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Hemistepsin A inhibits T0901317-induced lipogenesis in the liver
Jae Kwang Kim1,2,# (Researcher), Il Je Cho 1,# (Professor), Eun Ok Kim1 (Researcher), Dae Geon Lee1 (Post-Doc Researcher), Dae Hwa Jung1,3 (Researcher), Sung Hwan Ki4 (Professor), Sae Kwang Ku 1 (Professor), Sang Chan Kim 1,* (Professor)
1College of Korean Medicine, Daegu Haany University,
2Korean Medicine-Application Center, Korea Institute of Oriental Medicine,
3Research Center, Hani Bio,
4College of Pharmacy, Chosun University
Abstract
Hemistepsin A (HsA) is a guaianolide sesquiterpene lactone that inhibits hepatitis and liver fibrosis. We evaluated the effects of HsA on liver X receptor (LXR)-mediated hepatic lipogenesis in vitro and in vivo. Up to 10 レM, HsA did not affect the viability of HepG2 and Huh7 cells. Pretreatment with 5–10 レM HsA significantly decreased the luciferase activity of the LXR response element, which was transactivated by T0901317, GW3965, and LXRメ/retinoid X receptor メ overexpression. In addition, it significantly inhibited the mRNA expression of LXRメ in HepG2 and Huh7 cells. It also suppressed the expression of sterol regulatory element-binding protein-1c and lipogenic genes and reduced the triglyceride accumulation triggered by T0901317. Intraperitoneal injection of HsA (5 and 10 mg/kg) in mice significantly alleviated the T0901317-mediated increases in hepatocyte diameter and the percentage of regions in hepatic parenchyma occupied by lipid droplets. Furthermore, HsA significantly attenuated hepatic triglyceride accumulation by restoring the impaired expression of LXRメ-dependent lipogenic genes caused by T0901317. Therefore, based on its inhibition of the LXRメ-dependent signaling pathway, HsA has prophylactic potential for steatosis.
Abstract, Accepted Manuscript(in press) [Submitted on May 26, 2020, Accepted on July 21, 2020]
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