Inhibition by higenamine of lipopolysaccharide-induced iNOS and mRNA expression and NO production in rat aorta.
- Author:
Young Jin KANG
1
;
Goun Woo LEE
;
Eui Bon KU
;
Hoi Young LEE
;
Ki Churl CHANG
Author Information
1. Department of Pharmacology, College of Medicine, GyeongSang National University, Chinju 660-280, Korea.
- Publication Type:In Vitro ; Original Article
- Keywords:
Higenamine;
Nitric oxide;
Rheumatoid arthritis;
Lipopolysaccharide;
iNOS mRNA;
Rat;
Aorta
- MeSH:
Animals;
Aorta*;
Arthritis;
Arthritis, Rheumatoid;
Humans;
Muscle, Smooth, Vascular;
Nitric Oxide;
Nitric Oxide Synthase;
Rats*;
Relaxation;
RNA, Messenger*
- From:The Korean Journal of Physiology and Pharmacology
1997;1(3):297-302
- CountryRepublic of Korea
- Language:English
-
Abstract:
Higenamine was widely used as traditional remedy for the treatment of rheumatoid arthritis. Nitric oxide (NO) may be a critical mediator in this inflammatory disease. Synovial tissue from humans with inflammatory arthritis expresses NOS2 (iNOS) mRNA and protein, and generates NO in vitro. We therefore, investigated the effect of higenamine on the induction of nitric oxide synthase (NOS) promoted by lipopolysaccharide (LPS). Prophylactic application of higenamine selectively prevented LPS-primed initiation of L-arginine-induced relaxation and restored phenylephrine(PE)-induced contraction in rat aorta. LPS-stimulated nitrite production in the incubation medium was reduced by higenamine. Furthermore, RT-PCR and Northern analysis indicated that higenamine reduced iNOS expression primed by LPS in rat aorta. These results suggest that higenamine prevents LPS-promoted induction of NOS in vascular smooth muscle.
