Anti-Inflammatory Effects of Curcumin in the Inflammatory Diseases: Status, Limitations and Countermeasures

Abstract

Curcumin is a natural compound with great potential for disease treatment. A large number of studies have proved that curcumin has a variety of biological activities, among which anti-inflammatory effect is a significant feature of it. Inflammation is a complex and pervasive physiological and pathological process. The physiological and pathological mechanisms of inflammatory bowel disease, psoriasis, atherosclerosis, COVID-19 and other research focus diseases are not clear yet, and they are considered to be related to inflammation. The anti-inflammatory effect of curcumin can effectively improve the symptoms of these diseases and is expected to be a candidate drug for the treatment of related diseases. This paper mainly reviews the anti-inflammatory effect of curcumin, the inflammatory pathological mechanism of related diseases, the regulatory effect of curcumin on these, and the latest research results on the improvement of curcumin pharmacokinetics. It is beneficial to the further study of curcumin and provides new ideas and insights for the development of curcumin anti-inflammatory preparations.

Keywords:

• anti-inflammatory
• osteoarthritis
• psoriasis
• atherosclerotic
• pharmacokinetics
• prodrug

Acknowledgments

The authors acknowledge financial supports from the National special fund for intangible cultural heritage protection which organized by ministry of culture and tourism of the people’s Republic of China, fellowship of China Postdoctoral Science Foundation (no. 2020M673567XB), Key R & D projects (no. 20ZDYF1642) which organized by Science & Technology Department of Sichuan Province, Xinglin Scholar Research Premotion Project of Chengdu University of TCM (no. BSH2019026) and the Open Research Fund of Chengdu University of TCM State Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China (no. 2020QNJS005).

Abbreviations

IBD, inflammatory bowel disease; TLR, Toll-like receptors; NF-κB, Nuclear factor kappa-B; MAPKs, Mitogen-activated protein kinases; AP-1, Activator Protein 1; PPARγ, Peroxisome proliferator-activated receptor gamma; JAK/STAT, The Janus kinase/Signal transducer and activator of transcription; NLRP3, NOD-like receptor pyrin domain-containing 3; IL-1, Interleukin-1; TNF-α, Tumor necrosis factor-α; iNOS, Inducible nitric oxide synthase; RANTES, Regulated upon activation normal T cell expressed and secreted factor; G-CSF, Granulocyte colony-stimulating factor; MCP-1, Monocyte chemotactic protein‐1; CRP, C‐reactive protein; ROS, Reactive oxygen species; NADPH, Nicotinamide adenine dinucleotide phosphate; UC, Ulcerative colitis; CD, Crohn’s disease; DSS, dextran sulfate sodium salt; IBS, Irritable bowel syndrome; IBS-SSS, Irritable Bowel Syndrome- symptom severity score; OA, osteoarthritis; RA, rheumatoid arthritis; MMP, matrix metalloproteinase; ADAMTS, a disintegrin and metalloproteinase with thrombospondin-like motifs; CITED2, Cbp/p300 interacting transactivator with ED-rich tail 2; TGF-β, transforming growth factor-β; COX-2, cyclooxygenase-2; LPS, lipopolysaccharide; MSU, monosodium urate; PGE2, prostaglandin E2; IFN-γ, Interferon-gamma; GM-CSF, Granulocyte-macrophage colony stimulating factor; VEGF, Vascular endothelial growth factor; CCR6, CC Chemokine receptor 6; apoE-/-, apolipoprotein E homozygous knockout (−/−); Ldlr−/−, LDL receptor (−/−); HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; 5-LOX, 5-lipoxygenase; COVID-19, Coronavirus disease 19; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; ARDS, acute respiratory distress syndrome.

Disclosure

ChangJiang Hu is an employee of Neo-Green Pharmaceutical Co., Ltd. The authors report no other potential conflicts of interest for this work.