureas, glibenclamide and glipizide, have any effect on the systemic antinociception that is induced by diclofenac (30 mg/kg), lumiracoxib (56 mg/kg), meloxicam (30 mg/kg), metamizol (56 mg/kg) and indomethacin (30 mg/kg) using the non-diabetic and STZ-diabetic rat formalin test. Systemic injections of NSAIDs produced dose-dependent antinociception during the second phase of the test in both non-diabetic and STZ-diabetic rats. Systemic pretreatment with glibenclamide (10 mg/kg) and glipizide (10 mg/kg) blocked diclofenac-induced systemic antinociception in the second phase of the test (P 0.05) in both non-diabetic and STZ-diabetic rats. In contrast, pretreatment with glibenclamide or glipizide did not block lumiracoxib-, meloxicam-, metamizol-, and indomethacin-induced systemic antinociception (P 0.05) in both groups. Results showed that systemic NSAIDs are able to produce antinociception in STZ-diabetic rats. Likewise, data suggest that diclofenac, but not other NSAIDs, activated K + channels to induce its systemic antinociceptive effect in the non-diabetic and STZ-diabetic rat formalin test.
机译：有证据表明全身性磺酰脲类药物在正常大鼠中阻断双氯芬酸诱导的抗伤害感受，表明双氯芬酸激活了ATP敏感的K +通道。但是，没有证据表明链脲佐菌素（STZ）糖尿病大鼠中不同的非甾体类抗炎药（NSAID）与磺酰脲之间存在系统性相互作用。因此，这项工作是为了确定两种磺酰脲类，格列本脲和格列吡嗪对双氯芬酸（30 mg / kg），鲁美昔布（56 mg / kg），美洛昔康（30 mg / kg）诱导的全身抗伤害感受是否有任何作用。 ，非糖尿病和STZ糖尿病大鼠福尔马林测试中分别测定了甲硝唑（56 mg / kg）和消炎痛（30 mg / kg）。在非糖尿病和STZ糖尿病大鼠的试验的第二阶段，全身注射NSAID会产生剂量依赖性抗伤害感受。在试验的第二阶段，在非糖尿病和STZ糖尿病大鼠中，用格列苯脲（10 mg / kg）和格列吡嗪（10 mg / kg）进行的全身预处理可阻断双氯芬酸诱导的全身镇痛作用（P <0.05）。相比之下，两组均用格列本脲或格列吡嗪预处理并未阻断鲁美昔布，美洛昔康，美他唑和消炎痛引起的全身镇痛作用（P> 0.05）。结果表明，全身性NSAIDs能够在STZ糖尿病大鼠中产生抗伤害作用。同样，数据表明在非糖尿病和STZ糖尿病大鼠福尔马林试验中，双氯芬酸而非其他NSAID激活了K +通道，以诱导其全身性抗伤害作用。

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