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- Title
L-citrulline for protection of endothelial function from ADMA-induced injury in porcine coronary artery.
- Authors
Xuan, Chao; Lun, Li-Min; Zhao, Jin-Xia; Wang, Hong-Wei; Wang, Jue; Ning, Chun-Ping; Liu, Zhen; Zhang, Bei-Bei; He, Guo-Wei
- Abstract
Endogenous nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) is a cardiovascular risk factor. We tested the hypothesis that L-citrulline may ameliorate the endothelial function altered by ADMA in porcine coronary artery (PCA). Myograph study for vasorelaxation, electrochemical measurement for NO, RT-PCR, and Western blot analysis for expression of eNOS, argininosuccinate synthetase (ASS), and p-eNOSser1177 were performed. cGMP was determined by enzyme immunoassay. Superoxide anion (O2.−) production was detected by the lucigenin-enhanced chemiluminescence method. Compare with controls (96.03% ± 6.2%), the maximal relaxation induced by bradykinin was significantly attenuated (61.55% ± 4.8%, p < 0.01), and significantly restored by L-citrulline (82.67 ± 6.4%, p < 0.05) after 24 hours of ADMA exposure. Expression of eNOS, p-eNOSser1177, and ASS in PCA significantly increased after L-citrulline incubation. L-citrulline also markedly restored the NO production, and cGMP level which was reduced by ADMA. The increased O2.− production by ADMA was also inhibited by L-citrulline. L-citrulline restores the endothelial function in preparations treated with ADMA by preservation of NO production and suppression of O2.− generation. Preservation of NO is attributed to the upregulation of eNOS expression along with activation of p-eNOSser1177. L-citrulline improves endothelium-dependent vasodilation through NO/ cGMP pathway.
- Subjects
CITRULLINE; CORONARY artery injuries; ASYMMETRIC dimethylarginine; ARGININOSUCCINATE synthetase; SUPEROXIDES; BRADYKININ; WESTERN immunoblotting
- Publication
Scientific Reports, 2015, p10987
- ISSN
2045-2322
- Publication type
Article
- DOI
10.1038/srep10987