Mao Mei, Fan Wen, Zheng Yan, Qi Pan, Xi Min, Yao Yuanrong
Department of Neurology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, China.
Evid Based Complement Alternat Med. 2022 Jun 15;2022:8547095. doi: 10.1155/2022/8547095. eCollection 2022.
Guillain-Barré syndrome (GBS) is a common autoimmune disease of the peripheral nervous system, and there is still no effective treatment for GBS. This investigation intends to figure out the effect and mechanism of N-type voltage-gated calcium (Cav2.2) channels on neuropathic pain in GBS.
An experimental autoimmune neuritis (EAN) model was established in Lewis rats induced by myelin P2 peptide and complete Freund's adjuvant. Luxol fast blue (LFB) staining was used for observing the degree of cell infiltration and demyelination in the sciatic nerve of rats, ELISA for detecting IL-6 and TNF- expression in the serum, qRT-PCR, and Western blot for measuring the expression of iNOS, MCP-1, and Cav2.2 in the sciatic nerve, respectively.
EAN led to significant decreases in the mechanical withdrawal threshold, thermal withdrawal threshold, and mechanical hyperalgesia threshold and an increase in the withdrawal threshold to cold stimulation. The serum IL-6 and TNF- expression was significantly increased, and the mRNA and protein expression of iNOS, MCP-1, and Cav2.2 in the sciatic nerve were significantly increased in the EAN rats. However, silencing Cav2.2 expression could significantly reverse the above EAN-caused results.
Silencing Cav2.2 expression can significantly reduce the clinical score, pathological injury, and mechanical allodynia, reducing the release of inflammatory factors, thus improving neuropathic pain in EAN rats.
吉兰-巴雷综合征（GBS）是一种常见的周围神经系统自身免疫性疾病，目前仍无有效的治疗方法。本研究旨在探讨N型电压门控钙（Cav2.2）通道对GBS神经性疼痛的影响及机制。
采用髓鞘P2肽和完全弗氏佐剂诱导Lewis大鼠建立实验性自身免疫性神经炎（EAN）模型。用Luxol快速蓝（LFB）染色观察大鼠坐骨神经的细胞浸润和脱髓鞘程度，用酶联免疫吸附测定（ELISA）检测血清中白细胞介素-6（IL-6）和肿瘤坏死因子（TNF-）的表达，用实时定量聚合酶链反应（qRT-PCR）和蛋白质免疫印迹法（Western blot）分别检测坐骨神经中诱导型一氧化氮合酶（iNOS）、单核细胞趋化蛋白-1（MCP-1）和Cav2.2的表达。
EAN导致机械性缩足阈值、热缩足阈值和机械性痛觉过敏阈值显著降低，冷刺激缩足阈值升高。EAN大鼠血清IL-6和TNF-表达显著增加，坐骨神经中iNOS、MCP-1和Cav2.2的mRNA和蛋白表达显著增加。然而，沉默Cav2.2表达可显著逆转上述EAN所致结果。
沉默Cav2.2表达可显著降低临床评分、病理损伤和机械性异常性疼痛，减少炎症因子释放，从而改善EAN大鼠的神经性疼痛。
