Abnormal
collagen deposition, as well as
collagen metabolism, plays a crucial role in the formation and progression of vulnerable
atherosclerotic plaques (VAPs), which are susceptible to
rupture. According to our previous findings,
rosiglitazone, a
thiazolidinedione, can promote the stability of
atherosclerotic plaques in fat-fed ApoE-knockout mice; however, it is unknown whether it can modulate
collagen deposition and metabolism in VAPs. The present study was designed to determine the effect of
rosiglitazone on
collagen deposition and metabolism in the plaques of fat-fed ApoE-knockout mice. Following 13 weeks of the high-fat diet, the mice were randomized into three groups (10 mice/group) and intragastrically administered
rosiglitazone,
simvastatin and distilled water, respectively, for a further 13 weeks. The category of the
collagen present in the plaques was evaluated using the picro-Sirius red polarization method. Additionally, the
protein expression of
matrix metalloproteinase 9 (MMP-9) and
tissue inhibitor of metalloproteinase-1 (TIMP-1) in the plaques was determined using immunohistochemistry. The results showed that
rosiglitazone reduced the
lipid to
collagen and type III to
type I collagen ratios in the plaques, and these reductions were correlated with the reduction in the plaque MMP-9 to
TIMP-1 ratio. These results suggest that
rosiglitazone can modulate
collagen deposition and metabolism and promote the stabilization of VAPs.