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阿朴吗啡通过抗氧化活性以及抑制脊髓损伤后的细胞凋亡和炎症发挥治疗作用。

Therapeutic effect of apocynin through antioxidant activity and suppression of apoptosis and inflammation after spinal cord injury.

作者信息

Sun Yijun, Gong Futai, Yin Jichao, Wang Xiaoyan, Wang Xiangyang, Sun Qing, Zhu Zhiqiang, Su Xiaoqiang, Zheng Jie, Liu Li, Li Yang, Hu Xinglv, Li Jia

机构信息

Department of TCM Orthopedics and Traumatology, Xi'an City Hospital of Traditional Chinese Medicine, Xi'an, Shaanxi 710021, P.R. China.

出版信息

Exp Ther Med. 2017 Mar;13(3):952-960. doi: 10.3892/etm.2017.4090. Epub 2017 Jan 25.

DOI:10.3892/etm.2017.4090
PMID:28450925
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5403360/
Abstract

Spinal cord injury (SCI) is a devastating condition affecting hundreds of thousands of people worldwide annually. SCI results in activation of the inflammatory response and apoptosis, and generates oxidative stress, which has deleterious effects on the recovery of motor function. Apocynin, an inhibitor of NADPH oxidase, has been demonstrated to improve neuronal functional recovery in rat models of SCI. However, the efficacy of apocynin treatment post-SCI has not been investigated. The aim of this study was to observe the effects of apocynin on the repair of acute spinal cord damage in rats and to examine the potential beneficial effects. A rat model of SCI was established, and apocynin (50 mg/kg) was administered intraperitoneally at 30 min after SCI and then every 12 h for 3 days. In order to examine oxidative tissue injury, the levels of malondialdehyde and glutathione and activities of myeloperoxidase and superoxide dismutase in the spinal cord tissues were measured. Histological evaluations were also conducted. NeuN labeling, TUNEL staining and caspase 3 immunohistochemical staining were performed to analyze neuronal damage and apoptosis around the lesion. Immunohistochemical analysis was also carried out to observe the expression of CD11b and glial fibrillary acidic protein. The expression levels of bax, bcl-2, tumor necrosis-α, interleukin (IL)-1β and IL-6 in the spinal cord tissue were assayed by western blotting. Finally, locomotor function was evaluated using the inclined plane test and Basso, Beattie and Bresnahan scores. The results showed that treatment with apocynin decreased oxidative damage, alleviated neuronal apoptosis, inhibited the inflammatory response and resulted in the promotion of locomotor function. Therefore, this study confirmed the therapeutic efficacy of apocynin in the repair of SCI, which was probably mediated via the inhibition of apoptosis and the inflammatory response, thus promoting the restoration of nerve function.

摘要

脊髓损伤(SCI)是一种严重的疾病,每年影响着全球数十万人。SCI会导致炎症反应和细胞凋亡的激活,并产生氧化应激,这对运动功能的恢复具有有害影响。Apocynin是一种NADPH氧化酶抑制剂,已被证明可改善SCI大鼠模型中的神经元功能恢复。然而,尚未研究Apocynin在SCI后治疗的疗效。本研究的目的是观察Apocynin对大鼠急性脊髓损伤修复的影响,并探讨其潜在的有益作用。建立了SCI大鼠模型,并在SCI后30分钟腹腔注射Apocynin(50mg/kg),然后每12小时注射一次,持续3天。为了检测氧化组织损伤,测量了脊髓组织中丙二醛和谷胱甘肽的水平以及髓过氧化物酶和超氧化物歧化酶的活性。还进行了组织学评估。进行NeuN标记、TUNEL染色和caspase 3免疫组织化学染色以分析损伤周围的神经元损伤和凋亡。还进行了免疫组织化学分析以观察CD11b和胶质纤维酸性蛋白的表达。通过蛋白质印迹法检测脊髓组织中bax、bcl-2、肿瘤坏死-α、白细胞介素(IL)-1β和IL-6的表达水平。最后,使用斜面试验和Basso、Beattie和Bresnahan评分评估运动功能。结果表明,Apocynin治疗可降低氧化损伤,减轻神经元凋亡,抑制炎症反应,并促进运动功能。因此,本研究证实了Apocynin在SCI修复中的治疗效果,这可能是通过抑制细胞凋亡和炎症反应介导的,从而促进神经功能的恢复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/bb895d08a587/etm-13-03-0952-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/128de8fb22c1/etm-13-03-0952-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/3e1f1b0c7cc3/etm-13-03-0952-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/cf5e330a7bd3/etm-13-03-0952-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/7556522762cb/etm-13-03-0952-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/105e652769e6/etm-13-03-0952-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/bb895d08a587/etm-13-03-0952-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/128de8fb22c1/etm-13-03-0952-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/3e1f1b0c7cc3/etm-13-03-0952-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/cf5e330a7bd3/etm-13-03-0952-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/7556522762cb/etm-13-03-0952-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/105e652769e6/etm-13-03-0952-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70a7/5403360/bb895d08a587/etm-13-03-0952-g05.jpg

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