丁酸钠对小鼠脑缺血再灌注损伤的保护作用
发布时间：2018-07-25 09:39
【摘要】：目的研究不同剂量丁酸钠对脑缺血再灌注损伤急性期小鼠炎症反应、神经元凋亡保护机制。方法选取由ICR小鼠124只,将小鼠随机分为4组(每组31只):假手术组、模型组、低剂量实验组(丁酸钠5 mg·kg~(-1))和高剂量试验组(丁酸钠10 mg·kg~(-1));依据改良Zea-Longa线栓法制备大鼠大脑中动脉栓塞模型,血流阻断2 h后拔出线栓,形成再灌注。假手术组小鼠双侧的颈总动脉暴露但血管不进行结扎,表皮的切口正常的缝合,在24 h以后处死小鼠;模型组、低剂量试验组和高剂量试验组在假手术组基础上,结扎双侧颈总动脉,30 min以后解开结扎线,再灌注2 h后灌胃处理,24 h后处死小鼠。用WST-1检测超氧化物歧化酶(SOD)活力,用硫代巴比妥酸检测丙二醛(MDA)含量,用Western blot检测B淋巴细胞癌-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、丝氨酸/苏氨酸激酶(Akt)和磷酸化Akt(p-Akt)蛋白表达量,用ELISA法检测小鼠脑组织内白细胞介素8(IL-8)、白细胞介素1β(IL~(-1)β)和肿瘤坏死因子-α(TNF-α)的含量。结果模型组、假手术组与高剂量试验组SOD为(115.46±25.07),(153.65±34.81),(146.88±15.63)U·mg~(-1),MDA为(2.13±0.27),(1.42±0.07),(1.43±0.08)nmol·mg~(-1),IL~(-1)β分别为(17.82±3.60),(7.64±1.14),(10.15±2.05)pg·mg~(-1);TNF-α分别为(16.03±1.67),(7.95±0.85),(11.08±0.83)pg·mg~(-1),IL-8分别为(15.03±2.66),(9.52±1.05),(10.28±1.17)pg·mg~(-1);Bax/Bcl-2比值分别为0.67±0.05,1.00±0.00,1.13±0.10;p-Akt/Akt比值分别为0.72±0.06,1.00±0.00,1.18±0.12,模型组分别与假手术组和高剂量试验组比较,差异均有统计学意义(均P0.05)。结论丁酸钠能够抑制炎性因子与氧化应激,使Bcl-2蛋白的表达增加,Bax蛋白的表达减少,从而对神经元的凋亡起到抑制作用。
[Abstract]:Aim to study the protective mechanism of different doses of sodium butyrate on inflammatory response and neuronal apoptosis in mice with acute cerebral ischemia reperfusion injury. Methods 124 ICR mice were randomly divided into 4 groups (31 mice in each group): sham operation group, model group, and model group. Low dose sodium butyrate (5 mg kg ~ (-1) and high dose group (10 mg kg ~ (-1) sodium butyrate) were used to establish the model of middle cerebral artery embolization according to modified Zea-Longa thread embolization method. In sham-operation group, the common carotid artery was exposed but the blood vessel was not ligated, the incision of epidermis was sutured normally, and the mice were killed after 24 hours, while the model group, low-dose test group and high-dose experimental group were on the basis of sham-operation group. After 30 min of ligation of bilateral common carotid artery, the ligation line was untied, and the mice were killed after 24 h of gastric perfusion after 2 h reperfusion. The activity of superoxide dismutase (SOD) was detected by WST-1, malondialdehyde (MDA) by thiobarbituric acid, and the expression of (Bax), serine / threonine kinase (Akt) and phosphorylated Akt (p-Akt) by Western blot. The contents of interleukin-8 (IL-8), interleukin-1 尾 (IL-1 尾) and tumor necrosis factor- 伪 (TNF- 伪) in brain tissue of mice were detected by ELISA method. 缁撴灉妯″瀷缁，
本文编号：2143402
[Abstract]:Aim to study the protective mechanism of different doses of sodium butyrate on inflammatory response and neuronal apoptosis in mice with acute cerebral ischemia reperfusion injury. Methods 124 ICR mice were randomly divided into 4 groups (31 mice in each group): sham operation group, model group, and model group. Low dose sodium butyrate (5 mg kg ~ (-1) and high dose group (10 mg kg ~ (-1) sodium butyrate) were used to establish the model of middle cerebral artery embolization according to modified Zea-Longa thread embolization method. In sham-operation group, the common carotid artery was exposed but the blood vessel was not ligated, the incision of epidermis was sutured normally, and the mice were killed after 24 hours, while the model group, low-dose test group and high-dose experimental group were on the basis of sham-operation group. After 30 min of ligation of bilateral common carotid artery, the ligation line was untied, and the mice were killed after 24 h of gastric perfusion after 2 h reperfusion. The activity of superoxide dismutase (SOD) was detected by WST-1, malondialdehyde (MDA) by thiobarbituric acid, and the expression of (Bax), serine / threonine kinase (Akt) and phosphorylated Akt (p-Akt) by Western blot. The contents of interleukin-8 (IL-8), interleukin-1 尾 (IL-1 尾) and tumor necrosis factor- 伪 (TNF- 伪) in brain tissue of mice were detected by ELISA method. 缁撴灉妯″瀷缁，
本文编号：2143402
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