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Electroacupuncture suppresses glucose metabolism and GLUT-3 expression in medial prefrontal cortical in rats with neuropathic pain
Biological Research ( IF 4.3 ) Pub Date : 2021-08-06 , DOI: 10.1186/s40659-021-00348-0
Menghong Jiang 1 , Xiaomei Chen 1 , Liangping Zhang 1 , Weiting Liu 1 , Xiangmei Yu 1 , Zhifu Wang 1, 2 , Meifeng Zheng 1
Affiliation  

Accumulating evidence has demonstrated that the electroacupuncture (EA) stimulation could effectively alleviate neuropathic pain. The medial prefrontal cortex (mPFC) is a vital part of the cortical representation of pain in the brain, and its glucose metabolism is mostly affected in the progression of pain. However, the central mechanism of EA analgesia remains unclear. Fifty-four male SD rats were equally randomized into sham surgery (Sham) group, chronic constriction injury (CCI) group and EA stimulation (EA) group. The CCI model, involving ligature of the right sciatic nerve, was established in all animals except the Sham group. EA stimulation was applied on the right side acupoints of Huantiao (GB30) and Yanglingquan (GB34) in the EA group. Paw withdrawal threshold (PWT) and paw thermal withdrawal latency (PWL) were measured. The 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET) was used to evaluate glucose metabolism changes in the mPFC. The expression of glucose transporter 3 (GLUT-3) in the mPFC was determined by immune histochemistry and ELISA. Comparing with CCI groups, EA treatment was obviously reversed CCI-induced mechanical allodynia (P < 0.01), thermal hyperalgesia (P < 0.01) and the increase of glucose metabolism in the left mPFC (P < 0.05). Furthermore, EA treatment significantly decreased the protein expression of GLUT-3 in the left mPFC (P < 0.01). Our results indicate that EA analgesia effect may be related to suppressing the glucose metabolism and GLUT-3 expression in the mPFC. This study could provide a potential insight into the central mechanisms involved in the analgesic effect of EA.

中文翻译:

电针抑制神经病理性疼痛大鼠内侧前额叶皮质葡萄糖代谢及GLUT-3表达

越来越多的证据表明,电针(EA)刺激可以有效缓解神经性疼痛。内侧前额叶皮层 (mPFC) 是大脑疼痛皮层表征的重要组成部分,其葡萄糖代谢主要受疼痛进展影响。然而,电针镇痛的中心机制仍不清楚。54只雄性SD大鼠随机分为假手术(Sham)组、慢性缩窄性损伤(CCI)组和电针刺激(EA)组。除Sham组外,所有动物均建立右侧坐骨神经结扎CCI模型。电针组电针刺激右侧腧调(GB30)、阳陵泉(GB34)。测量爪子缩回阈值(PWT)和爪子热缩回潜伏期(PWL)。18 F-氟脱氧葡萄糖正电子发射断层扫描 (FDG-PET) 用于评估 mPFC 中的葡萄糖代谢变化。葡萄糖转运蛋白 3 (GLUT-3) 在 mPFC 中的表达通过免疫组织化学和 ELISA 确定。与CCI组相比,电针治疗明显逆转了CCI引起的机械性异常性疼痛(P < 0.01)、热痛觉过敏(P < 0.01)和左侧mPFC葡萄糖代谢的增加(P < 0.05)。此外,电针治疗显着降低了左侧 mPFC 中 GLUT-3 的蛋白质表达(P < 0.01)。我们的结果表明,电针镇痛作用可能与抑制 mPFC 中的葡萄糖代谢和 GLUT-3 表达有关。这项研究可以提供对 EA 镇痛作用所涉及的中心机制的潜在见解。
更新日期:2021-08-07
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