中国现代医学杂志2017，Vol.27Issue(23)：1-6,6.DOI:10.3969/j.issn.1005-8982.2017.23.001
NF-κB在右美托咪定抑制利多卡因神经毒性中的作用
Role of NF-kappa B in Dexmedetomidine-induced inhibition of Lidocaine neurotoxicity
摘要
Abstract
Objective To investigate the role of NF-κB in regulation of Lidocaine-induced spinal cord neurotoxicity of rats with sciatic nerve injury (SNI). Methods Forty male SD rats were randomly divided into 5 groups (8 in each): healthy control group (group C), SNI model group (group S), SNI+Lidocaine group (group SL), SNI+Lidocaine+Dexmedetomidine group (group SLD), SNI+Lidocaine+Dexmedetomidine+NF-κB blocker group (group SLDB) with the random number generator in SPSS 17.0 software. All rats had epidural catheterization. But the group C had no other intervention. After the pain was stable, the rats in the group S were intrathecally injected with saline 20 μl, those in the group SL were intrathecally injected with 10%Lidocaine 20 μl, those in the group SLD were intrathecally injected with 10% Lidocaine 20 μl and then intraperitoneally injected with 75μg/kg Dexmedetomidine, those in the group SLDB were intrathecally injected with 40μg of Pyrrolidine dithiocarbamate (PDTC) on the basis of the group SLD. The drugs were injected once a day for 7 d. Then L4-L6 segments of the spinal cord were extracted from the rats after anesthesia. Morphological changes of the spinal cord were observed by transmission electron microscope. TUNEL fluorescence staining was used to observe the apoptosis of spinal dorsal horn cells. The expressions of Bax and caspase-1 were detected by Western blot. TNF-α and IL-1β levels in spinal cord homogenate were detected by ELISA. Results Compared with the group S, the mechanical threshold of the groups SL, SLD and SLDB increased, so did the number of apoptic cells and the expressions of Bax, caspase-1, TNF-α and IL-1β ( <0.05). Compared with the group SL, the number of apoptic cells and the expressions of Bax, caspase-1, TNF-α and IL-1β in the groups SLD and SLDB decreased ( <0.05). Compared with the group SLD, the number of apoptic cells and the expression of Bax, caspase-1, TNF-α and IL-1β increased in the group SLDB ( <0.05). Conclusions Activation of NF-κB pathway, inhibition of inflammation and apoptosis may be the mechanism of Dexmedetomidine's inhibition of Lidocaine-induced neurotoxicity in SNI model rats.关键词
核转录因子-κB/利多卡因/右美托咪定/凋亡/炎症/神经毒性Key words
NF-κB/Lidocaine/Dexmedetomidine/apoptosis/inflammation/neurotoxicity分类
医药卫生引用本文复制引用
覃思平,周增华,蒋宗滨,张爱民,何睿林..NF-κB在右美托咪定抑制利多卡因神经毒性中的作用[J].中国现代医学杂志,2017,27(23):1-6,6.基金项目
广西自然科学基金(No:2013GXNSFAA019137) （No:2013GXNSFAA019137）
