Cardiology Center, The People's Hospital of Liaoning Province, Shenyang, 110016, China,
Chin J Integr Med. 2015 Feb;21(2):139-46. doi: 10.1007/s11655-014-1774-2. Epub 2014 Jun 3.
To investigate whether ginsenoside-Rb1 (Gs-Rb1) inhibits the apoptosis of hypoxia cardiomyocytes by up-regulating apelin-APJ system and whether the system is affected by hypoxia-induced factor 1α (Hif-1α).
Neonatal rat cardiomyocytes were randomly divided into 6 groups: a control group, a simple CoCl group, a simple Gs-Rb1 group, a CoCl and Gs-Rb1 hypoxia group, a CoCl and 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (YC-1) group, a CoCl and YC-1 group and a Gs-Rb1 group, in which YC-1 inhibits the synthesis and accelerates the degradation of Hif-1a. The concentration of CoCl, Gs-Rb1 and YC-1 was 500 μmol/L, 200 μmol/L and 5 μmol/L, respectively; the apoptosis ratio was analyzed with a flow cytometer; and apelin, APJ and Hif-1α were assayed with immunocytochemistry, Western blot assays and reverse transcription polymerase chain reaction (RT-PCR).
(1) The anti-apoptosis effect of Gs-Rb1 on hypoxia cardiomyocytes was significantly inhibited by YC-1; (2) Hypoxia significantly up-graded the expression of mRNA and protein of apelin; this effect was further reinforced by Gs-Rb1 and significantly inhibited by YC-1; (3) Gs-Rb1 further strengthened the expression of APJ mRNA and APJ proteins once hypoxia occurred, which was significantly inhibited by YC-1; (4) Gs-Rb1 significantly increased the expression of Hif-1α, which was completely abolished by YC-1; (5) There was a negative relationship between AR and apelin (or APJ, including mRNA and protein), a positive correlation between apelin (or APJ) protein and Hif-1a protein, in hypoxia cardiomyocytes.
The apelin-APJ system plays an important role in the anti-apoptosis effect of Gs-Rb1 on hypoxia neonatal cardiomyocytes, which was partly adjusted by Hif-1α.
探讨人参皂苷 Rb1（Gs-Rb1）是否通过上调孤啡肽（apelin）-孤啡肽受体（APJ）系统抑制缺氧心肌细胞凋亡，以及该系统是否受缺氧诱导因子 1α（Hif-1α）影响。
将乳鼠心肌细胞随机分为 6 组：对照组、单纯 CoCl2 组、单纯 Gs-Rb1 组、CoCl2 和 Gs-Rb1 缺氧组、CoCl2 和 3-(5'-羟甲基-2'-呋喃基)-1-苯并吲哚（YC-1）组、CoCl2 和 YC-1 组及 Gs-Rb1 组，YC-1 抑制 Hif-1α的合成并加速其降解。CoCl2、Gs-Rb1 和 YC-1 的浓度分别为 500μmol/L、200μmol/L 和 5μmol/L；采用流式细胞仪分析细胞凋亡率；免疫细胞化学法、Western blot 法和逆转录聚合酶链反应（RT-PCR）法检测孤啡肽、APJ 和 Hif-1α。
（1）YC-1 明显抑制 Gs-Rb1 对缺氧心肌细胞的抗凋亡作用；（2）缺氧显著上调孤啡肽的 mRNA 和蛋白表达，Gs-Rb1 进一步增强该作用，YC-1 则明显抑制该作用；（3）一旦发生缺氧，Gs-Rb1 进一步增强 APJ mRNA 和蛋白的表达，YC-1 则明显抑制该作用；（4）Gs-Rb1 显著增加 Hif-1α的表达，YC-1 完全消除了这一作用；（5）缺氧心肌细胞中 AR 与孤啡肽（或 APJ，包括 mRNA 和蛋白）呈负相关，孤啡肽（或 APJ）蛋白与 Hif-1α蛋白呈正相关。
孤啡肽-APJ 系统在 Gs-Rb1 抑制缺氧新生心肌细胞凋亡中起重要作用，部分受 Hif-1α调节。
