Open AccessBerberine attenuates mitochondrial dysfunction by inducing autophagic flux in myocardial hypoxia/reoxygenation injury
Author(s) -
Na Zhu,
Xueming Cao,
Peiyuan Hao,
Yuwei Zhang,
Yan Chen,
Jing Zhang,
Jiang Li,
Chuanyu Gao,
Li Li
Publication year - 2020
Publication title -
cell stress and chaperones
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.994
H-Index - 87
eISSN - 1466-1268
pISSN - 1355-8145
DOI - 10.1007/s12192-020-01081-5
Subject(s) - autophagy , rhodamine 123 , berberine , hypoxia (environmental) , flow cytometry , chemistry , microbiology and biotechnology , flux (metallurgy) , pharmacology , apoptosis , mitochondrion , membrane potential , reactive oxygen species , downregulation and upregulation , green fluorescent protein , biology , biochemistry , oxygen , gene , organic chemistry , multiple drug resistance , antibiotics
Berberine (BBR) is routinely prescribed in many Asian countries to treat diarrhea. Evidence from both animal and clinical investigations suggests that BBR exerts diverse pharmacological activities, including antidiabetic, antineoplastic, antihypertensive, and antiatherosclerotic effects. This study aimed to explore the cardioprotective mechanisms of BBR and to elucidate the modulations between autophagy and mitochondrial function during hypoxia/reoxygenation (H/R) in H9c2 cells. The degree of autophagic flux was assessed by pretreating H9c2 cells with BBR prior to H/R exposure and measuring the expression levels of Beclin-1 and green fluorescent protein (GFP)-labeled LC3B fusion proteins as well as the LC3II/LC3I ratio. The mitochondrial membrane potential (△Ψm) in H9c2 cells was evaluated by detecting rhodamine-123 fluorescence using flow cytometry. The results revealed that pretreatment with BBR upregulated autophagic flux and protected against the loss of the △Ψm in H9c2 cells subjected to H/R. We conclude that BBR attenuates mitochondrial dysfunction by inducing autophagic flux.