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. 2018 Jan;15(1):520-526.
doi: 10.3892/etm.2017.5414. Epub 2017 Nov 1.

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

Dayan Zhou  1 , Zongjie Qu  1 , Hao Wang  1 , Yong Su  1 , Yazhu Wang  1 , Weiwei Zhang  1 , Zhe Wang  1 , Qiang Xu  1
Affiliations

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

Dayan Zhou et al. Exp Ther Med. 2018 Jan.

Abstract

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.

Keywords: B-cell lymphoma 2; B-cell lymphoma-like protein 4; coronary heart disease; hydroxy safflower yellow A; inflammation; peroxisome proliferator-activated receptor-γ.

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Figures

Figure 1.
Figure 1.
Chemical structure of hydroxy safflower yellow A.
Figure 2.
Figure 2.
Effect of HSYA on LVIDs and LVEF in coronary heart disease model. The effect of HSYA on (A) LVIDs and (B) LVEF in a coronary heart disease model. **P<0.01 vs. sham; ##P<0.01 vs. model. HSYA, hydroxy safflower yellow A; LVEF, left ventricular ejection fraction; LVID, left ventricular systolic internal diameter; sham, sham group; model, coronary heart disease model group; HSYA-L, low dose HSYA group; HSYA-H, high dose HSYA group.
Figure 3.
Figure 3.
Effect of HSYA on biochemical composition in coronary heart disease model. The effect of HSYA on (A) Scr, (B) BUN and (C) urine in a coronary heart disease model. **P<0.01 vs. sham; ##P<0.01 vs. model. HSYA, hydroxy safflower yellow A; Scr, plasma creatine; BUN, blood urea nitrogen; sham, sham group; model, coronary heart disease model group; HSYA-L, low dose HSYA group; HSYA-H, high dose HSYA group.
Figure 4.
Figure 4.
Effect of HSYA on the mRNA levels of IL-1β, IL-6, IL-10 and TNF-α in coronary heart disease model. The effect of HSYA on the mRNA levels of (A) IL-1β, (B) IL-6, (C) TNF-α and (D) IL-10 in a coronary heart disease model. **P<0.01 vs. sham; ##P<0.01 vs. model. HSYA, hydroxy safflower yellow A; IL, interleukin; TNF, tumor necrosis factor; sham, sham group; model, coronary heart disease model group; HSYA-L, low dose HSYA group; HSYA-H, high dose HSYA group.
Figure 5.
Figure 5.
Effect of HSYA on the mRNA levels of COX-2 in a coronary heart disease model. **P<0.01 vs. sham; ##P<0.01 vs. model. HSYA, hydroxy safflower yellow A; COX, cyclooxygenase; sham, sham group; Model, coronary heart disease model group; HSYA-L, low dose HSYA group; HSYA-H, high dose HSYA group.
Figure 6.
Figure 6.
Effect of HSYA on the mRNA levels of iNOS in a coronary heart disease model. **P<0.01 vs. sham; ##P<0.01 vs. model. HSYA, hydroxy safflower yellow A; iNOS, inducible nitric oxide synthase; sham, sham group; model, coronary heart disease model group; HSYA-L, low dose HSYA group; HSYA-H, high dose HSYA group.
Figure 7.
Figure 7.
Effect of HSYA on the Bcl-2/Bax ratio and PPAR-γ in coronary heart disease model. The effect of HSYA on the Bcl-2/Bax and PPAR-γ protein expression by (A) western blotting assays and statistical analysis of (B) Bcl-2/Bax and (C) PPAR-γ protein expression in coronary heart disease model. **P<0.01 vs. sham; ##P<0.01 vs. model. HSYA, hydroxy safflower yellow A; Bcl-2, B-cell lymphoma 2; Bax, Bcl-2-like protein 4; Sham, sham group; Model, coronary heart disease model group; HSYA-L, low dose HSYA group; HSYA-H, high dose HSYA group.
Figure 8.
Figure 8.
Effect of HSYA on the phosphorylation of JAK2 and STAT3 protein expression in coronary heart disease model. (A) Western blotting and statistical analysis of (B) p-JAK2 and (C) p-STAT3 protein expression in the coronary heart disease model. **P<0.01 vs. sham; ##P<0.01 vs. model. HSYA, hydroxyl safflower yellow A; JAK, Janus kinase; STAT, signal transducer and activator of transcription; p-, phosphorylated; sham, sham group; model, coronary heart disease model group; HSYA-L, low dose HSYA group; HSYA-H, high dose HSYA group.
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