Sinapic Acid Derivative Inhibits EC Activation
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Fig. 6. SA9 inhibited the expression of ICAM-1 on mouse aortic intima
induced by LPS in vivo. C57B mice were fed 50 mg·kg21 body weight SA9
for 1 hour; then, the inflammation was induced by intraperitoneal
injection of LPS (10 mg·kg21 body weight) for 8 hours. Sections of aortic
endothelial underwent en face immunostaining for ICAM-1. The red
fluorescent staining indicates surface ICAM-1 immunoreactivity, and blue
staining represents nuclear staining by Hoechst dye 33258. Images are
representative of results from six mice. Bar graphs show the mean density
of ICAM-1 relative expression. *P , 0.05.
regulation of COX-2 mRNA stability (Singer et al., 2003). We
found that SA9 mainly inhibited TNF-a-induced phosphory-
lation of IKB but also attenuated phosphorylation of JNK and
ERK to a certain degree, which suggests the involvement of
the AP-1 pathway (c-Jun/c-Fos). Our results also indicate the
induction of COX-2 and VCAM-1/ICAM-1 by cytokines via
different mechanisms.
In conclusion, we demonstrated that SA9, a new SA de-
rivative, could efficiently prevent endothelial oxidative stress in
vitro and in vivo. In addition, SA9 could inhibit the TNF-
a-induced NF-kB activation and the expression of cell adhesion
molecules for a potential endothelial protective effect. SA9 may
provide a new therapeutic approach for preventing endothelial
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Authorship Contributions
Pober JS, Min W, and Bradley JR (2009) Mechanisms of endothelial dysfunction,
injury, and death. Annu Rev Pathol 4:71–95.
Participated in research design: Zhu, Zheng, Zeng.
Conducted experiments: Zeng, Fu, Su, Sun, Zhang, Hou.
Contributed new reagents or analytic tools: Zeng, Fu, Su, Sun,
Zhang, Hou.
Performed data analysis: Zeng, Fu, Su, Sun, Zhang, Zhu.
Wrote or contributed to the writing of the manuscript: Zeng, Fu,
Sun, Zhu.
Praticò
D (2005) Antioxidants and endothelium protection. Atherosclerosis 181:
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