Chlorogenic acid: a review on its mechanisms of anti-inflammation, disease treatment, and related delivery systems

Abstract

Chlorogenic acid is a bioactive compound ubiquitously present in the natural realm, lauded for its salient anti-inflammatory and antioxidant attributes. It executes its anti-inflammatory function by moderating the synthesis and secretion of inflammatory mediators, namely, TNF-α, IL-1β, IL-6, IL-8, NO, and PGE2. Concurrently, it modulates key signaling pathways and associated factors, including NF-κB, MAPK, Nrf2, and others, bestowing protection upon cells and tissues against afflictions such as cardio-cerebrovascular and diabetes mellitus. Nevertheless, the inherent low bioavailability of chlorogenic acid poses challenges in practical deployments. To surmount this limitation, sophisticated delivery systems, encompassing liposomes, micelles, and nanoparticles, have been devised, accentuating their stability, release mechanisms, and bioactivity. Given its innate anti-inflammatory prowess and safety profile, chlorogenic acid stands as a promising contender for advanced biomedical investigations and translational clinical endeavors.

Keywords: chlorogenic acid; disease treatment; inflammatory response; related delivery systems; signaling pathways.

FIGURE 1

Molecular structure of chlorogenic acid and its isomers.

FIGURE 2

Anti-inflammatory mechanism of chlorogenic acid compounds.:promote; :inhibit; CGA:chlorogenic acid; VCAM-1:vascular cell adhesion molecule 1; MDA:malonaldehyde; NADPH:nicotinamide adenine dinucleotide phosphate; ROS:reactive oxygen species; TLR4:toll like receptor 4; MyD88:myeloid differentiation primary response gene (88); P-P38:phosphorylated P38 kinase; P-PERK1:phosphorylated extracellular signal-regulated protein kinase-1; P-PERK2:phosphorylated extracellular signal-regulated protein kinase-2; p-JNK:phosphorylated c-Jun amino-terminal kinase.