一种磷酸二酯酶抑制剂异去甲蟛蜞菊内酯对HT-22细胞的保护作用

Protective Effect of Phosphodiesterase Inhibitor DWEL on HT-22 Cells Damage

磷酸二酯酶(PDEs)是催化水解细胞内第二信使cAMP和cGMP的唯一途径,而磷酸二酯酶抑制剂可通过改变cAMP和cGMP的浓度从而调节学习与认知功能障碍等多种生理过程。异去甲蟛蜞菊内酯(Demethylwedelolactone,DWEL)是墨旱莲的主要成分之一。实验采用Alpha试剂盒确认DWEL对PDE2A有一定的抑制作用,其IC50为9.17μmol·L^-1;而对PDE4D和PDE10A无明显抑制作用,说明DWEL对磷酸二酯酶的抑制具有一定选择性。可的松诱导HT-22细胞模型发现,不同浓度的DWEL给药后细胞活力不断提高,浓度到达20μmol·L^-1时,细胞活力为76.98%(P<0.05),结果表明DWEL对神经细胞有一定保护作用。

Phosphodiesterase PDEs are the only pathways that catalyze the hydrolysis of second messenger cAMP and cGMP in cells.Phosphodiesterase(PDE)inhibitors can regulate learning and cognitive dysfunction(AD)by altering the concentrations of cAMP and cGMP.Demethylwedelolactone(DWEL)is one of the main components of Eclipta prostrata L.Alpha kit test confirmed the inhibition effect of Demethylwedelolactone on PDE2A with IC 50 value 9.17μmol·L^-1.However,no obvious inhibition effect was found on PDE4D and PDE10A which indicate Demethylwedelolactone can inhibit PDE2A selectively.HT-22 cell model induced by cortisone showed that Demethylwedelolactone could increase the survival rate of HT-22 cell cells.When the concentration reached 20μmol·L^-1,the cell viability was 76.98%(P<0.05).These results suggested that DWEL could protect HT-22 cell indured by cortisone.