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• W2800182458 abstract "BACKGROUND:Acute liver injury in the setting of hepatic fibrosis is an intriguing and still unsettled issue. We previously have demonstrated the protective effects conferred by M2-like macrophages in the fibrotic liver. In the present work, we further decipher the cellular mechanisms governing this hepatoprotection. MATERIAL AND METHODS:Macrophages were isolated from control mice (M0 macrophages), then polarized into M1 or M2 phenotype using IFN-γ or IL-4, respectively. Conditioned media (CM) from M0, M1, and M2 macrophages were harvested and applied to M1 macrophages. Cell apoptosis was evaluated by immunostaining and real-time PCR. Similarly, human monocyte-derived macrophages were isolated and polarized, then M0, M1, and M2 CM were applied to HL-7702 or HepG2 cells followed by apoptosis induction. Cell apoptosis was assessed by flow cytometry. RESULTS:For the mouse conditioned medium experiment, stronger expression of cleaved caspase 3 and higher Bax/Bcl-2 mRNA ratio were found in M1 macrophages pretreated with M2 CM compared to those in M1 macrophages pretreated with M0 or M1 CM. Similarly, exposure of HL-7702 and HepG2 cells to either M0 or M1 CM had no significant effect on cell apoptosis. Nevertheless, the frequency of hepatocyte apoptosis was substantially reduced in HL-7702 (from 32.23±2.99 to 15.37±0.69 for Annexin V+/PI+ staining, p<0.01) and HepG2 cells (from 36.1±7.26 to 15.2±1.2 for Annexin V+/PI+ staining, p<0.01) with M2 CM pretreatment. CONCLUSIONS:M2-like macrophages exert their hepatoprotective effect by promoting M1-like macrophage apoptosis but protecting against hepatocyte apoptosis." @default.
• W2800182458 created "2018-05-17" @default.
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• W2800182458 date "2018-04-30" @default.
• W2800182458 modified "2023-10-14" @default.
• W2800182458 title "Cellular Mechanisms of Hepatoprotection Mediated by M2-Like Macrophages" @default.
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• W2800182458 doi "https://doi.org/10.12659/msm.907222" @default.
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