Melatonin Suppresses Macrophage M1 Polarization and ROS-Mediated Pyroptosis via Activating ApoE/LDLR Pathway in Influenza A-Induced Acute Lung Injury

Figure 6

Melatonin promoted the activation of the ApoE/LDLR pathway in H3N2-induced ALI. (a) Representative immunohistochemical images of ApoE in lung tissues of wild-type (WT) mice as indicated by the brown staining (black arrows) from the control (PBS) group, PBS+Mel group, H3N2 infection group, and H3N2+Mel group, bar 50 μm (original magnification ×50, ×200). (b) Western blot analysis of the expression of ApoE and LDLR to β-actin in lung tissue homogenate of WT mice. (c) Quantitative ELISA detection of ApoE levels in the serum from the control (PBS) group, PBS+Mel group, H3N2 infection group, and H3N2+Mel group. (d) Quantitative RT-PCR measurement of the relative mRNA level of ApoE in Raw264.7 cells infected with influenza A (H3N2) (, 12 h) with/without melatonin pretreatment (100 μM, 200 μM, or 400 μM, 3 h before H3N2 infection). (e) Western blot analysis of the expression of ApoE and LDLR to β-actin in Raw264.7 cells. Data expressed as (). , , and compared with influenza A- (H3N2-) infected mice or Raw264.7 cells.

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