Treatment with Commelina communis Extract Exerts Anti-inflammatory Effects in Murine Macrophages via Modulation of the Nuclear Factor-κB Pathway.

Ji-Hee Kim,Bog-Im Park,Yong-Ouk You,Eduardo Dalmarco

doi:10.1155/2022/2028514

Abstract

The incidence of severe inflammatory diseases caused by chronic inflammation has increased owing to unprecedented changes brought about by industrialization. In this study, we aimed to assess the effect of treatment of lipopolysaccharide- (LPS-) induced murine macrophages with Commelina communis Linne extract (CCE) on synthesis of nitric oxide (NO), hypersecretion of proinflammatory cytokines, intranuclear transition of the p65 subunit of nuclear factor- (NF-) κB, and degradation of the NF-κB inhibitor IκBα. Notably, CCE treatment did not affect cell viability even at a final concentration of 1.5 mg/mL. At a high concentration of CCE, the LPS-induced high levels of NO, tumor necrosis factor-α, interleukin- (IL-) 1β, and IL-6 were decreased via downregulation of inducible NO synthase and proinflammatory cytokine mRNA expression. Furthermore, phosphorylation of IκBα was significantly decreased upon CCE treatment, and the intranuclear transition of NF-κB p65 triggered by LPS was inhibited at a high concentration of CCE. Polyphenols and flavonoids, secondary metabolites in CCE that regulate the NF-κB pathway, may be responsible for its anti-inflammatory activity. We suggest that CCE has anti-inflammatory effects related to suppression of the NF-κB pathway and can be used to treat chronic inflammation.

Highlights

A portion of the extract was used for analysis of secondary metabolites of Commelina communis Linne extract (CCE), and the rest of the extract was mixed with dimethyl sulfoxide
Macrophages are activated by LPS resulting in the induction of proinflammatory cytokines and inflammatory responses via the nuclear factor- (NF-)κB signaling pathway [29, 30]
IκBα phosphorylation and nuclear p65 subunit levels were inhibited by CCE treatment in a dose-dependent manner. These results suggested that CCE treatment inhibits the intranuclear transition of the NF-κB p65 subunit by regulating the upstream events of IκBα phosphorylation and decomposition

Summary

Introduction

Inflammation is an innate defense response in living organisms. It protects the human body against pathogenic infections and provides adaptive immunity against specific pathogens. Humans are experiencing unprecedented environmental changes involving exposure to unhealthy diet, air pollution, fabrics made from synthetic fibers, and hygienerelated products that are harsh on the skin as well as ease of access to antibiotics, general pharmaceuticals, and quasidrugs [2]. These changes in environmental factors may be unregulated and lead to induction of inflammatory processes that can in turn lead to homeostatic imbalance and pathologies such as chronic colitis [3], rheumatic diseases and arterial stiffness [4], fatty liver diseases [5], cancer [6], obesity and asthma [7], and sepsis [8]. It has increased the proportion of population that experiences the negative effects of chronic inflammatory diseases [2]

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