2,3-Seco and 3-nor guaianolides fromAchillea alpina with antidiabetic activity.
10.1016/S1875-5364(23)60411-X
- Author:
Guimin XUE
1
;
Chenguang ZHAO
2
;
Jinfeng XUE
2
;
Jiangjing DUAN
2
;
Hao PAN
2
;
Xuan ZHAO
2
;
Zhikang YANG
2
;
Hui CHEN
2
;
Yanjun SUN
2
;
Weisheng FENG
3
Author Information
1. College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou 450046, China. Electronic address: xueguimin123@126.com.
2. College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou 450046, China.
3. College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou 450046, China. Electronic address: fwsh@hactcm.edu.cn.
- Publication Type:Journal Article
- Keywords:
Achillea alpina;
Antidiabetic activity;
Glucose consumption;
Seco-guaianolide
- MeSH:
Humans;
Hypoglycemic Agents/pharmacology*;
Circular Dichroism;
Cytokines;
Glucose;
Hep G2 Cells;
Insulin Resistance
- From:
Chinese Journal of Natural Medicines (English Ed.)
2023;21(8):610-618
- CountryChina
- Language:English
-
Abstract:
In this study, we presented the isolation and characterization of eight novel seco-guaianolide sesquiterpenoids (1-8) and two known guaianolide derivatives (9 and 10), from the aerial part of Achillea alpina L.. Compounds 1-3 were identified as guaianolides bearing an oxygen insertion at the 2, 3 position, while compounds 4-8 belonged to a group of special 3-nor guaianolide sesquiterpenoids. The structural elucidation of 1-8, including their absolute configurations, were accomplished by a combination of spectroscopic data analysis and quantum electronic circular dichroism (ECD) calculations. To evaluate the potential antidiabetic activity of compounds 1-10, we investigated their effects on glucose consumption in palmitic acid (PA)-mediated HepG2-insulin resistance (IR) cells. Among the tested compounds, compound 7 demonstrated the most pronounced ability to reverse IR. Moreover, a mechanistic investigation revealed that compound 7 exerted its antidiabetic effect by reducing the production of the pro-inflammatory cytokine IL-1β, which was achieved through the suppression of the NLRP3 pathway.
