异甘草素对PC12细胞缺氧前后LDH和SOD活性的影响  被引量:12

Effect of isoliquiritigenin on LDH and SOD activity in PC12 cells before and after hypoxia

在线阅读下载全文

作  者:季玮[1] 李长栋[1] 荔志云[1] 孙建军[1] 付亚杰[1] 

机构地区:[1]兰州军区兰州总医院神经外科,甘肃兰州730050

出  处:《中华神经外科疾病研究杂志》2016年第2期132-135,共4页Chinese Journal of Neurosurgical Disease Research

摘  要:目的观察异甘草素对缺氧诱导神经细胞损伤过程中乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)的影响。方法采用体外培养PC12细胞;建立细胞缺氧损伤模型。将细胞分为C(对照组)、H(模型组,即单纯缺氧组)、H1(异甘草素低剂量组)、H2(异甘草素中剂量组)、H3(异甘草素高剂量组)。即H1、H2、H3加入对应浓度的异甘草素后与H一同放入缺氧环境中,培养时间结束后,再进行统一处理。光学显微镜观察PC12细胞形态;测定上清液中LDH、SOD的含量。结果 PC12细胞在缺氧后乳酸脱氢酶(LDH)显著升高,超氧化物歧化酶(SOD)明显减低,而经异甘草素(ISL)干预后,细胞上清液中LDH水平明显下降,SOD含量有所提高。结论缺氧对PC12细胞的增殖具有一定的抑制作用,使超氧化物歧化酶(SOD)活性降低,乳酸脱氢酶(LDH)漏出增加。异甘草素(ISL)能够逆转缺氧对PC12细胞的抑制作用,可能通过提高培养液中SOD活性,防止脂质过氧化,稳定细胞膜,降低LDH的释放,而起到细胞保护作用。Objective Effect of isoliquiritigenin( ISL) on lactate dehydrogenase( LDH) and superoxide dismutase( SOD) in hypoxia-induced nerve cell damage was discussed.Methods PC12 cells were cultured in vitro to establish hypoxic injury model.The cells were divided into C( control group),H( model group,namely the hypoxia group),H1( isoliquiritigenin low dose group),H2( isoliquiritigenin middle dose group),H3( isoliquiritigenin high dose group).H1,H2,H3 with corresponding concentration of hormone and H were put in hypoxic environment for culture.Morphology of PC12 were observed under microscope.Lactate dehydrogenase and SOD in the supernatant lactate were determined.Results LDH in PC12 cells after hypoxia treatment was increased significantly,while SOD was significantly decreased.After adding isoliquiritigenin( ISL),LDH in the cell supernatant lactate was significantly decreased,but SOD was increased.Conclusion Hypoxia inhibits the proliferation of PC12 cells to some extent,by reducing SOD activity and increasing lactate LDH leakage.ISL can reverse the inhibition of hypoxia on PC12 cells.It may protect the cells by improving the SOD activity in culture medium,preventing lipid peroxidation,maintaining membrane stability,and reducing LDH release.

关 键 词:缺氧 PC12细胞 异甘草素 

分 类 号:R651[医药卫生—外科学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象