Atractylenolide II-ameliorated hyperlipidemia in mice by regulating AMPK/PPARα/SREBP-1C signaling pathway

In this paper, we present our study on the effect of atractylenolide II on hyperlipidemic model mice. After 8 weeks, the blood of these mice was taken to detect four lipids. Pathological changes were detected in the aortas and livers of the mice. Expression of PPARα and SREBP-1C was detected in the liver by western blot. An enzyme-linked immunosorbent assay was used to detect the effects of atractylenolide II on blood lipids in hyperlipidemia mice. Hematoxylin and eosin staining was used to detect pathological changes in the aortas and livers of mice with hyperlipidemia after treatment with atractylenolide II. Changes in PPARα and SREBP-1C expression were found in mice with dyslipidemia. As the results shown, atractylenolide II administration reduced body weight and hyperlipidemia in hyperlipidemic model mice. In addition, atractylenolide II effectively relieved fat deposition and damage in aortic and liver tissues. Therefore, atractylenolide II had a beneficial therapeutic effect in reducing hyperlipidemia in hyperlipidemic model mice, which may be related to its ability to inhibit SREBP-1C expression by activating PPARα. The molecular mechanism driving the therapeutic effect of atractylenolide II may involve upregulation of PPARα and activation of the AMPK/PPARα/SREBP-1C signaling pathway. Our research demonstrated the development of therapeutic agents that can be used to improve hyperlipidemia.