کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5637996 1583273 2017 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Dexamethasone promotes regeneration of crushed inferior alveolar nerve by inhibiting NF-κB activation in adult rats
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی دندانپزشکی، جراحی دهان و پزشکی
پیش نمایش صفحه اول مقاله
Dexamethasone promotes regeneration of crushed inferior alveolar nerve by inhibiting NF-κB activation in adult rats
چکیده انگلیسی


- Local administration of dexamethasone could promote inferior alveolar nerve regeneration.
- Dexamethasone could inhibit NF-κB more effectively than PDTC.
- Dexamethasone could be a promising treatment of inferior alveolar nerves regeneration.

PurposeNuclear factor kappa B (NF-κB), which is closely related to inflammation, has become a topic of interest for research. The aim of this study is to investigate the effects of dexamethasone (Dex), an inhibitor of NF-κB, on inferior alveolar nerve injury in adult rats.Materials and methodsThe crushed inferior alveolar model is established in Wistar rats and they are randomly divided into three groups according to treatment: pyrrolidine dithiocarbamate (PDTC), dexamethasone (Dex), and saline (physiological saline). After treatment, the rats are respectively sacrificed at 3, 7, and 14 d, and inferior alveolar nerves are extracted for histochemical and western blot analysis.ResultCompared with the PDTC and saline groups, nerve fibers in the Dex group are regularly arranged with few vacuoles, which is similar to normal inferior alveolar nerves. Immunofluorescent results show significantly decreased NF-κB expression in the Dex group. Western bolt shows higher expression of GAP-43 and lower expression of NF-κB.ConclusionTaken together, all results show that dexamethasone significantly improved the regeneration of crushed inferior alveolar nerves by inhibiting NF-κB activation in adult rats.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Archives of Oral Biology - Volume 80, August 2017, Pages 101-109
نویسندگان
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