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Life Sci. 2019 Dec 15;239:117014. doi: 10.1016/j.lfs.2019.117014. Epub 2019 Oct 31.

Protective effects of epigallocatechin gallate against ischemia reperfusion injury in rat skeletal muscle via activating Nrf2/HO-1 signaling pathway.

Author information

1
School of Sports and Health, Nanjing Sport Institute, Nanjing, 210014, Jiangsu China.
2
Department of Emergency Medicine and Critical Care, Shanghai East Hospital, Tongji University School of Medicine, 150 Jimo Road, Shanghai, 200120, China.
3
Department of Emergency Medicine and Critical Care, Shanghai East Hospital, Tongji University School of Medicine, 150 Jimo Road, Shanghai, 200120, China. Electronic address: 13917947179@139.com.
4
Department of Emergency Medicine and Critical Care, Shanghai East Hospital, Tongji University School of Medicine, 150 Jimo Road, Shanghai, 200120, China. Electronic address: yanyanli77@126.com.

Abstract

AIMS:

Previous studies have demonstrated that epigallocatechin gallate (EGCG) had certain protective effects on myocardial and renal ischemia reperfusion (I/R) injury. We aimed to research the special effects and underling mechanisms of EGCG on skeletal muscle I/R injury.

MAIN METHOD:

We established an experimental rat model of I/R skeletal muscle injury and treated with different doses of EGCG. Hematoxylin eosin staining, TUNEL assay, ELISA, qRT-PCR and Western blotting were used to evaluate the effects of EGCG.

KEY FINDINDS:

EGCG significantly improved skeletal muscle function of I/R injury rats. Moreover, EGCG had positive effects on decreasing apoptosis of skeletal muscle tissues, alleviating oxidative stress damage and suppressing the production of inflammatory cytokines. Further, EGCG had positive effects on activating Nrf2/HO-1 signaling pathway.

SIGNIFICANCE:

EGCG might be a powerful candidate compound for alleviating I/R injury in rat skeletal muscle.

KEYWORDS:

Apoptosis; Epigallocatechin gallate; Inflammatory response; Nrf2/HO-1 signaling pathway; Oxidative stress; Skeletal muscle ischemia reperfusion injury

PMID:
31678278
DOI:
10.1016/j.lfs.2019.117014
[Indexed for MEDLINE]

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