RETRACTED: Astragalus polysaccharide alleviates LPS-induced inflammation injury by regulating miR-127 in H9c2 cardiomyoblasts

Abstract

Astragalus polysaccharide (APS) has been widely reported to play an important role in inflammatory response. In this study, we aimed to explore the effects and underlying mechanisms of APS on lipopolysaccharide (LPS)-induced inflammation injury in H9c2 cardiomyoblasts. H9c2 cells were treated with different concentrations of APS, and cell viability was detected by the Cell Counting Kit-8 (CCK-8) assay. Then, the effect of APS on cell viability and apoptosis induced by LPS was determined by CCK-8, flow cytometry, and western blot. The expression and release of inflammatory cytokines were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and enzyme-linked immunosorbent assay (ELISA). Furthermore, expression of miR-127 in H9c2 cells was analyzed by qRT-PCR, and knocked down by transfection with miR-127 inhibitor. Western blot was used to analyze signaling pathway molecules. APS had no effect on H9c2 cells viability. However, APS could alleviate LPS-induced inflammation injury by increasing cell viability, reducing apoptosis, and inhibiting release of inflammatory cytokines in H9c2 cells (P < 0.05). Additionally, we found that APS increased toll-like receptor 4 (TLR4) expressions in LPS-treated H9c2 cells. Mechanistically, we found that APS exerted the protective effect by down-regulating LPS-increased expression of miR-127 (P < 0.05), inhibiting nuclear factor kappa B (NF-κB), JNK and promoting phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathways in LPS-treated H9c2 cells. The results demonstrated that APS could protect H9c2 cells against LPS-induced inflammation injury, which might be partially due to miR-127 down-regulation and regulation of NF-κB, JNK, and PI3K/AKT signaling pathways. These findings indicated that APS might be a potential therapeutic drug for treatment of myocarditis.

Exploring Molecular Mechanism of Huangqi in Treating Heart Failure Using Network Pharmacology

“…Although astragalus polysaccharide and cycloastragenol were not recruited by TCMSP, and targets corresponding to astragalus polysaccharide, cycloastragenol, and astragaloside IV were not obtained from TCMSP, they were also considered the critical compounds of Huangqi for their strong cardioprotective effect. Astragalus polysaccharide was proved to protect myocardium through reducing oxidant stress and cardiomyocyte apoptosis, inhabiting the generation of inflammatory factors like phosphorylated NF-κB, IL-1β, IL-6, TNF-α, and so on, restoring normal autophagic flux [21,[32][33][34][35][36]. In addition, research confirms that cycloastragenol improves cardiac defect and remodeling by enhancing autophagy in myocardial cells and reduces the production of MMP-2 and MMP-9 [24].…”

Schizandrin A Alleviates LPS-Induced Injury in Human Keratinocyte Cell Hacat Through a MicroRNA-127-Dependent Regulation

“…Among all these identified miRNAs, abnormal expression of miR-127 was reported to be link to inflammatory disorders [16]. In addition, miR-127 was found to be involved in LPS-induced inflammation injury in ATDC cells [17] and in H9c2 cardiomyoblasts [18]. Of note, recent studies indicated that miR-127 had a potential role in autoimmune diseases, such as lupus, nephritis and oral pemphigus [19,20].…”

Astragalus Polysaccharides/Chitosan Microspheres for Nasal Delivery: Preparation, Optimization, Characterization, and Pharmacodynamics

“…Allergic rhinitis is a chronic inflammatory disease of the upper respiratory tract resulting from various environmental factors. APS can effectively correct the imbalance of Th1/Th2 cells and reduce inflammatory infiltration, and it has been widely used in the clinical treatment of AR Ren et al, 2018). CTS microspheres can overcome rapid mucociliary clearance and provide longer contact time for drug transport.…”

“…Astragalus polysaccharides (APS), a main active extract of Astragalus membranaceus, can enhance the immune response by increasing the serum antibody titer and enhancing the secretion of a wide range of cytokines (Tan et al, 2017;Zhou et al, 2017). APS can also regulate the balance of Th1/Th2 cells and inhibit the expression of inflammatory factors and inflammation injury (Liu, 2017;Ren et al, 2018). APS ameliorated palmitate-induced proinflammatory responses through AMP-activated protein kinase (AMPK) activity (Lu et al, 2013).…”