Abstract
This paper aims to observe the changes of the inflammatory cytokines in microglial BV2 cells stimulated by apelin, and investigate the mechanism of inflammatory cytokines secretion after apelin stimulation. Immunofluorescence and quantitative real-time PCR were performed to observe expression of TNF-α, IL-1β, IL-10, MIP-1α, and MCP-1 in BV2 cells. Western blot was used to investigate the expression of phosphorylation PI-3K/Akt and phosphorylation Erk signaling pathways in BV2 cells after stimulation by apelin. Furthermore, PI-3K/Akt inhibitor (LY294402) and Erk inhibitor (U0126) were used as antagonists to detect the secretion mechanisms of cytokines in BV2 cells stimulated by apelin. Exogenous recombinant apelin activated the expression of TNF-α, IL-1β, MCP-1 and MIP-1α in BV2 cells by the detection of fluorescence expression and mRNA. Apelin also unregulated the protein expression of p-PI-3K/Akt and p-Erk in BV2 cells induced by apelin. LY294002 and U0126 inhibited activation of p-PI-3K/Akt and p-Erk expression by Western blot and attenuated the expression of inflammation factors in BV2 cells by fluorescence staining. This study demonstrates that apelin is a potential activator of inflammation factors through the PI3K/Akt and Erk signaling pathway and is potential therapeutically relevant to inflammatory responses of microglia cells.
Highlights
This paper aims to observe the changes of the inflammatory cytokines in microglial BV2 cells stimulated by apelin, and investigate the mechanism of inflammatory cytokines secretion after apelin stimulation
The expression of IL-1β, TNF-α, MCP-1, macrophage inflammatory protein-1α (MIP-1α) and IL-10 were investigated by immunofluorescence staining in microglial BV2 cells
After the microglial BV2 cells incubation with apelin, the result showed that IL-1β, TNF-α, MCP-1, MIP-1α were up-regulated, but IL-10 was downregulated (Figure 2)
Summary
This paper aims to observe the changes of the inflammatory cytokines in microglial BV2 cells stimulated by apelin, and investigate the mechanism of inflammatory cytokines secretion after apelin stimulation. This study demonstrates that apelin is a potential activator of inflammation factors through the PI3K/Akt and Erk signaling pathway and is potential therapeutically relevant to inflammatory responses of microglia cells. Studies have demonstrated that microglial cells are involved in phagocytosis, removal of apoptotic neuronal remnants and involved in remodeling [10] When they are over-activated, microglial cells release soluble cytotoxins, such as tumor necrosis factor-alpha (TNF-α), interleukin1β (IL-1β), and IL-6 that can contribute to neuronal and vascular cell death and the progression of diabetic retinopathy (DR) [11]. Park et al [16] indicated that fucoidan treatment significantly attenuated expression of iNOS, COX-2, MCP-1, IL-1β and TNF-α in LPS-stimulated BV2 microglia through down-regulation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and AKT pathways. The present study was designed to investigate whether apelin could effectively regulate the pro- and anti-inflammatory factors in BV2 cells and to study the mechanism of apelin on the expression of inflammatory cytokines in BV2 cells
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