All-trans retinoic acid attenuates cardiac allograft vasculopathy and myocardial fibrosis
10.3760/cma.j.issn.0254-1785.2009.07.002
- VernacularTitle:全反式维甲酸减轻大鼠移植心脏血管病变及纤维化
- Author:
Mingkui ZHANG
;
Qingyu WU
;
Jianguo HU
- Publication Type:Journal Article
- Keywords:
Heart transolantation;
Vascular diseases;
Fibrosis;
Tretinoin;
Rats
- From:
Chinese Journal of Organ Transplantation
2009;30(7):394-397
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism of albtrans retinoic acid (atRA)attenuating cardiac allograft vasculopathy and myocardial fibrosis. Methods With inbred Wistar rats as donors and Sprague Dawley (SD) rats as recipients, heterotopic heart transplantation model was rejection group received same doses of cyclosporine A for 60 days. Grafts were removed on the day 60 post-transplant. Paraffin-embedded sections of cardiac allograft were stained with Masson's trichrome and Van Gieson for examination of myocardial fibrosis and vascular stenosis. Immunohistochemistry was performed to observe CD68 positive cell infiltration. Platelet-derived growth factor-A (PDGF-A)mRNA was detected by using reverse transcription-polymerase chain reaction (RT-PCR). Results The index of fibrosis in chronic rejection group and atRA-treated group was 64. 0 ± 11.9 and 34. 7 ±6. 3 respectively with the significant difference (P<0. 01). Chronic rejection all,grafts showed severe vessel disease. The luminal occlusion index of coronary arteries in chronic rejection group was 62. 9 4± 17. 2, and 40. 1± 8. 2 in atRA-treated group with significant difference (P<0. 01). CD68-positive cell count in atRA-treated group and chronic rejection group was 17. 6 4± 4. 2 and 32. 1 ± 9. 3 with significant difference (P<0. 01). The relative expression levels of PDGF-A mRNA in atRA-treated group and chronic rejection group were 0. 46 ± 0. 08 and 0. 94 4±0. 11 respectively with significant difference (P<0. 01). Conclusion AtRA attenuates cardiac all,graft vasculopathy and myocardial fibrosis. The effects might be induced by inhibition of CD68 positive cell infiltration and PDGF-A mRNA expression.
