Rosiglitazone impedes Porphyromonas gingivalis-accelerated atherosclerosis by downregulating the TLR/NF-κB signaling pathway in atherosclerotic mice

Rosiglitazone treatment was associated with less atherosclerotic plaque formation in both P. gingivalis-treated and untreated ApoE-/- mice.

• Inoculation with P. gingivalis was linked to increased atherosclerotic plaque formation and higher levels of pro-inflammatory cytokines in serum.
• Serum lipid profiles remained unchanged despite P. gingivalis infection.
• Higher levels of inflammatory markers and Toll-like receptors were found in aortic tissues of mice exposed to P. gingivalis.
• Rosiglitazone treatment resulted in lower serum inflammatory cytokines and cholesterol levels, as well as enhanced levels of PPARγ in both treated groups.
• The treatment also led to decreased amounts of Toll-like receptors and reduced nuclear factor-κB activity in aortic tissues.

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