Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK

Wu, Yue; Yang, Ying; Li, Fang; Zhang, Jie; Wang, Yuhao; Xu, Mengxia; Wang, Yonglun; Li, Ruixi; Sun, Yuting; Lü, Shun; Zhang, Yuanyuan; Sun, Xiaodong

doi:10.14218/jcth.2021.00050

Cited by 6 publications

(6 citation statements)

References 20 publications

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“…The role of autophagy in obesity is shown in a recent study by Zhang et al demonstrating that inhibition of autophagy through the downregulation of FOXO3 leads to lipid accumulation in adipocytes of mice ( 61 ). The association between autophagy inhibition and adipocyte lipid accumulation was also described in a study by Wu et al The use of icaritin, an osteoinductive agent, attenuated lipid accumulation with an increase in autophagy flux ( 62 ). As adipocyte lipid accumulation is closely related to obesity, this suggests that autophagy may participate in regulating obesity condition by inhibiting lipid accumulation.…”

Section: Sirt1-mediated Autophagy and Endocrine Disordersmentioning

confidence: 71%

SIRT1 and Autophagy: Implications in Endocrine Disorders

et al. 2022

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Autophagy is a cellular process involved in the selective degradation and recycling of dysfunctional intracellular components. It plays a crucial role in maintaining cellular homeostasis and survival by removing damaged and harmful proteins, lipids, and organelles. SIRT1, an NAD+-dependent multifunctional enzyme, is a key regulator of the autophagy process. Through its deacetylase activity, SIRT1 participates in the regulation of different steps of autophagy, from initiation to degradation. The levels and function of SIRT1 are also regulated by the autophagy process. Dysregulation in SIRT1-mediated autophagy hinders the proper functioning of the endocrine system, contributing to the onset and progression of endocrine disorders. This review provides an overview of the crosstalk between SIRT1 and autophagy and their implications in obesity, type-2 diabetes mellitus, diabetic cardiomyopathy, and hepatic steatosis.

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Section: Sirt1-mediated Autophagy and Endocrine Disordersmentioning

confidence: 71%

SIRT1 and Autophagy: Implications in Endocrine Disorders

et al. 2022

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“…Our previous study also demonstrated that ICT regulates autophagy depending on the cell status of 3 T3-L1 cells and C2C12 cells. 33 ICT has been reported to regulate autophagy via AMPK. 14,33 ICT has also been reported to inhibit skin fibrosis by regulating AMPK and the Wnt/β-catenin pathway.…”

Section: Discussionmentioning

confidence: 99%

“…33 ICT has been reported to regulate autophagy via AMPK. 14,33 ICT has also been reported to inhibit skin fibrosis by regulating AMPK and the Wnt/β-catenin pathway. 34 We therefore assumed that ICT alleviates DTX-induced skin injury through activating AMPK.…”

Section: Discussionmentioning

confidence: 99%

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Icaritin alleviates docetaxel‐induced skin injury by suppressing reactive oxygen species via estrogen receptors

Zhang

et al. 2021

Thoracic Cancer

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Background: Docetaxel (DTX) exhibits antitumor effects against breast cancer by stabilizing microtubules and increasing the accumulation of reactive oxygen species (ROS). DTX extravasation during infusion often causes skin injury. The present study aimed to investigate the effects and mechanisms of icaritin (ICT) on DTX-induced skin injury. Methods: The effects of ICT on the viability and apoptosis of HaCaT cells were measured by SRB assay and flow cytometry, respectively. Endogenous LC3 puncta and microtubules were determined by immunofluorescence. The number of mitochondria was measured by MitoTracker orange staining. ROS were determined by dihydroethidium staining. The expression of markers of ROS and autophagy were measured by western blotting. Chloroquine, compound D, and tamoxifen were employed as the inhibitor for autophagy and AMPK, estrogen receptors (ERs) modulator, respectively. Results: DTX inhibited the viability and decreased apoptosis of HaCaT cells, which can be rescued by ICT. ICT decreased microtubule bundles, increased the number of mitochondria, and attenuated ROS of HaCaT cells induced by DTX. ICT blocks autophagy and the autophagic flux. Compound C or tamoxifen diminished the protection effects of ICT on DTX-treated HaCaT cells. Conclusion: ICT alleviates DTX-induced skin injury by suppressing ROS, reducing microtubule bundles, and blocking autophagy via ERs. Our study indicated that ICT may be a potential candidate for DTX-induced skin injury.

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“…Although vitamin E and pioglitazone have been demonstrated to be beneficial for NAFLD patients, the United States Food and Drug Administration hasn’t approved any specific drugs [ 6 ]. However, our previous studies have demonstrated that flavonoids such as naringenin and icaritin have obvious effects on ameliorating NAFLD [ 7 , 8 ]. As a kind of flavonoid, psoralen is the major antioxidant of Medik (syn.…”

Section: Introductionmentioning

confidence: 99%

Psoralen Suppresses Lipid Deposition by Alleviating Insulin Resistance and Promoting Autophagy in Oleate-Induced L02 Cells

Wang

et al. 2022

Cells

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Non-alcoholic fatty liver disease (NAFLD) held a high global prevalence in recent decades. Hepatic lipid deposition is the major characteristic of NAFLD. We aim to explore the mechanisms of psoralen on lipid deposition in NAFLD. The effects of psoralen on insulin resistance, lipid deposition, the expression and membrane translocation of glucose transporter type 4 (GLUT4), autophagy, and lipogenesis enzymes were determined on sodium oleate-induced L02 cells. Chloroquine and 3-MA were employed. The AMP-activated protein kinase alpha (AMPKα) was knocked down by siRNA. Psoralen alleviated insulin resistance in sodium oleate-induced L02 hepatocytes by upregulating the expression and membrane translocation of GLUT4. Psoralen inhibited lipid accumulation by decreasing the expression of key lipogenesis enzymes. Psoralen promotes autophagy and the autophagic flux to enhance lipolysis. Psoralen promoted the fusion of the autophagosome with the lysosome. Both chloroquine and 3-MA blocked the effects of psoralen on autophagy and lipid accumulation. The AMPKα deficiency attenuated the effects of psoralen on autophagy and lipid accumulation. Our study demonstrated that as an antioxidant, psoralen attenuates NAFLD by alleviating insulin resistance and promoting autophagy via AMPK, suggesting psoralen to be a promising candidate for NAFLD.

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Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK

Cited by 6 publications

References 20 publications

SIRT1 and Autophagy: Implications in Endocrine Disorders

SIRT1 and Autophagy: Implications in Endocrine Disorders

Icaritin alleviates docetaxel‐induced skin injury by suppressing reactive oxygen species via estrogen receptors

Psoralen Suppresses Lipid Deposition by Alleviating Insulin Resistance and Promoting Autophagy in Oleate-Induced L02 Cells

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