羟基红花黄色素A对脑组织蛋白质羰基化影响的体外研究
发布时间：2018-10-26 07:47
【摘要】：目的研究羟基红花黄色素A(HSYA)对体外ONOO~-途径和亚铁血红素/亚硝酸钠/过氧化氢(heme/NaNO_2/H_2O_2)途径引起脑组织蛋白质羰基化的影响。方法分别模拟体内ONOO~-、heme/NaNO_2/H_2O_2羰基化途径,以脑组织蛋白为羰基化底物,分为空白对照组、对照组及低、高浓度组(以HSYA 0.1 mmol/L、1 mmol/L干预)。以2、4-二硝基苯肼(2、4-dinitrophenylhydrazine,DNPH)法检测蛋白质羰基化水平。结果 ONOO~-途径和heme/NaNO_2/H_2O_2途径均可以增加脑组织匀浆中羰基蛋白的含量。HSYA预处理可浓度依赖性地降低ONOO~-途径诱导的蛋白质羰基化水平,低、高浓度组羰基蛋白含量分别降低了26.13%、46.23%,差异有统计学意义(F=14.265,P0.05)。HSYA预处理对体外heme/NaNO_2/H_2O_2途径诱导的蛋白质羰基化没有明显抑制作用,差异无统计学意义(P0.05)。结论 HSYA可剂量依赖性地抑制ONOO~-途径在体外对脑组织蛋白的羰基化修饰;提示HSYA抑制蛋白质羰基化反应可能是其对抗脑血管疾病与神经系统变性疾病的分子机制之一。
[Abstract]:Objective to study the effects of hydroxysafflor yellow A (HSYA) on the carbonylation of protein in brain tissue induced by ONOO~- pathway and hemin / sodium nitrite / hydrogen peroxide (heme/NaNO_2/H_2O_2) pathway in vitro. Methods ONOO~-,heme/NaNO_2/H_2O_2 carbonylation pathway was simulated in vivo, and brain tissue protein was used as carbonylation substrate. It was divided into blank control group, control group and low and high concentration groups (treated with HSYA 0.1 mmol/L,1 mmol/L). The level of carbonylation of protein was determined by DNPH method with 2o 4-dinitrophenylhydrazinehydrazinehydrazineine (DNPH). Results both ONOO~- pathway and heme/NaNO_2/H_2O_2 pathway could increase the content of carbonyl protein in brain homogenate, HSYA pretreatment could decrease the level of protein carbonylation induced by ONOO~- pathway in a concentration-dependent manner. The content of carbonyl protein in high concentration group decreased 26.13% and 46.23%, respectively, and the difference was statistically significant (F < 14.265, P < 0.05). P05). HSYA pretreatment had no significant inhibitory effect on protein carbonylation induced by heme/NaNO_2/H_2O_2 pathway in vitro, but the difference was not statistically significant (P0.05). Conclusion HSYA can inhibit the carbonylation modification of brain tissue proteins by ONOO~- pathway in vitro in a dose-dependent manner, suggesting that the inhibition of protein carbonylation by HSYA may be one of its molecular mechanisms against cerebrovascular diseases and neurodegenerative diseases.
【作者单位】： 河北省邢台市人民医院神经内二科;河北省邢台市第三医院神经内一科;天津医科大学总医院天津市神经病学研究所;
【分类号】：R741
，
本文编号：2295042
[Abstract]:Objective to study the effects of hydroxysafflor yellow A (HSYA) on the carbonylation of protein in brain tissue induced by ONOO~- pathway and hemin / sodium nitrite / hydrogen peroxide (heme/NaNO_2/H_2O_2) pathway in vitro. Methods ONOO~-,heme/NaNO_2/H_2O_2 carbonylation pathway was simulated in vivo, and brain tissue protein was used as carbonylation substrate. It was divided into blank control group, control group and low and high concentration groups (treated with HSYA 0.1 mmol/L,1 mmol/L). The level of carbonylation of protein was determined by DNPH method with 2o 4-dinitrophenylhydrazinehydrazinehydrazineine (DNPH). Results both ONOO~- pathway and heme/NaNO_2/H_2O_2 pathway could increase the content of carbonyl protein in brain homogenate, HSYA pretreatment could decrease the level of protein carbonylation induced by ONOO~- pathway in a concentration-dependent manner. The content of carbonyl protein in high concentration group decreased 26.13% and 46.23%, respectively, and the difference was statistically significant (F < 14.265, P < 0.05). P05). HSYA pretreatment had no significant inhibitory effect on protein carbonylation induced by heme/NaNO_2/H_2O_2 pathway in vitro, but the difference was not statistically significant (P0.05). Conclusion HSYA can inhibit the carbonylation modification of brain tissue proteins by ONOO~- pathway in vitro in a dose-dependent manner, suggesting that the inhibition of protein carbonylation by HSYA may be one of its molecular mechanisms against cerebrovascular diseases and neurodegenerative diseases.
【作者单位】： 河北省邢台市人民医院神经内二科;河北省邢台市第三医院神经内一科;天津医科大学总医院天津市神经病学研究所;
【分类号】：R741
，
本文编号：2295042
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