Alisol A 24-acetate stimulates lipolysis in 3 T3-L1 adipocytes

Abstract Background Alisol A 24-acetate (AA-24-a), one of the main active triterpenes isolated from the well-known medicinal plant Alisma orientale (Sam.) Juz., exhibits multiple biological activities including hypolipidemic activity. However, its effect on lipid metabolism in adipocytes remains unc...

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Main Authors: Hai-xia Lou, Wen-cheng Fu, Jia-xiang Chen, Tian-tian Li, Ying-ying Jiang, Chun-hui Liu, Wen Zhang
Format: Article
Language:English
Published: BMC 2021-04-01
Series:BMC Complementary Medicine and Therapies
Subjects:
Online Access:https://doi.org/10.1186/s12906-021-03296-0
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author Hai-xia Lou
Wen-cheng Fu
Jia-xiang Chen
Tian-tian Li
Ying-ying Jiang
Chun-hui Liu
Wen Zhang
author_facet Hai-xia Lou
Wen-cheng Fu
Jia-xiang Chen
Tian-tian Li
Ying-ying Jiang
Chun-hui Liu
Wen Zhang
author_sort Hai-xia Lou
collection DOAJ
description Abstract Background Alisol A 24-acetate (AA-24-a), one of the main active triterpenes isolated from the well-known medicinal plant Alisma orientale (Sam.) Juz., exhibits multiple biological activities including hypolipidemic activity. However, its effect on lipid metabolism in adipocytes remains unclear. The present study aimed to clarify the effect of AA-24-a on adipocyte lipolysis and to determine its potential mechanism of action using 3 T3-L1 cells. Methods We assayed the release of glycerol into culture medium of 3 T3-L1 cells under treatment with AA-24-a. Protein and mRNA expression and phosphorylation levels of the main lipases and kinases involved in lipolysis regulation were determined by quantitative polymerase chain reaction and western blotting. Specific inhibitors of protein kinase A (PKA; H89) and extracellular signal-regulated kinase (ERK; PD98059), which are key enzymes in relevant signaling pathways, were used to examine their roles in AA-24-a-stimulated lipolysis. Results AA-24-a significantly stimulated neutral lipolysis in fully differentiated adipocytes. To determine the underlying mechanism, we assessed the changes in mRNA and protein levels of key lipolysis-related genes in the presence or absence of H89 and PD98059. Both inhibitors reduced AA-24-a-induced lipolysis. Moreover, pretreatment with H89 attenuated AA-24-a-induced phosphorylation of hormone-sensitive lipase at Ser660, while pretreatment with PD98059 attenuated AA-24-a-induced downregulation of peroxisome proliferator-activated receptor-γ and perilipin A. Conclusions Our results indicate that AA-24-a promoted neutral lipolysis in 3 T3-L1 adipocytes by activating PKA-mediated phosphorylation of hormone-sensitive lipase and ERK- mediated downregulation of expression of perilipin A.
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spelling doaj.art-ef5d6e0451c74b09b62725fb35ff9f3c2022-12-21T21:56:33ZengBMCBMC Complementary Medicine and Therapies2662-76712021-04-0121111110.1186/s12906-021-03296-0Alisol A 24-acetate stimulates lipolysis in 3 T3-L1 adipocytesHai-xia Lou0Wen-cheng Fu1Jia-xiang Chen2Tian-tian Li3Ying-ying Jiang4Chun-hui Liu5Wen Zhang6School of Life Sciences, East China Normal UniversitySchool of Life Sciences, East China Normal UniversitySchool of Life Sciences, East China Normal UniversitySchool of Life Sciences, East China Normal UniversitySchool of Life Sciences, East China Normal UniversityChina National Institute of StandardizationSchool of Life Sciences, East China Normal UniversityAbstract Background Alisol A 24-acetate (AA-24-a), one of the main active triterpenes isolated from the well-known medicinal plant Alisma orientale (Sam.) Juz., exhibits multiple biological activities including hypolipidemic activity. However, its effect on lipid metabolism in adipocytes remains unclear. The present study aimed to clarify the effect of AA-24-a on adipocyte lipolysis and to determine its potential mechanism of action using 3 T3-L1 cells. Methods We assayed the release of glycerol into culture medium of 3 T3-L1 cells under treatment with AA-24-a. Protein and mRNA expression and phosphorylation levels of the main lipases and kinases involved in lipolysis regulation were determined by quantitative polymerase chain reaction and western blotting. Specific inhibitors of protein kinase A (PKA; H89) and extracellular signal-regulated kinase (ERK; PD98059), which are key enzymes in relevant signaling pathways, were used to examine their roles in AA-24-a-stimulated lipolysis. Results AA-24-a significantly stimulated neutral lipolysis in fully differentiated adipocytes. To determine the underlying mechanism, we assessed the changes in mRNA and protein levels of key lipolysis-related genes in the presence or absence of H89 and PD98059. Both inhibitors reduced AA-24-a-induced lipolysis. Moreover, pretreatment with H89 attenuated AA-24-a-induced phosphorylation of hormone-sensitive lipase at Ser660, while pretreatment with PD98059 attenuated AA-24-a-induced downregulation of peroxisome proliferator-activated receptor-γ and perilipin A. Conclusions Our results indicate that AA-24-a promoted neutral lipolysis in 3 T3-L1 adipocytes by activating PKA-mediated phosphorylation of hormone-sensitive lipase and ERK- mediated downregulation of expression of perilipin A.https://doi.org/10.1186/s12906-021-03296-0Alisma orientale (Sam.) Juz.Alisol A 24-acetateLipolysis3 T3-L1 adipocyteObesity
spellingShingle Hai-xia Lou
Wen-cheng Fu
Jia-xiang Chen
Tian-tian Li
Ying-ying Jiang
Chun-hui Liu
Wen Zhang
Alisol A 24-acetate stimulates lipolysis in 3 T3-L1 adipocytes
BMC Complementary Medicine and Therapies
Alisma orientale (Sam.) Juz.
Alisol A 24-acetate
Lipolysis
3 T3-L1 adipocyte
Obesity
title Alisol A 24-acetate stimulates lipolysis in 3 T3-L1 adipocytes
title_full Alisol A 24-acetate stimulates lipolysis in 3 T3-L1 adipocytes
title_fullStr Alisol A 24-acetate stimulates lipolysis in 3 T3-L1 adipocytes
title_full_unstemmed Alisol A 24-acetate stimulates lipolysis in 3 T3-L1 adipocytes
title_short Alisol A 24-acetate stimulates lipolysis in 3 T3-L1 adipocytes
title_sort alisol a 24 acetate stimulates lipolysis in 3 t3 l1 adipocytes
topic Alisma orientale (Sam.) Juz.
Alisol A 24-acetate
Lipolysis
3 T3-L1 adipocyte
Obesity
url https://doi.org/10.1186/s12906-021-03296-0
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