Department of Physical Therapy, China Medical University, Taichung, Taiwan; Department of Medical Research, Chi-Mei Medical Center, Tainan, Taiwan.
Neurosci Lett. 2013 Sep 27;552:62-5. doi: 10.1016/j.neulet.2013.07.030. Epub 2013 Jul 31.
Diphenidol has been shown to block voltage-gated Na(+) channels, which are associated with specific types of pain. Here, we evaluated the effects of diphenidol on chronic constriction injury (CCI)-evoked allodynia and expression of tumor necrosis factor-α (TNF-α). A peripheral nerve injury was elicited in rats by placing four loosely constrictive ligatures around the sciatic nerve. After intraperitoneal injection of diphenidol, rats were tested for evidence of mechanical allodynia prior to surgery, and on postoperative days 3, 6, 7, 11, 13 and 14. We showed that CCI rats received diphenidol caused dose-dependent increases in mechanical withdrawal threshold. Both diphenidol 2 and 10 μmol/kg groups, but not 0.4 μmol/kg diphenidol, displayed lower TNF-α level in the sciatic nerve than the CCI group (P<0.05) on day 7 after CCI. Our results support the conclusion that systemic diphenidol produced a dose-related inhibition of mechanical allodynia following chronic constriction injury of the sciatic nerve. This antiallodynic effect is related to the decrease of TNF-α expression in the sciatic nerve of CCI rats.
地芬诺酯已被证明可以阻断电压门控钠离子通道，而这种通道与特定类型的疼痛有关。在这里，我们评估了地芬诺酯对慢性缩窄性损伤（CCI）诱发的痛觉过敏和肿瘤坏死因子-α（TNF-α）表达的影响。通过在坐骨神经周围放置四个宽松的结扎线，在大鼠中诱发周围神经损伤。在腹腔注射地芬诺酯后，在手术前和术后第 3、6、7、11、13 和 14 天对大鼠进行机械性痛觉过敏的证据进行测试。我们表明，CCI 大鼠接受地芬诺酯导致机械性撤回阈值呈剂量依赖性增加。CCI 后第 7 天，地芬诺酯 2 和 10 μmol/kg 组，但不是 0.4 μmol/kg 地芬诺酯组，坐骨神经中的 TNF-α水平低于 CCI 组（P<0.05）。我们的结果支持这样的结论，即全身给予地芬诺酯可产生与慢性缩窄性坐骨神经损伤相关的机械性痛觉过敏的剂量相关抑制。这种抗痛觉过敏作用与 CCI 大鼠坐骨神经中 TNF-α表达的降低有关。
