The effect of hydroxy safflower yellow A on coronary heart disease through Bcl-2/Bax and PPAR-γ.

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)-gamma. 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)-alpha, interleukin (IL)-1 beta, 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-gamma, 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-1 beta (P< 0.01), IL-6 (P< 0.01), TNF-alpha (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-gamma 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-gamma signaling pathway.