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Published on: March 28, 2013
β-Glucan attenuates inflammatory responses in oxidized LDL-induced THP-1 cells via the p38 MAPK pathway
1Oncology Institute, The Affiliated Hospital of Nanjing Medical University, Changzhou No. 2 People's Hospital, Changzhou 213003, China; Central Lab, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou 213003, China.
Aim:
To investigate the immunomodulatory effects of β-(1,3/1,6)-d-glucan on atherosclerosis as well as on the molecular mechanisms of its transition.
Methods And Results:
Human monocytic leukemia (THP-1) cells were differentiated into the macrophage phenotype by incubation with oxLDL in the absence or presence of β-glucan. β-glucan attenuated CD86 and CD80 expression and simultaneously reduced secretion of the inflammatory cytokines IL-2, IL-8, IL-12, TNF-α and IFN-γ. Western blot analysis showed that oxLDL treatment induced phosphorylation of p38 MAPK and ERK1/2 in PMA-differentiated THP-1 cells. However, β-glucan inhibited p38 MAPK activation. In experiments with monocytes derived from healthy donors, β-glucan inhibited IL-8, IL-12 and TNF-α production. The anti-inflammatory effects of β-glucan were also observed in atherosclerotic plaque cells.
Conclusions:
β-glucan inhibited oxLDL-induced pro-inflammatory effects in macrophages via regulation of p38 MAPK phosphorylation. This novel finding may provide insight for new therapeutic strategies.
