Emodin suppresses LPS-induced inflammation in RAW264.7 cells through a PPARγ-dependent pathway

Inflammation is a defense and protective response to multiple harmful stimuli. Over and uncontrolled inflammation can lead to local tissues or even systemic damages and injuries. Actually, uncontrolled and self-amplified inflammation is the fundament of the pathogenesis of a variety of inflammatory diseases, including sepsis shock, acute lung injury and acute respiratory distress syndrome (ALI/ARDS). Our recent study showed that emodin, the main active component of Radix rhizoma Rhei, could significantly ameliorate LPS-induced ALI/ARDS in mice. However, its underlying signal pathway was not still very clear. Then, the aim of current study was to explore whether emodin could attenuate LPS-induced inflammation in RAW264.7 cells, and its involved potential mechanism. The mRNA and protein expression of ICAM-1, MCP-1 and PPAR gamma were measured by qRCR and western blotting, the production of TNF-alpha was evaluated by ELISA. Then, the phosphorylation of NF-kappa B p65 was also detected by western blotting. And NF-kappa B p65 DNA binding activity was analyzed by ELISA as well. Meanwhile, siRNA-PPAR gamma transfection was performed to knockdown PPAR gamma expression in cells. Our data revealed that LPS-induced the up-regulation of ICAM-1, MCP-1 and TNF-alpha, LPS-induced the down-regulation of PPAR gamma, and LPS-enhanced NF-kappa B p65 activation and DNA binding activity were substantially suppressed by emdoin in RAW264.7 cells. Furthermore, our data also figured out that these effects of emdoin were largely abrogated by siRNA-PPAR gamma transfection. Taken together, our results indicated that LPS-induced inflammation were potently compromised by emodin very likely through the PPAR gamma-dependent inactivation of NF-kappa B in RAW264.7 cells. (C) 2016 Elsevier B.V. All rights reserved.