Abstract
It has been shown that antioxidant agents act inhibitorily against neointimal formation after balloon injury, suggesting the role of oxidative stress as a promotor of intimal cell proliferation. Heme oxygenase-1 (HO-1) is an inducible form of heme catabolizing enzyme that is induced by and acts against oxidative tissue injury. In this set of experiments, we showed that HO-1 was present in newly formed neointima; however, arterial HO-1 expression did not increase in response to balloon injury in rat carotid artery. Intraperitoneal administration of hemin, a HO-1 inducer, for 5 consecutive days resulted in about a 4-fold increase of serum bilirubin concentration. In addition, hemin injection increased HO-1 protein expression in the carotid artery, the heart, the kidney, and the liver. In this condition, balloon injury-induced neointimal formation was markedly inhibited. Local application of tin protoporphyrin, a HO inhibitor, blocked this effect, suggesting that induced HO-1 in the carotid artery was responsible for the inhibition of neointimal formation after balloon injury. This study suggests that induction of the endogenous antioxidant gene can suppress neointimal formation after balloon injury.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
