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Effect of Rig-I on Proliferation， Apoptosis and Function of LPS-induced Macrophages
Wang Jinxia, Zhang Hongxin, Lu Shunyuan, Tang Lingyun, Wang Zhugang*
Research Center for Experimental Medicine of Rui Jin Hospital Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
Abstract: To investigate the biology function and mechanism of Rig-I on lipopolysaccharide (LPS)-induced macrophages such as proliferation， apoptosis and cytokines secretion， macrophages (Raw264.7) with Rig-I gene knock-down or overexpression were treated with different doses of LPS for indicated times. The viability was analyzed by CCK-8 and apoptosis was measured by flow cytometry. The expression levels of related cytokines were examined by qPCR. The Toll like receptor-4 (TLR4) signaling induced by LPS was detected by Western blot. CCK- 8 and flow cytometry analyses showed that Rig-I promoted the proliferation of macrophages and inhibited LPSinduced apoptosis. qPCR results indicated that Rig-I upregulated the expression of TNF-α， IL-10， IL-1 and IL-6 in macrophage cells. These effects caused by Rig-I were further demonstrated by activation of AKT and its downstream p-38， NF-κB and Bcl-xL. These data firstly suggested that Rig-I could regulate proliferation， apoptosis and function of LPS-induced macrophages through AKT signaling pathway.
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