| 党双双,易 甫,武 锋,陈 伟,李敬霞.芒果苷通过PI3K/Akt/mTOR通路抑制缺氧缺血性脑损伤大鼠神经细胞凋亡及炎症反应[J].现代生物医学进展英文版,2020,(10):1820-1823. |
| 芒果苷通过PI3K/Akt/mTOR通路抑制缺氧缺血性脑损伤大鼠神经细胞凋亡及炎症反应 |
| Mangiferin Inhibits Neuronal Apoptosis and Inflammatory Response in Rats with Hypoxic-ischemic Brain Injury Via PI3K/Akt/mTOR Pathway |
| Received:November 23, 2019 Revised:December 18, 2019 |
| DOI：10.13241/j.cnki.pmb.2020.10.005 |
| 中文关键词: 芒果苷 缺氧缺血性脑损伤 氧化应激 神经细胞凋亡 |
| 英文关键词: Mangiferin Hypoxic ischemic brain damage Oxidative stress Neuron apoptosis |
| 基金项目:陕西省社会发展科技攻关基金项目(2014K12-07) |
| Author Name | Affiliation | E-mail | | DANG Shuang-shuang | Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710032, China | 564601855@qq.com | | YI Fu | Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710032, China | | | WU Feng | Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710032, China | | | CHEN Wei | Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710032, China | | | LI Jing-xia | Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710032, China | |
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| 中文摘要: |
| 摘要 目的：探讨芒果苷抑制缺氧缺血性脑损伤大鼠神经细胞凋亡的机制。方法：将144只SD新生大鼠分为空白组、模型对照组、阳性对照组(尼莫地平，0.4 mg?kg-1?d--1)、芒果苷低、中、高剂量组(50、100、200 mg?kg-1?d-1)。检测脑组织中超氧化物歧化酶(SOD)水平、细胞凋亡率、PI3K/Akt/mTOR通路分子表达量。结果：与空白对照组比较，模型组大鼠脑组织中SOD的含量显著降低、细胞凋亡率显著增加，p-PI3K、p-AKT、p-mTOR的表达量显著减少（P<0.05）；与模型组比较，芒果苷低、中、高剂量组大鼠脑组织中SOD的含量显著增加，细胞凋亡率均显著减少，p-PI3K、p-AKT、p-mTOR的表达量显著增加且芒果苷剂量越大，上述变化越显著（P<0.05）。结论：芒果苷对缺氧缺血性脑损伤大鼠的细胞凋亡及炎症反应具有抑制作用且该抑制作用与抑制PI3K/Akt/mTOR通路有关。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the inhibitory effect of mangiferin on the neuronal apoptosis in rats with hypoxic-ischemic brain damage and its mechanisms. Methods: 144 neonatal rats were divided into four groups: control group, model control group, positive control group(Nimodipine, 0.4 mg?kg-1?d-1), low, middle and high dose of mangiferin group(50, 100, 200 mg?kg-1?d-1). The content of Superoxide dismutase (SOD), apoptosis rate and the expression of PI3K/Akt/mTOR pathway molecular were measured. Results: Compared with the blank control group, the contents of SOD in the brain tissue of the model group was significantly decreased, the apoptosis rate in the brain tissue of the model group was significantly increased, the expression of p-PI3K, p-Akt, p-mTOR significantly decreased (P<0.05); compared with the model group, the contents of SOD was significantly increased, the apoptosis rate in the brain tissue of the low, middle and high dose mangiferin group significantly was decreased, and the expression of p-PI3K, p-Akt, p-mTOR significantly increased and the higher the dose of mangiferin was, the more significant the changes were(P<0.05). Conclusion: Mangiferin can inhibit the apoptosis and inflammatory response in rats with hypoxic-ischemic brain damage, which may ne related to the inhibition of PI3K/Akt/mTOR pathway. |
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