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首页> 外文期刊>Drug Design, Development and Therapy >The effects of vasoactive intestinal peptide in the rat model of experimental autoimmune neuritis and the implications for treatment of acute inflammatory demyelinating polyradiculoneuropathy or Guillain–Barré syndrome
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The effects of vasoactive intestinal peptide in the rat model of experimental autoimmune neuritis and the implications for treatment of acute inflammatory demyelinating polyradiculoneuropathy or Guillain–Barré syndrome

机译：血管活性肠肽在实验性自身免疫性神经炎大鼠模型中的作用及其对急性炎症性脱髓鞘性多发性神经根神经病或格林-巴利综合征的治疗意义

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Background: Guillain–Barré syndrome is an acute inflammatory demyelinating polyneuropathy that is characterized histologically by demyelination of peripheral nerves and nerve roots, infiltrates of T lymphocytes, and an inflammatory response that includes macrophage infiltrates. The aim of this study was to evaluate the effects of vasoactive intestinal peptide (VIP) in a rat model of experimental autoimmune neuritis (EAN). Methods: Forty male Lewis rats were divided into a control group (N=10), an EAN group (N=10), an EAN group treated with 15 nmol of VIP (N=10), and an EAN group treated with 30 nmol of VIP (N=10). The rat model was created by subcutaneous injection of P2 polypeptide (200 μg P257–81) into the base of the tail. Intraperitoneal injection of VIP was given on day 7. Rats were weighed and functionally evaluated using an EAN score (0–10). On day 16, the rats were euthanized. The sciatic nerve was examined histologically and using immunohistochemistry with antibodies against CD8, CD68, and forkhead box p3 (Foxp3). Serum concentrations of IL-17 and interferon-α (IFN-α) were measured by ELISA on day 16 after creating the EAN model. Results: The VIP-treated EAN groups had increased body weight and improved EAN scores compared with the untreated EAN group. CD8-positive and CD68-positive cells were significantly reduced in the EAN group treated with 30 nmol of VIP compared with 15?nmol of VIP. Foxp3-positive cells were significantly decreased in both EAN groups treated with VIP, and serum concentrations of IL-17 and IFN-α were significantly lower compared with the untreated EAN group ( P 0.05). Conclusion: In a rat model of EAN, treatment with VIP resulted in functional improvement, reduced nerve inflammation, and decreased serum levels of inflammatory cytokines.
机译：背景：格林-巴利综合征是一种急性炎症性脱髓鞘性多发性神经病，其组织学特征是周围神经和神经根脱髓鞘，T淋巴细胞浸润以及包括巨噬细胞浸润的炎症反应。这项研究的目的是评估血管活性肠肽（VIP）在实验性自身免疫性神经炎（EAN）大鼠模型中的作用。方法：40只雄性Lewis大鼠分为对照组（N = 10），EAN组（N = 10），用15 nmol VIP组治疗的EAN组（N = 10）和EAN 30 mol组治疗的EAN组。 VIP（N = 10）。通过将P2多肽（200μgP257–81）皮下注射到尾根中来创建大鼠模型。在第7天进行腹膜内注射VIP。对大鼠称重并使用EAN评分（0-10）进行功能评估。在第16天，将大鼠安乐死。组织学检查坐骨神经，并用免疫组织化学方法检测抗CD8，CD68和叉头盒p3（Foxp3）的抗体。在建立EAN模型后的第16天，通过ELISA测定血清IL-17和干扰素-α（IFN-α）的浓度。结果：与未治疗的EAN组相比，VIP治疗的EAN组体重增加，并且EAN得分提高。与15nmol VIP组相比，用30 nmol VIP组治疗的EAN组CD8阳性和CD68阳性细胞明显减少。与未治疗的EAN组相比，用VIP治疗的两个EAN组中Foxp3阳性细胞均显着减少，并且IL-17和IFN-α的血清浓度显着降低（P <0.05）。结论：在EAN大鼠模型中，VIP治疗可改善功能，减少神经炎症，并降低血清炎性细胞因子水平。

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