title: Picroside Ⅱ inhibits hypoxia/reoxygenation-induced cardiomyocyte apoptosis by ameliorating mitochondrial function through a mechanism involving a decrease in reactive oxygen species production.
abstract: Reactive oxygen species (ROS)‑induced mitochondrial dysfunction plays an important role in cardiomyocyte apoptosis during myocardial ischemia/reperfusion (I/R) injury. Picroside Ⅱ, isolated from Picrorhiza scrophulariiflora Pennell (Scrophulariaceae), has been reported to protect cardiomyocytes from hypoxia/reoxygenation (H/R)‑induced apoptosis, but the exact mechanism is not fully clear. The aim of the present study was to explore the protective effects of picroside Ⅱ on H/R‑induced cardiomyocyte apoptosis and the underlying mechanism. In the H9c2 rat cardiomyocyte cell line, picroside Ⅱ (100 µg/ml) was added for 48 h prior to H/R. The results showed that picroside Ⅱ markedly inhibited H/R‑induced cardiomyocyte apoptosis. In addition, picroside Ⅱ was also able to decrease the opening degree of mitochondrial permeability transition pore (mPTP), increase the mitochondrial membrane potential, inhibit cytochrome c release from mitochondria to cytosol and downregulate caspase‑3 expression and activity concomitantly with the decreased ROS production. These results suggested that picroside Ⅱ inhibited H/R‑induced cardiomyocyte apoptosis by ameliorating mitochondrial function through a mechanism involving a decrease in ROS production.
authors.affiliation: Department of Pharmacy, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China.
authors.forename: Jian-Zhe
authors.initials: JZ
authors.lastname: Li
authors.affiliation: Modern Analysis and Testing Center, Central South University, Changsha, Hunan 410078, P.R. China.
authors.forename: Shu-Yi
authors.initials: SY
authors.lastname: Yu
authors.affiliation: Department of Surgery, Maternal and Child Health Hospital of the Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530003, P.R. China.
authors.forename: Dan
authors.initials: D
authors.lastname: Mo
authors.affiliation: Department of Pharmacy, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China.
authors.forename: Xiu-Neng
authors.initials: XN
authors.lastname: Tang
authors.affiliation: Department of Pharmacy, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China.
authors.forename: Qing-Rui
authors.initials: QR
authors.lastname: Shao
mesh_terms: D000818:Animals; D053148:Caspase 3 / Q000378:metabolism; D015687:Cell Hypoxia / Q000187:drug effects; D002460:Cell Line; D002934:Cinnamates / Q000494:pharmacology*; D057888:Iridoid Glucosides / Q000494:pharmacology*; D008929:Mitochondria, Heart / Q000378:metabolism* / Q000473:pathology; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D002934:Cinnamates; D057888:Iridoid Glucosides; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D017382:Reactive Oxygen Species; C416837:picroside II; C505410:Casp3 protein, rat; D053148:Caspase 3