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表木栓醇通过下调神经元凋亡和NMDA受体改善神经性疼痛并恢复脊髓损伤后的功能。

Epifriedelinol Ameliorates the Neuropathic Pain and Recovers the Function in Spinal Cord Injury by Downregulation of Neuronal Apoptosis and NMDA Receptor.

作者信息

Guan Haiying, Yan Ting, Wu Dongyang, Tripathi Alok Shiomurti

机构信息

Department of Spine Surgery, Xi'an Hospital of Traditional Chinese Medicine.

Department of Ultrasound, Xi'an Honghui Hospital.

出版信息

Tohoku J Exp Med. 2022 Sep 29;258(2):143-148. doi: 10.1620/tjem.2022.J065. Epub 2022 Aug 11.

DOI:10.1620/tjem.2022.J065
PMID:35965095
Abstract

Spinal cord injury (SCI) is commonly associated with neuropathic pain, which affects large population. Thus, the presented investigation evaluates the beneficial effect of epifriedelinol against SCI-associated neuropathic pain. SCI injury was induced in rats by clip-compression and rats were treated with epifriedelinol 100 and 200 mg/kg, i.p. for 21 days after the induction of SCI. The effect of epifriedelinol was assessed on neuropathic pain by mechanical allodynia and locomotor function. Level of inflammatory cytokines were assessed in the neuronal tissue using enzyme linked immunosorbent assay (ELISA) and expression of caspase-3 and Bcl2 protein were assessed by western blot assay. Data of investigation reveals that epifriedelinol reduces mechanical allodynia in SCI injured rats. Moreover, it also improves locomotor function in SCI injured rats. There was significant decrease in level of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α in the neuronal tissues of epifriedelinol-treated group than negative control group. Moreover, treatment with epifriedelinol ameliorates the altered expression of caspase 3, Bcl2 and GluN1 and level of glutamate in neuronal tissue of SCI-injured rats. In conclusion, data reveal that epifriedelinol treatment protects neuropathic pain associated with spinal cord injury by downregulating the N-methyl-D-aspartate (NMDA) receptor function.

摘要

脊髓损伤(SCI)通常与神经性疼痛相关,这影响着大量人群。因此,本研究评估了表木栓醇对SCI相关神经性疼痛的有益作用。通过夹压法在大鼠中诱导脊髓损伤,在脊髓损伤诱导后,大鼠腹腔注射100和200 mg/kg的表木栓醇,持续21天。通过机械性异常性疼痛和运动功能评估表木栓醇对神经性疼痛的影响。使用酶联免疫吸附测定(ELISA)评估神经元组织中炎性细胞因子的水平,并通过蛋白质印迹法评估caspase-3和Bcl2蛋白的表达。研究数据表明,表木栓醇可减轻SCI损伤大鼠的机械性异常性疼痛。此外,它还可改善SCI损伤大鼠的运动功能。与阴性对照组相比,表木栓醇治疗组神经元组织中白细胞介素(IL)-1β、IL-6和肿瘤坏死因子(TNF)-α的水平显著降低。此外,表木栓醇治疗可改善SCI损伤大鼠神经元组织中caspase 3、Bcl2和GluN1的表达变化以及谷氨酸水平。总之,数据表明表木栓醇治疗通过下调N-甲基-D-天冬氨酸(NMDA)受体功能来保护与脊髓损伤相关的神经性疼痛。

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