Department of Physiology and Pathophysiology, University of Manitoba, Winnipeg, MB, Canada.
Food Funct. 2018 Jun 20;9(6):3466-3480. doi: 10.1039/c8fo00730f.
The present study investigated the effects of cyanidin 3-O-glucoside (C3G) in cardiomyocytes (CM) and fibroblasts exposed to endothelin 1 (ET1), as well as in the spontaneously hypertensive rat (SHR) model, alone or in combination with hydrochlorothiazide (HCT). Adult rat CM and cardiac fibroblasts (CF) were pretreated with C3G and co-incubated with ET1 (10-7 M) for 24 hours. Five-week-old male SHR and their normotensive controls, Wistar-Kyoto rats (WKY), received one of 4 treatments via oral gavage daily for 15 weeks: (1) water (control); (2) C3G (10 mg per kg per day); (3) HCT (10 mg per kg per day); (4) C3G + HCT (10 mg per kg per day each). Blood pressure (BP) was measured at 1, 8 and 15 weeks. Echocardiography measurements were performed at 15 weeks. C3G prevented ET1-induced CM death and hypertrophy. Stimulating CF with ET1 did not induce their phenoconversion; nevertheless, C3G inhibited un-stimulated CF differentiation. HCT slowed the rise of systolic BP (SBP) in the SHR over time (week 1: SHRs control = 161 ± 6.3 mmHg, SHRs HCT = 129 ± 6.3 mmHg; week 15: SHRs control = 201 ± 7.3 mmHg, SHRs HCT = 168 ± 7.3 mmHg), but C3G had no effect on SBP (week 1: SHRs control = 161 ± 6.3 mmHg, SHRs C3G = 126 ± 6.3 mmHg; week 15: SHRs control = 201 ± 7.3 mmHg, SHRs C3G = 186 ± 7.3 mmHg). SHRs treated with C3G, HCT, and C3G + HCT had lower left ventricular mass and shorter isovolumetric relaxation time compared to control SHRs. C3G ameliorated cardiac hypertrophy and diastolic dysfunction in SHRs.
本研究旨在探讨矢车菊素-3-O-葡萄糖苷（C3G）在暴露于内皮素 1（ET1）的心肌细胞（CM）和纤维母细胞中的作用，以及在自发性高血压大鼠（SHR）模型中的作用，单独或与氢氯噻嗪（HCT）联合使用。成年大鼠 CM 和心脏成纤维细胞（CF）用 C3G 预处理，并与 ET1（10-7 M）共孵育 24 小时。5 周龄雄性 SHR 和其正常血压对照，Wistar-Kyoto 大鼠（WKY），通过口服灌胃每天接受 4 种治疗中的 1 种，持续 15 周：（1）水（对照）；（2）C3G（10 毫克/公斤/天）；（3）HCT（10 毫克/公斤/天）；（4）C3G+HCT（10 毫克/公斤/天）。在 1、8 和 15 周时测量血压（BP）。在 15 周时进行超声心动图测量。C3G 可预防 ET1 诱导的 CM 死亡和肥大。用 ET1 刺激 CF 不会诱导其表型转化；然而，C3G 抑制了未受刺激的 CF 分化。随着时间的推移，HCT 减缓了 SHR 的收缩压（SBP）升高（第 1 周：SHR 对照组=161±6.3mmHg，SHR HCT 组=129±6.3mmHg；第 15 周：SHR 对照组=201±6.3mmHg，SHR HCT 组=168±6.3mmHg），但 C3G 对 SBP 没有影响（第 1 周：SHR 对照组=161±6.3mmHg，SHR C3G 组=126±6.3mmHg；第 15 周：SHR 对照组=201±6.3mmHg，SHR C3G 组=186±6.3mmHg）。与对照组 SHR 相比，用 C3G、HCT 和 C3G+HCT 治疗的 SHR 左心室质量较低，等容舒张时间较短。C3G 改善了 SHR 的心脏肥大和舒张功能障碍。
