论文部分内容阅读
目的探讨急性砷暴露小鼠脾脏核转录因子NF-E2相关因子2(NF-E2-related factor 2,Nrf2)及其下游血红素单加氧酶-1(HO-1)和谷胱甘肽-S-转移酶(GST)蛋白的表达。方法将48只健康8周龄清洁级昆明雌性小鼠按体重随机分为4组,分别为对照(生理盐水)组和5、10、20 mg/kg亚砷酸钠染毒组,每组12只。给予小鼠一次性灌胃亚砷酸钠24 h后,测定脾组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力以及Nrf2、HO-1和GST蛋白的表达水平。结果与对照组相比,各剂量亚砷酸钠染毒组小鼠脾组织中MDA含量均增加,差异有统计学意义(P<0.05);20 mg/kg亚砷酸钠染毒组小鼠脾组织中SOD活力和10、20 mg/kg亚砷酸钠染毒组小鼠脾组织中GSH-Px活力均减少,差异有统计学意义(P<0.05)。且随着亚砷酸钠染毒剂量的升高,小鼠脾组织中SOD和GSH-Px活力均呈下降趋势,而MDA含量呈上升趋势。与对照组相比,各剂量亚砷酸钠染毒组小鼠脾组织中HO-1和GSTO1/2蛋白的表达水平及10、20 mg/kg亚砷酸钠染毒组小鼠脾组织中Nrf2蛋白的表达水平均增加,差异有统计学意义(P<0.05);且随着亚砷酸钠染毒剂量的升高,小鼠脾组织中Nrf2、HO-1和GSTO1/2蛋白的表达水平均呈上升趋势。结论急性砷暴露在导致小鼠脾脏发生氧化损伤的同时,能够活化Nrf2信号通路,诱导下游抗氧化相关酶类蛋白表达,这可能是砷暴露刺激机体产生的一种防御应答反应。
Objective To investigate the expression of NF-E2-related factor 2 (Nrf2) and its downstream heme oxygenase-1 (HO-1) and glutathione- S-transferase (GST) protein expression. Methods Forty eight healthy 8-week-old female Kunming mice were randomly divided into 4 groups according to body weight: control (saline) group and 5, 10, 20 mg / kg sodium arsenite exposure group, with 12 only. The mice were given a single intragastric administration of sodium arsenite for 24 h. The contents of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) Nrf2, HO-1 and GST protein expression levels. Results Compared with the control group, the content of MDA in the spleen of mice in each dose of sodium arsenite increased, the difference was statistically significant (P <0.05); 20 mg / kg of sodium arsenite in mice The activity of SOD in spleen tissue and GSH-Px activity in spleen tissue of 10, 20 mg / kg sodium arsenite-treated mice decreased significantly, with statistical significance (P <0.05). And with the dose of sodium arsenite increased, the activity of SOD and GSH-Px in mice spleen showed a downward trend, while the content of MDA showed an upward trend. Compared with the control group, the expression levels of HO-1 and GSTO1 / 2 in the spleen of mice exposed to sodium arsenite at various doses and the concentrations of HO-1 and GSTO1 / 2 in the spleen of 10,20 mg / kg sodium arsenite- (P <0.05). The expression of Nrf2, HO-1 and GSTO1 / 2 in mice spleen was increased with the dose of sodium arsenite increased The levels are on the rise. Conclusions Acute exposure to arsenic can activate the Nrf2 signaling pathway and induce the expression of antioxidant enzymes in downstream tissues. This may be a defensive response to arsenic exposure.