CARDIOVASCULAR ENGINEERING Journal for Extracorporeal Circulation, Assist Devices,Transplantation and Artificial Organs
	Volume 5, 2000, No 1

Low-dose Cyclosporine and Triptolide Inhibit Cardiac Graft Rejection and Coronary Arteriosclerosis
M. Hachida, K. Yasumoto

Graft coronary arteriosclerosis (GCA) is a major limiting factor for long-term survival after heart transplantation. In this study, we investigated the effect of triptolide in combination with cyclosporine on GCA and platelet-derived growth factor-A (PDGF-A) mRNA chain expression of cardiac allograft in a rat model. Twenty-one heterotopic heart transplantations were conducted using Lewis rats as a recipient and Wistar-King donors as donor. Cyclosporine (10 mg/kg/day) was administrated in control group and triptolide 3.75 µg/kg/day and 37.5 µg/kg/day were administrated in triptolide group A and B respectively. Histological evaluations of rejection and coronary arteriosclerosis were performed and graft PDGF-A mRNA expression was evaluated using Northern blot analysis on day 60 after transplantation. Morphometric findings indicated no significant difference in rejection between the control and triptolide treated groups. However, the extent of graft coronary arteriosclerosis in the triptolide treated groups was significantly less than that seen in the control group (p < 0.01). The expression of PDGF-A mRNA chain of cardiac allograft was also significantly suppressed in the triptolide treated groups when compared with the control group (P < 0.01 respectively). The combined use of Triptolide with cyclosporine showed significant inhibitory effect on graft coronary arteriosclerosis following heart transplantation by inhibiting expression of graft PDGF-A chain mRNA. 

Key words: coronary arteriosclerosis, heart transplantation, platelet-derived growth factor, immunosuppressants

Address for Correspondence:
Mitsuhiro Hachida, M.D.
Second Department of Surgery
Sangyow Medical University
1-1, Iseigaoka , Yahatanishiku , Kitakyushuw, Fukuoka, 817-8555
Japan
E-mail: hachidam@med.uoeh-u.ac.jp

Reference:
(CVE. 2000; 5 (1): 36-40)

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