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Lycium barbarum polysaccharides inhibit ischemia/reperfusion-induced myocardial injury via the Nrf2 antioxidant pathway

Authors :
Hao Yu Gong
Yi Lu
Lei Lei He
Gong Xiao Zhao
Zheng Wang
Jin Jun Liu
Chun Fang Li
Abdoulaye Issotina Zibrila
Bai Chun Niu
Lynn Soong
Jing Ning Xu
Source :
Toxicology Reports, Vol 8, Iss, Pp 657-667 (2021), Toxicology Reports
Publication Year :
2021
Publisher :
Elsevier BV, 2021.

Abstract

Graphical abstract LBP attenuated myocardial ischemia/reperfusion injury by restoring redox status, ultimately improving cardiac function. CAT: catalase; GPX: glutathione peroxidase; HO1: heme oxygenase 1; IL-6: interleukin-6; I/R: ischemia/reperfusion; LBP: Lycium barbarum polysaccharides; Nrf2: nuclear factor erythroid 2-related factor 2; NQO1: NADPH dehydrogenase quinone 1; ROS: reactive oxygen species; SOD: superoxide dismutase; TNF-α: tumor necrosis factor α.<br />Highlights • LBP attenuated myocardial oxidative stress and apoptosis induced by I/R. • LBP improved cardiac function by reducing oxidative stress and apoptosis. • LBP ameliorated myocardial I/R injury via activation the Nrf2 signal pathway.<br />Oxidative stress is considered to be one of main pathophysiological mechanisms in myocardial ischemia/reperfusion (I/R) injury. Lycium barbarum polysaccharides (LBP), the main ingredient of Lycium barbarum, have potential antioxidant activity. We aimed to investigate the effects of LBP on myocardial I/R injury and explore the underlying mechanisms. Myocardial I/R group was treated with or without LBP to evaluate oxidative stress markers and the role of Nrf2 signal pathway. Our results showed that I/R increased infarct size and the activities of creatine kinase (CK) and lactate dehydrogenase (LDH) when compared with control group. Meanwhile, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were enhanced and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT) were decreased. These changes were associated with a significant increase in myocardial apoptosis, ultimately leading to cardiac dysfunction. LBP reduced infarct size (38.4 ± 2 % versus 19.4 ± 1.8 %, p < 0.05), CK and LDH activities and myocardial apoptotic index. Meanwhile, LBP suppressed the production of ROS and restored redox status. Additionally, LBP increased protein level of nuclear Nrf2 in vivo (2.1 ± 0.3 versus 3.8 ± 0.4, p < 0.05) and in vitro (1.9 ± 0.2 versus 3.8 ± 0.1, p < 0.05) and subsequently upregulated heme oxygenase 1 and NADPH dehydrogenase quinone 1 compared to I/R group. Interestingly, Nrf2 siRNA abolished the protective effects of LBP. LBP suppressed oxidative stress damage and attenuated cardiac dysfunction induced by I/R via activation of the Nrf2 antioxidant signal pathway.

Details

ISSN :
22147500
Volume :
8
Database :
OpenAIRE
Journal :
Toxicology Reports
Accession number :
edsair.doi.dedup.....e2da051aa6af4dfc1153ce28bafd2828