کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4323504 1292348 2016 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Electroacupuncture inhibits pruritogen-induced spinal microglial activation in mice
ترجمه فارسی عنوان
الکترواسکولار مهار فعال سازی میکروگلالیال ستون فقرات ناشی از پرییتوتن را در موش ها متوقف می کند
کلمات کلیدی
الکترو ساکشن، پروریتوژن، فعال سازی میکروگلیال، نخاع
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
چکیده انگلیسی


• Electroacupuncture (EA) reduces 5′-guanidinonaltrindole-induced scratching in mice.
• EA reduces 5′-guanidinonaltrindole-induced microglial activation in the spinal cord.
• EA may be a useful treatment for sensory disorders including itch.

In this study, we examined whether electroacupuncture (EA) represses pruritogen-induced microglial activation. Immunohistochemical studies revealed that a subcutaneous (s.c.) injection of the pruritogen 5′-guanidinonaltrindole (GNTI; 0.3 mg/kg) to the back of the neck in mice induced acute expression of the ionized calcium-binding adaptor molecule 1 (Iba1) in both gray and white matter of the spinal cord, with the highest expression in the dorsal horn area. EA application (2 Hz) to LI4 and LI11 attenuated GNTI-induced scratching behavior and repressed GNTI-induced Iba1 expression and Iba1 (+) microglia in the dorsal horn. In contrast, EA at the ST36 acupoint had no such effects. Confocal image analysis revealed co-expression of phosphorylated p38 and Iba1 in microglia with EA at the ST36 acupoint, but not at the LI4 or LI11 acupoints. In Western blot analysis, s.c. injection of GNTI to the back of the neck increased Iba1 and phospho-p38 expression in the spinal cord as compared with injection of saline, while EA at LI4 and LI11 reduced GNTI-induced expression of Iba1 and phospho-p38. These findings indicate that EA at LI4 and LI11, but not at ST36, reduces GNTI-induced microglial activation in the mouse spinal cord.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1649, Part A, 15 October 2016, Pages 23–29
نویسندگان
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