p-Asarone protects PC12 cells against OGD/ R-induced injury via attenuating Beclin-l-dependent autophagy  

作　　者：Zhen-tao MO Yong-qi FANG Yu-ping HE ShengZHANG 

机构地区：[1]The First Affiliated Hospital of Guangzhou University of Chinese Medicine,Guangzhou 510405,China

出　　处：《Acta Pharmacologica Sinica》2012年第6期737-742,共6页中国药理学报（英文版）

摘　　要：Aim： To explore the effects of β-asarone from Acorus Tatarinowii Schott on autophagy in an ischemic stroke model of PC12 cells. Methods： The ischemic stroke model of PC12 cells was made by OGD/R （2 h oxygen-glucose deprivation followed by 24 h reperfu- sion）. Drug administration was started 1 h before OGD and last for 3 h. Then the cells were incubated in the drug-free and full culture medium under normoxic conditions for 24 h. After the treatments, Beclin-1, intracellular free calcium concentration （[Ca2＋]1） and mitochondrial membrane potential （MMP） were analyzed using flow cytometry. Cell viability was measured using MTT assay. Cell morphology was studied under inverted phase contrast microscope, and autophagosomes were observed under transmission electron microscope. Results： Pretreatment with β-asarone （20, 30, or 45 pg/mL） or the calcium channel antagonist nimodipine （10 pmol/L） significantly increased the cell viability and MMP, and decreased Beclin-1 expression and [Ca2＋]i in OGD/R-treated PC12 cells. Under inverted phase contrast microscope, pretreatment with β-asarone or nimodipine dramatically increase the number of cells and improved the cellular morphology. Autophagosomes were found in OGD/R-treated PC12 cells as well as in drug plus OGD/R-treated PC12 cells. Conclusion： β-Asarone protects PC12 cells against OGD/R-induced injury partly due to attenuating Beclin-l-dependent autophagy caused by decreasing [Ca2＋] and increasing MMP.Aim： To explore the effects of β-asarone from Acorus Tatarinowii Schott on autophagy in an ischemic stroke model of PC12 cells. Methods： The ischemic stroke model of PC12 cells was made by OGD/R （2 h oxygen-glucose deprivation followed by 24 h reperfu- sion）. Drug administration was started 1 h before OGD and last for 3 h. Then the cells were incubated in the drug-free and full culture medium under normoxic conditions for 24 h. After the treatments, Beclin-1, intracellular free calcium concentration （[Ca2＋]1） and mitochondrial membrane potential （MMP） were analyzed using flow cytometry. Cell viability was measured using MTT assay. Cell morphology was studied under inverted phase contrast microscope, and autophagosomes were observed under transmission electron microscope. Results： Pretreatment with β-asarone （20, 30, or 45 pg/mL） or the calcium channel antagonist nimodipine （10 pmol/L） significantly increased the cell viability and MMP, and decreased Beclin-1 expression and [Ca2＋]i in OGD/R-treated PC12 cells. Under inverted phase contrast microscope, pretreatment with β-asarone or nimodipine dramatically increase the number of cells and improved the cellular morphology. Autophagosomes were found in OGD/R-treated PC12 cells as well as in drug plus OGD/R-treated PC12 cells. Conclusion： β-Asarone protects PC12 cells against OGD/R-induced injury partly due to attenuating Beclin-l-dependent autophagy caused by decreasing [Ca2＋] and increasing MMP.

关 键 词：Β-ASARONE PC12 cells oxygen-glucose deprivation/reperfusion AUTOPHAGY Beclin-1 [Ca2＋]i MMP NIMODIPINE 

分 类 号：Q421[生物学—神经生物学] S567.239[生物学—生理学]