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Ginkgo biloba Pretreatment Attenuates Myocardial Ischemia-Reperfusion Injury via mitoBKCa.

Authors
  • Li, Tonghua1, 2
  • Zhang, Yuyang2
  • Tian, Jianwei3
  • Yang, Lu4
  • Wang, Jianchang5
  • 1 *School of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, P. R. China. , (China)
  • 2 ‡Department of Cardiology, Xi'an No.1 Hospital, Xi'an, Shaanxi 710002, P. R. China. , (China)
  • 3 §Department of Cardiology, Air Force Medical Center, PLA, Beijing 100142, P. R. China. , (China)
  • 4 †Department of Physiology, Fourth Military Medical University, Xi'an 710032, P. R. China. , (China)
  • 5 ¶Geriatrics Research Center, Air Force Medical Center, PLA, Beijing 100142, P. R. China. , (China)
Type
Published Article
Journal
The American journal of Chinese medicine
Publication Date
Jan 01, 2019
Volume
47
Issue
5
Pages
1057–1073
Identifiers
DOI: 10.1142/S0192415X1950054X
PMID: 31327236
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Ginkgo biloba extracts (EGb) alleviate myocardial ischemia/reperfusion (MI/R) injury. However, the underlying mechanisms have not yet been characterized. This study aimed to investigate whether activation of large-conductance Ca2+-activated K+ channels at the inner mitochondrial membrane (mitoBKCa) of cardiomyocytes is involved in Ginkgo biloba extract-mediated cardioprotection. Shuxuening injection (SXNI, 12.5ml/kg/d), a widely prescribed herbal medicine containing Ginkgo biloba extracts in China, or vehicle, was administered to C57BL/6 mice via tail vein injection for one week prior to surgical procedures. The mitoBKCa blocker paxilline (PAX) (1ml/kg, 115 nM) was administered via tail vein injection 30min prior to the onset of ischemia. The mice were randomly divided into the following groups: Sham, MI/R, MI/R+SXNI, and MI/R+SXNI+PAX. MI/R was induced by ligating the left anterior descending coronary artery for 30min with subsequent reperfusion for 24h. SXNI pretreatment conferred cardioprotective effects against MI/R injury as evidenced by reduced infarct size, improved cardiac function, and improved mitochondrial function. However, these effects were abrogated by co-administration with PAX. In addition, activation of mitoBKCa by Ginkgo biloba extract EGb761 reduced hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury in vitro through the inhibition of mitochondrial fragmentation, restoration of the mitochondrial membrane potential, decreased generation of superoxide, and inhibition of apoptosis which is associated with alleviating mitochondrial Ca2+ overload. These results indicated that Ginkgo biloba extracts pretreatment protected against MI/R injury via activation of mitoBKCa.

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