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首页> 外文期刊>Diabetes >Protein Kinase Cβ Selective Inhibitor LY333531 Attenuates Diabetic Hyperalgesia Through Ameliorating cGMP Level of Dorsal Root Ganglion Neurons
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Protein Kinase Cβ Selective Inhibitor LY333531 Attenuates Diabetic Hyperalgesia Through Ameliorating cGMP Level of Dorsal Root Ganglion Neurons

机译：蛋白激酶Cβ选择抑制剂LY333531通过改善背根神经节神经元的cGMP水平减轻糖尿病痛觉过敏

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Streptozocin (STZ)-induced diabetic rats show hyper-algesia that is partially attributed to altered protein kinase C (PKC) activity. Both attenuated neuronal nitric oxide synthase (nNOS)-cGMP system and tetro-dotoxin-resistant (TTX-R) Na channels in dorsal root ganglion neurons may be involved in diabetic hyperal-gesia. We examined whether PKCβ inhibition ameliorates diabetic hyperalgesia and, if so, whether the effect is obtained through action on neurons by testing noci-ceptive threshold in normal and STZ-induced diabetic rats treated with or without PKCβ-selective inhibitor LY333531 (LY) and by assessing the implication of LY in either nNOS-cGMP system or TTX-R Na channels of isolated dorsal root ganglion neurons. The decreased nociceptive threshold in diabetic rats was improved either after 4 weeks of LY treatment or with a single intradermal injection into the footpads. The treatment of LY for 6 weeks significantly decreased p-PKCβ and ameliorated a decrease in cGMP content in dorsal root ganglia of diabetic rats. The latter effect was confirmed in ex vivo condition. The treatment with NO donor for 4 weeks also normalized both diabetic hyperalgesia and decreased cGMP content in dorsal root ganglions. The expressions of nNOS and TTX-R Na channels were not changed with LY treatment. These results suggest that LY is effective for treating diabetic hyperalgesia through ameliorating the decrease in the nNOS-cGMP system.
机译：链脲佐菌素（STZ）诱导的糖尿病大鼠表现出痛觉过敏，其部分归因于蛋白激酶C（PKC）活性的改变。背根神经节神经元中的减弱型神经元一氧化氮合酶（nNOS）-cGMP系统和抗河豚毒素（TTX-R）Na通道都可能参与糖尿病性痛觉过敏。我们检查了PKCβ抑制作用是否改善了糖尿病的痛觉过敏，如果是的话，是否通过在接受或不接受PKCβ选择抑制剂LY333531（LY）治疗的正常和STZ诱导的糖尿病大鼠中通过测试伤害感受性阈值，通过对神经元的作用获得效果？评估LY在孤立的背根神经节神经元的nNOS-cGMP系统或TTX-R Na通道中的意义。 LY治疗4周后或单次皮内注射足垫可改善糖尿病大鼠的伤害感受性阈值。 LY治疗6周可显着降低糖尿病大鼠背根神经节中p-PKCβ的表达，并改善cGMP含量的降低。在离体条件下证实了后者的作用。用NO供体治疗4周也使糖尿病性痛觉过敏正常并且背根神经节中的cGMP含量降低。 LY处理未改变nNOS和TTX-R Na通道的表达。这些结果表明，LY通过改善nNOS-cGMP系统的减少而有效治疗糖尿病痛觉过敏。

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