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Review
. 2020 Oct 2;9(10):950.
doi: 10.3390/antiox9100950.

Key Developments in the Potential of Curcumin for the Treatment of Peripheral Neuropathies

Martial Caillaud  1 , Yu Par Aung Myo  1 , Bryan D McKiver  1 , Urszula Osinska Warncke  1 , Danielle Thompson  1 , Jared Mann  1 , Egidio Del Fabbro  2   3 , Alexis Desmoulière  4 , Fabrice Billet  4 , M Imad Damaj  1   3
Affiliations
Review

Key Developments in the Potential of Curcumin for the Treatment of Peripheral Neuropathies

Martial Caillaud et al. Antioxidants (Basel). .

Abstract

Peripheral neuropathies (PN) can be triggered after metabolic diseases, traumatic peripheral nerve injury, genetic mutations, toxic substances, and/or inflammation. PN is a major clinical problem, affecting many patients and with few effective therapeutics. Recently, interest in natural dietary compounds, such as polyphenols, in human health has led to a great deal of research, especially in PN. Curcumin is a polyphenol extracted from the root of Curcuma longa. This molecule has long been used in Asian medicine for its anti-inflammatory, antibacterial, and antioxidant properties. However, like numerous polyphenols, curcumin has a very low bioavailability and a very fast metabolism. This review addresses multiple aspects of curcumin in PN, including bioavailability issues, new formulations, observations in animal behavioral tests, electrophysiological, histological, and molecular aspects, and clinical trials published to date. The, review covers in vitro and in vivo studies, with a special focus on the molecular mechanisms of curcumin (anti-inflammatory, antioxidant, anti-endoplasmic reticulum stress (anti-ER-stress), neuroprotection, and glial protection). This review provides for the first time an overview of curcumin in the treatment of PN. Finally, because PN are associated with numerous pathologies (e.g., cancers, diabetes, addiction, inflammatory disease...), this review is likely to interest a large audience.

Keywords: anti-ER-stress; anti-inflammatory; antioxidant; clinical trial; curcumin; peripheral neuropathy.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
A suggested model summarizing the sites of action of curcumin in peripheral neuropathies as reported in the literature: curcumin reduces neuropathic pain and improves sensitivity in in vivo models of PN, by improving sensory nerve conduction velocity (SNCV), reducing the loss of neurons and satellite cells in dorsal roots ganglia (DRG), and promoting the regrowth of sensory nerve fibers. In addition, curcumin improves motor functions in in vivo models of PN, by improving motor nerve conduction velocity (MNCV), reducing nerve fibers demyelination, loss of motor neurons in spinal cord, muscle atrophy and neurogenic lesions, and improving motor nerves fibers regrowth.
Figure 2
Figure 2
A proposed model summarizing the molecular targets of curcumin in peripheral neuropathies reported in the literature: tumor necrosis factors (TNFα), interferon (INF-γ), interleukins (IL-1α, IL-1β, IL-6, IL_10), granulocyte-macrophage colony-stimulating factor (GM-CSF), monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein (MIP-1α), Toll-like receptor (TLR, TLR1, TLR3, TLR4, and TLR7), nuclear factor-kappa B (NF-κB), NF-κB inhibitor-α (IκB-α), nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), lipooxygenase (LOX), cyclooxygenase (COX), nitric oxide synthase (NOS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), transient receptor potential cation channel subfamily-M-2 (TRMP2), nuclear factor erythroid 2–related factor 2 (Nrf2), reactive oxygen species (ROS), reactive nitrogen species (RNS), peripheral myelin protein 22 (PMP22), myelin protein zero (MPZ), myelin basic protein (MBP), extracellular signal regulated kinase (ERK), c-Jun-N-terminal kinase (JNK), α7-nicotinic acetylcholine receptors (α7-nAchR), tropomyosin receptor kinase A (TrkA), phosphoinositide 3-kinase (PI3K), activating transcription factor 3 (ATF3), ER-residing protein endoplasmic oxidoreductin-1 (Ero-1β), activating transcription factor 6 (ATF6) cleavage, X-Box binding protein 1 (XBP1) splicing, and C/EBP homologous protein (CHOP).
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