Abstract:
:Pro‑inflammatory (M1) macrophages have key roles in atherogenesis. As β‑glucan has been demonstrated to exert pro‑inflammatory effects, the present study examined whether β‑glucan exerts atherogenic effects via converting macrophages into M1 phenotype. The results from reverse transcription‑quantitative polymerase chain reaction, flow cytometry, western blotting and transmission electron microscope indicated that M1 macrophage markers inducible nitric oxide synthase and cluster of differentiation 80 were upregulated, dectin‑1 (a receptor for β‑glucan) expression and nuclear factor (NF)‑κB nuclear translocation were promoted, and autophagy level was inhibited following β‑glucan treatment of macrophages. Additionally, dectin‑1 small interfering RNA (siRNA), autophagy inducer rapamycin and NF‑κB inhibitor SN50 reversed the effects of β‑glucan on autophagy level and macrophage M1 polarization, suggesting that dectin‑1 and NF‑κB are upstream of autophagy in β‑glucan‑induced macrophage M1 polarization. Notably, simultaneous treatment with dectin‑1 siRNA and SN50 exhibited similar effects on β‑glucan‑reduced autophagy compared with dectin‑1 siRNA treatment alone. These findings demonstrate that dectin‑1 may mediate β‑glucan‑reduced autophagy through NF‑κB in macrophages. Accordingly, results from hematoxylin and eosin staining, western blotting and immunofluorescence staining demonstrated that β‑glucan accelerated the progress of atherosclerosis in apolipoprotein E‑deficient mice and modulated expression of dectin‑1, beclin‑1 and light chain 3II/I in aortas similarly to that observed in macrophages. These results indicate that dectin‑1 activation by β‑glucan exerts atherogenic effects via converting macrophages into M1 phenotype in an NF‑κB‑autophagy‑dependent pathway.
journal_name
Int J Oncoljournal_title
International journal of oncologyauthors
Li X,Luo H,Ye Y,Chen X,Zou Y,Duan J,Xiang Ddoi
10.3892/ijo.2018.4630subject
Has Abstractpub_date
2019-01-01 00:00:00pages
271-282issue
1eissn
1019-6439issn
1791-2423journal_volume
54pub_type
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