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姜酮通过调节神经炎症和氧化应激缓解创伤性脑损伤后的神经功能缺损。

Germacrone alleviates neurological deficits following traumatic brain injury by modulating neuroinflammation and oxidative stress.

机构信息

Department of Neurology, Linyi Central Hospital, Linyi, 276400, Shandong, China.

Department of Anesthesiology, Linyi Central Hospital, Linyi, 276400, Shandong, China.

出版信息

BMC Complement Med Ther. 2021 Jan 5;21(1):6. doi: 10.1186/s12906-020-03175-0.

DOI:10.1186/s12906-020-03175-0
PMID:33402180
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7786997/
Abstract

BACKGROUND

Germacrone (GM) is a terpenoid compound which is reported to have anti-inflammatory and anti-oxidative effects. However, its role in treating traumatic brain injury (TBI) remains largely unknown.

METHODS

Male C57BL/6 mice were divided into the following groups: control group, TBI group [controlled cortical impact (CCI) model], CCI + 5 mg/kg GM group, CCI + 10 mg/kg GM group and CCI + 20 mg/kg GM group. GM was administered via intraperitoneal injection. The neurological functions (including motor coordination, spatial learning and memory abilities) and brain edema were measured. Nissl staining was used to detect the neuronal apoptosis. Colorimetric assays and enzyme linked immunosorbent assay (ELISA) kits were used to determine the expression levels of oxidative stress markers including myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD), as well as the expressions of inflammatory markers, including tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). Additionally, protein levels of Nrf2 and p-p65 were detected by Western blot assay.

RESULTS

GM significantly ameliorated motor dysfunction, spatial learning and memory deficits of the mice induced by TBI and it also reduced neuronal apoptosis and microglial activation in a dose-dependent manner. Besides, GM treatment reduced neuroinflammation and oxidative stress compared to those in the CCI group in a dose-dependent manner. Furthermore, GM up-regulated the expression of antioxidant protein Nrf2 and inhibited the expression of inflammatory response protein p-p65.

CONCLUSIONS

GM is a promising drug to improve the functional recovery after TBI via repressing neuroinflammation and oxidative stress.

摘要

背景

大根香叶烯(GM)是一种萜烯类化合物,据报道具有抗炎和抗氧化作用。然而,其在治疗创伤性脑损伤(TBI)中的作用在很大程度上尚不清楚。

方法

雄性 C57BL/6 小鼠分为以下几组:对照组、TBI 组(皮质撞击伤模型)、CCI+5mg/kg GM 组、CCI+10mg/kg GM 组和 CCI+20mg/kg GM 组。GM 通过腹腔注射给药。测量神经功能(包括运动协调、空间学习和记忆能力)和脑水肿。尼氏染色法用于检测神经元凋亡。比色法和酶联免疫吸附测定(ELISA)试剂盒用于测定氧化应激标志物髓过氧化物酶(MPO)、丙二醛(MDA)和超氧化物歧化酶(SOD)的表达水平,以及炎症标志物肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的表达水平。此外,通过 Western blot 测定法检测 Nrf2 和 p-p65 的蛋白水平。

结果

GM 显著改善了 TBI 诱导的小鼠运动功能障碍、空间学习和记忆缺陷,并呈剂量依赖性减少神经元凋亡和小胶质细胞激活。此外,GM 治疗以剂量依赖性方式降低了神经炎症和氧化应激,与 CCI 组相比。此外,GM 上调了抗氧化蛋白 Nrf2 的表达并抑制了炎症反应蛋白 p-p65 的表达。

结论

GM 是一种有前途的药物,可通过抑制神经炎症和氧化应激来改善 TBI 后的功能恢复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/627a6de10d80/12906_2020_3175_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/19fcceba4e29/12906_2020_3175_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/1b2945ec1efa/12906_2020_3175_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/bba0caf3b89a/12906_2020_3175_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/a783055f304b/12906_2020_3175_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/35282df07fce/12906_2020_3175_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/627a6de10d80/12906_2020_3175_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/19fcceba4e29/12906_2020_3175_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/1b2945ec1efa/12906_2020_3175_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/bba0caf3b89a/12906_2020_3175_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/a783055f304b/12906_2020_3175_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/35282df07fce/12906_2020_3175_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/267d/7786997/627a6de10d80/12906_2020_3175_Fig6_HTML.jpg

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