Zhou Dayan, Qu Zongjie, Wang Hao, Su Yong, Wang Yazhu, Zhang Weiwei, Wang Zhe, Xu Qiang
Department of Cardiology, The Fifth People's Hospital of Chongqing, Chongqing 400062, P.R. China.
Exp Ther Med. 2018 Jan;15(1):520-526. doi: 10.3892/etm.2017.5414. Epub 2017 Nov 1.
The aim of the present study was to investigate the effect of hydroxy safflower yellow A (HSYA) on coronary heart disease through assessing the expression of B-cell lymphoma 2 (Bcl-2)/Bcl-2-like protein 4 (Bax) and peroxisome proliferator-activated receptor (PPAR)-γ. Coronary heart disease was induced in male Bama miniature swines via thoracoscope to serve as an animal model. Coronary heart disease swine were lavaged with 20 or 40 mg/kg HSYA. The mRNA levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-10, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were detected using reverse transcription-quantitative polymerase chain reaction. The protein expression of Bcl-2, Bax, PPAR-γ, phosphorylation of Janus kinase (JAK)2 and phosphorylation of signal transducer and activator of transcription (STAT)3 were detected using western blot analysis. Treatment with HSYA significantly suppressed the mRNA levels of IL-1β (P<0.01), IL-6 (P<0.01), TNF-α (P<0.01), COX-2 (P<0.01) and iNOS (P<0.01), and significantly increased IL-10 mRNA level in the coronary heart disease model (P<0.01). Furthermore, HSYA treatment significantly decreased the Bcl-2/Bax ratio (P<0.01) in the coronary heart disease model group, and enhanced the phosphorylation of JAK2/STAT3 pathway (P<0.01). However, HSYA had no significant effect on the expression of PPAR-γ protein. The results of the present study suggest that HSYA is able to weaken coronary heart disease via inflammation, Bcl-2/Bax and the PPAR-γ signaling pathway.
本研究旨在通过评估B细胞淋巴瘤2(Bcl-2)/Bcl-2样蛋白4(Bax)和过氧化物酶体增殖物激活受体(PPAR)-γ的表达,探讨羟基红花黄色素A(HSYA)对冠心病的影响。通过胸腔镜诱导雄性巴马小型猪患冠心病,作为动物模型。给冠心病猪灌胃20或40mg/kg HSYA。采用逆转录-定量聚合酶链反应检测肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β、IL-6、IL-10、环氧化酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)的mRNA水平。采用蛋白质印迹分析检测Bcl-2、Bax、PPAR-γ、Janus激酶(JAK)2的磷酸化和信号转导子及转录激活子(STAT)3的磷酸化。HSYA治疗显著抑制了冠心病模型中IL-1β(P<0.01)、IL-6(P<0.01)、TNF-α(P<0.01)、COX-2(P<0.01)和iNOS(P<0.01)的mRNA水平,并显著提高了IL-10 mRNA水平(P<0.01)。此外,HSYA治疗显著降低了冠心病模型组的Bcl-2/Bax比值(P<0.01),并增强了JAK2/STAT3信号通路的磷酸化(P<0.01)。然而,HSYA对PPAR-γ蛋白的表达没有显著影响。本研究结果表明,HSYA能够通过炎症、Bcl-2/Bax和PPAR-γ信号通路减轻冠心病。