Abstract
A hypernomic reaction or an abnormal inflammatory process could cause a series of diseases, such as cardiovascular disease, neurodegeneration, and cancer. Additionally, oxidative stress has been identified to induce severe tissue injury and inflammation. Carpesium cernuum L. (C. cernuum) is a Chinese folk medicine used for its anti-inflammatory, analgesic, and detoxifying properties. However, the underlying molecular mechanism of C. cernuum in inflammatory and oxidative stress conditions remains largely unknown. The aim of this study was to examine the effects of a methanolic extract of C. cernuum (CLME) on lipopolysaccharide- (LPS-) induced RAW 264.7 mouse macrophages and a sepsis mouse model. The data presented in this study indicated that CLME inhibited LPS-induced production of proinflammatory mediators such as nitric oxide (NO) and prostaglandin E2 (PGE2) in RAW 264.7 cells. CLME treatment also reduced reactive oxygen species (ROS) generation and enhanced the expression of heme oxygenase-1 (HO-1) protein in a dose-dependent manner in the LPS-stimulated RAW 264.7 cells. Moreover, CLME treatment abolished the nuclear translocation of nuclear factor-κB (NF-κB), enhanced the activation of nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), and reduced the expression of extracellular signal-related kinase (ERK) and ERK kinase (MEK) phosphorylation in LPS-stimulated RAW 264.7 cells. These outcomes implied that CLME could be a potential antioxidant and anti-inflammatory agent.
Highlights
Inflammation is a multistep process occurring in many animals
Only 60% of septic mice with CLME-treated groups were dead within 41 h of LPS injection, indicating that CLME improved the survival of mice suffering from lethal endotoxic shock (Figure 1(a))
In cells pretreated with CLME, the level of cell spreading and pseudopodia induced by LPS was decreased, indicating inhibition of cell activation or differentiation (Fig. S1B)
Summary
Inflammation is a multistep process occurring in many animals. It is one of the first lines of defense against harmful stimuli, such as trauma, bacteria, and irritants [1]. Acute inflammation is a finite process, leading to the return of tissue homeostasis. It has been reported that unrestrained inflammation occurs during chronic inflammatory milieu, such as allergies, asthma, arthritis, atherosclerosis, multiple sclerosis, metabolic syndromes, and obesity [2, 3]. Lipopolysaccharide (LPS), a well-known inflammatory ligand, can activate macrophages to release a variety of inflammatory cytokines [5]. We can Mediators of Inflammation mimic inflammatory and oxidative stress milieu using RAW 264.7 macrophage cells, which demonstrate a highly reproducible response to LPS
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