A narrative review of the protective effects of curcumin in treating ischemia-reperfusion injury

Abstract

Background and objective: Ischemia-reperfusion (IR) injury is the cause of morbidity and mortality in a variety of diseases and surgical procedures including organ transplantation surgeries, acute coronary syndrome, strokes, and limb injuries. IR injury causes dysfunction of tissues and organs, and oxidative stress plays an important role in driving this process. Curcumin (CUR), a polyphenolic compound derived from turmeric, protects against IR injury by alleviating oxidative stress, reactive oxygen species (ROS) inflammation, apoptosis, and fibrosis. We review the protective effects of CUR against IR.

Methods: We searched PubMed, ScienceDirect, and Web of Science databases using the keywords: ischemic reperfusion, CUR and summarized the results.

Key content and findings: The effects of CUR during IR have been reported for animal models in vitro and in vivo and the compound has been shown in various organs by suppression of oxidative stress, prevention of inflammation, inhibition of apoptosis and autophagy. CUR with nanocarriers showed many advantages than free CUR in the treatment of IR injury, such as improved bioavailability, sustained-release, better water solubility, better target organ accumulation, improved permeability across the blood-brain-barrier and more effective.

Conclusions: Nanotechnology offers significant improvements and promising strategies to improve drug delivery to IR-injured tissues and achieve the desired protective effects. Thus, it is necessary to promote further clinical trials to promote the clinical application of CUR with nanocarriers.

Keywords: Ischemia; curcumin (CUR); reperfusion; review.

Figure 1

Molecular mechanism demonstrating the protective function of CUR against ischemia-reperfusion injury. TNF-R, tumor necrosis factor receptor; PPAR, peroxisome proliferators-activated receptors; TGF, transforming growth factor; IL-6R, interleukin 6 receptor; CUR, curcumin; ATP, adenosine triphosphate; ER, endoplasmic reticulum; NF-κB, nuclear factor κB; I-κB, inhibitor of NF-κB; Casp, caspase; ROS, reactive oxygen species; JNK, c-Jun N-terminal kinase; Cyto-c, cytochrome c; ERK, extracellular signal-regulated kinase; BCL2, b-cell lymphoma-2; BAX, BCL2 associated X; AKT (PKB), protein kinase B; HSP, heat shock protein; PI3K, phosphoinositide 3-kinase; JAK, janus kinase; STAT, signal transducer and activator of transcription; RAS, rat sarcoma; MAPK, mitogen activated protein kinase; MTOR, mammalian target of rapamycin.