title: Puerarin attenuates myocardial hypoxia/reoxygenation injury by inhibiting autophagy via the Akt signaling pathway.
abstract: Puerarin (Pur), which is the major bioactive ingredient extracted from the root of Pueraria lobata (Willd.) Ohwi, has been demonstrated to relieve myocardial ischemia/reperfusion (I/R) injury. Macroautophagy, or autophagy, is an evolutionarily conserved cellular catabolic mechanism that is involved in myocardial I/R injury. The present study evaluated the involvement of autophagy in the protective mechanisms of Pur during myocardial hypoxia/reoxygenation (H/R). The results revealed that Pur and 3‑methyladenine pretreatment exerted a cardioprotective effect against H/R‑induced cell viability loss. Pur also decreased the ratio of light chain 3 (LC3) ‑II/LC3‑I and the degradation of p62 during H/R, which was accompanied by an increased level of phosphorylated‑protein kinase B (Akt). These findings suggested that autophagy during myocardial H/R was inhibited by Pur, and this was further confirmed by the results of transmission electron microscopy and adenovirus‑monomeric red fluorescent protein‑green fluorescent protein‑light chain 3 transfection. Furthermore, Pur inhibited the increased levels of autophagy induced by rapamycin, and the autophagy‑inhibiting effects of Pur during myocardial H/R were abolished by the Akt signaling inhibitor API‑2. Collectively, these data indicate that Pur pretreatment may attenuate myocardial H/R injury by inhibiting autophagy via the Akt signaling pathway.
authors.affiliation: Department of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
authors.forename: Huixiong
authors.initials: H
authors.lastname: Tang
authors.affiliation: Department of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
authors.forename: Xudong
authors.initials: X
authors.lastname: Song
authors.affiliation: Department of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
authors.forename: Yuanna
authors.initials: Y
authors.lastname: Ling
authors.affiliation: Department of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
authors.forename: Xianbao
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
authors.forename: Pingzhen
authors.initials: P
authors.lastname: Yang
authors.affiliation: Division of Cardiology, Department of Medicine, University of California Irvine Medical Center, Orange, CA 92868, USA.
authors.forename: Tao
authors.initials: T
authors.lastname: Luo
authors.affiliation: Department of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
authors.forename: Aihua
authors.initials: A
authors.lastname: Chen
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D000225:Adenine / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001343:Autophagy / Q000187:drug effects*; D015415:Biomarkers; D002470:Cell Survival / Q000187:drug effects; D004195:Disease Models, Animal; D005260:Female; D007529:Isoflavones / Q000737:chemistry / Q000494:pharmacology*; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects*; D014665:Vasodilator Agents / Q000737:chemistry / Q000494:pharmacology*
chemical_list: D015415:Biomarkers; D007529:Isoflavones; D014665:Vasodilator Agents; C025946:3-methyladenine; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D055372:AMP-Activated Protein Kinases; D000225:Adenine; C033607:puerarin