TY - JOUR
T1 - Systemic diphenidol reduces neuropathic allodynia and TNF-alpha overexpression in rats after chronic constriction injury
AU - Chen, Yu Wen
AU - Tzeng, Jann Inn
AU - Liu, Kuo Sheng
AU - Yu, Shu Han
AU - Hung, Ching Hsia
AU - Wang, Jhi Joung
N1 - Funding Information:
The authors gratefully acknowledge the financial support provided for the experiment by the National Science Council of Taiwan ( NSC 100-2314-B-039-017-MY3 and NSC 101-2815-C-039-015-B ). No author has any conflict of interest related to the content of this paper.
PY - 2013/9/27
Y1 - 2013/9/27
N2 - 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 10μmol/kg groups, but not 0.4μmol/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.
AB - 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 10μmol/kg groups, but not 0.4μmol/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.
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U2 - 10.1016/j.neulet.2013.07.030
DO - 10.1016/j.neulet.2013.07.030
M3 - Article
C2 - 23916656
AN - SCOPUS:84884332840
SN - 0304-3940
VL - 552
SP - 62
EP - 65
JO - Neuroscience Letters
JF - Neuroscience Letters
ER -