Anti-influenza A Virus Effects and Mechanisms of Emodin and Its Analogs via Regulating PPARα/γ-AMPK-SIRT1 Pathway and Fatty Acid Metabolism

Figure 3

Interference of PPARα/γ-AMPK pathway impaired the inhibitory effect of emodin on IAV replication and cell injury. A549 cells were infected with IAV (PR8, ) and treated with or without emodin (25 μg/mL). (a, b) In the inhibitor-treated assays, A549 cells were simultaneously further treated with the inhibitors of PPARα (MK886, 10 μM), PPARγ (GW9662, 30 μM), and AMPK (Compound C, CC, 10 μM) for 48 h, respectively. The cytotoxicity of these inhibitors was determined (Supplement Figure 6). (c, d) In the siRNA assay, A549 cells were first transfected with the siRNA for PPARα, PPARγ, and AMPKα1. After 12 h, the cells were infected with IAV (PR8, ) and treated with emodin (25 μg/mL) for 48 h. (a, c) The vRNA levels of the IAV matrix protein (MP) gene were quantified by a qRT-PCR assay. (b, d) The counteracting effects of the inhibitors and siRNAs on cell viability were quantified by a MTT method. All data shown were the of three independent experiments each in triplicate. vs. the only IAV-infected group; ^# vs. the IAV+emodin group; ^Δ vs. the IAV+emodin+siRNA control group.

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