Emodin Ameliorates LPS-Induced Acute Lung Injury, Involving the Inactivation of NF-κB in Mice

Abstract

Acute lung injury (ALI) and its severe manifestation of acute respiratory distress syndrome (ARDS) are well-known illnesses. Uncontrolled and self-amplified pulmonary inflammation lies at the center of the pathology of this disease. Emodin, the bio-active coxund of herb Radix rhizoma Rhei, shows potent anti-inflammatory properties through inactivation of nuclear factor-κB (NF-κB). The aim of this study was to evaluate the effect of emodin on lipopolysaccharide (LPS)-induced ALI in mice, and its potential bio-mechanism. In our study, BALB/c mice were stimulated with LPS to induce ALI. After 72 h of LPS stimulation, pulmonary pathological changes, lung injury scores, pulmonary edema, myeloperoxidase (MPO) activity, total cells, neutrophils, macrophages, TNF-α, IL-6 and IL-1β in bronchoalveolar lavage fluid (BALF), and MCP-1 and E-selectin expression were notably attenuated by emodin in mice. Meanwhile, our data also revealed that emodin significantly inhibited the LPS-enhanced the phosphorylation of NF-κB p65 and NF-κB p65 DNA binding activity in lung. Our data indicates that emodin potently inhibits OPEN ACCESS Int. J. Mol. Sci. 2014, 15 19356 LPS-induced pulmonary inflammation, pulmonary edema and MCP-1 and E-selectin expression, and that these effects were very likely mediated by inactivation of NF-κB in mice. These results suggest a therapeutic potential of emodin as an anti-inflammatory agent for ALI/ARDS treatment.

Emodin mitigates diesel exhaust particles-induced increase in airway resistance, inflammation and oxidative stress in mice

“…Our results are in line with recent studies which reported that emodin attenuates lung edema, inflammation and enhances alveolar epithelial barrier function in rats with experimental pancreatitis (Xia et al, 2010). It has also been demonstrated that emodin protects from LPS-induced lung injury (Xiao et al, 2014).…”

“…The dose of particle (20 g/mouse) we used here has been selected from our previous study (Nemmar et al, 2009a) and is comparable to the doses employed in previous animal models of particulate air pollution exposure (Kido et al, 2011;Mutlu et al, 2007;Nemmar et al, 2011a). Emodin (1,3,8-trihydroxy-6-methyl-anthraquinone), an anthraquinone derivative from many herbs, is known to inhibit the production of inflammatory cytokines such as TNF␣, IL-6 and IL1␤ (Li et al, 2013;Xiao et al, 2014) and to have strong antioxidant and antiapoptotic actions Chang et al, 2011). In the present study, we elected to test emodin against DEP-induced lung toxicity, as the latter is associated with oxidative stress and inflammation (Nemmar et al, 2009a(Nemmar et al, , 2011a(Nemmar et al, , 2012b.…”

“…Emodin has also been shown to protect against inflammation in several conditions, e.g. atherosclerosis, asthma and lipopolysaccharide (LPS)-induced lung injury (Chu et al, 2012;Meng et al, 2010;Xiao et al, 2014). Since it is well established that exposure to DEP causes lung inflammation and oxidative stress (Nemmar et al, 2013b), we wanted, in the present study, to assess whether and to what extent emodin treatment can prevent/ameliorate DEP-induced pulmonary inflammation and oxidative stress.…”

Antimicrobial Peptide CMA3 Derived from the CA-MA Hybrid Peptide: Antibacterial and Anti-inflammatory Activities with Low Cytotoxicity and Mechanism of Action in Escherichia coli

“…In addition, in vivo studies showed that CMA3 has strong endotoxin-neutralizing activity. LPS is located on the Gram-negative bacterial membrane, strongly induces inflammation (49), and is responsible for the physiological manifestations of various diseases, including pneumonia (50). Here, we show that serum levels of the inflammatory marker NO are significantly reduced when mice administered E. coli-derived LPS are pretreated with CMA3.…”

Emodin Bidirectionally Modulates Macrophage Polarization and Epigenetically Regulates Macrophage Memory

“…Lin et al (46) showed that emodin shifted the Th1/Th2 balance toward Th2 by decreasing IFN␥ and IL2 and increasing IL4 levels in the serum of rats that received orthotopic liver transplantation. Emodin has also shown effectiveness in treating acute models of inflammation in the pancreas, lungs, kidneys, and liver at least partly through inhibiting NFB signaling (47)(48)(49)(50). Our laboratory has shown that emodin is able to attenuate liver inflammation in an experimental model of non-alcoholic fatty liver disease by inhibiting inflammatory cell infiltration in the liver (31).…”