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Review

Anti-Inflammatory Influences of Culinary Spices and Their Bioactives

Pages 1-17 | Published online: 04 Nov 2020
 

ABSTRACT

This review summarizes all the available evidence for the anti-inflammatory potential of culinary spices or their bioactives by considering in vitro, translational, and human intervention studies. An exhaustive search of the available literature was performed using PubMed, Google Scholar, and Scopus databases. The review considers information from clinical, translational, and in vitro studies especially on the commonly used spices: Curcuma longa L., Capsicum annuum L., Zingiber officinale L., Syzygium aromaticum L., Nigella sativum, and Piper nigrum L. Both in vitro studies on LPS-challenged macrophages and in vivo animal edema models have documented the anti-inflammatory potential of spice principles curcumin, capsaicin, 6-gingerol, eugenol, thymoquinone, and piperine. Studies on animal inflammation models have revealed that curcumin and capsaicin delay the onset, lower the incidence and severity of arthritis. The anti-inflammatory effects of these spices bioactives were accompanied by an inhibition of inflammatory cytokines (TNF-α, IL-1β and IL-6) and the transcription factor (NFκB). The available evidences strongly recommend that a diet rich in specific anti-inflammatory spices may reduce the inflammation and exert preventive effect on inflammation-related diseases. Although these spices are traditionally used for inflammatory disorders for centuries, their therapeutic application to prevent or treat inflammatory diseases warrants further in-depth investigation.

Abbreviations

CEO, Clove essential oil; COX, Cyclooxygenase; CRP, C-Reactive protein; CVD, Cardiovascular disease; DMEM, Dulbecco’s modified Eagle medium; DMSO, Dimethyl sulfoxide; IL, Interleukin; IP-10, Interferon γ-induced protein-10; I-TAC, Interferon-inducible T-cell α-chemoattractant; iNOS, Inducible nitric oxide synthase; IRF, Interferon regulatory factor; LPS, Lipopolysaccharide; M-CSF, Macrophage colony-stimulating factor; MIG, Monokine induced by γ-interferon; MMP, Matrix metalloproteinase; MTT, 3-(4, 5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; NF-κB, Nuclear factor- κB; NO, Nitric oxide; NSAID, Nonsteroidal anti-inflammatory drug; PDA, Pancreatic ductal adenocarcinoma; PGE2, Prostaglandin E2; PLA2, Phospholipase A2; PPAR, Peroxisome proliferator-activated receptor; SAID, Steroidal anti-inflammatory drug; TIMP-2, Tissue inhibitor of metalloproteinase-2; TNF-α, Tumor necrosis factor-α; TQ, Thymoquinone; TX, Thromboxane; VCAM-1, Vascular cell adhesion molecule-1; VEGF, Vascular endothelial growth factor

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