Epimedium koreanum Nakai and its main constituent icariin suppress lipid accumulation during adipocyte differentiation of 3T3-L1 preadipocytes

Cao

et al. 2018

Front. Pharmacol.

Both thioredoxin-interacting protein (TXNIP) and endoplasmic reticulum (ER) stress are implicated in skeletal muscle insulin resistance. Icariin has been found to mimic insulin action in normal skeletal muscle C2C12 cells and display anti-diabetic properties in diet-induced obese mice. However, the underlying molecular mechanism remains to be well-established. Herein, we tested the hypothesis that the protective effects of icariin on free fatty acid-induced insulin resistance were attributed to its regulation on TXNIP protein levels and ER stress in skeletal muscle cells. We found that TXNIP mediated the saturated fatty acid palmitate (PA)-induced insulin resistance in C2C12 myotubes. Icariin treatment significantly restored PA-reduced proteasome activity resulting in reduction of TXNIP protein and suppression of ER stress, as well as improvement of insulin sensitivity. Proteasome inhibition by its specific inhibitor MG132 obviously abolished the inhibitory effect of icariin on PA-induced insulin resistance. In addition, MG132 supplementation markedly abrogated the impacts of icariin on ER stress and TXNIP-mediated downstream events such as inflammation and STAT3 phosphorylation. These results clearly indicate that icariin improves PA-induced skeletal muscle insulin resistance through a proteasome-dependent mechanism, by which icariin downregulats TXNIP levels and inhibits ER stress.

Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

RETRACTED: Icariin Ameliorates Palmitate-Induced Insulin Resistance Through Reducing Thioredoxin-Interacting Protein (TXNIP) and Suppressing ER Stress in C2C12 Myotubes

Cao

et al. 2018

Front. Pharmacol.

“…The potential mechanisms could be twofold. On the one hand, Icariin could inhibit cholesterol synthesis and uptake via sterol regulatory element-binding protein (SREBP) ( Han et al, 2016 ) and scavenger receptor (CD36) ( Yang et al, 2015 ), respectively. On the other hand, Icariin could promote SR-BI-mediated cholesterol efflux ( Yang et al, 2015 ) and facilitate cholesterol excretion.…”

Section: Potential Molecular Targets Of Icariinmentioning

confidence: 99%

Icariin, an Anti-atherosclerotic Drug from Chinese Medicinal Herb Horny Goat Weed

Fang

2017

Front. Pharmacol.

Icariin is a major bioactive pharmaceutical constituent isolated from Chinese medicine Horny Goat Weed (Ying Yang Huo) with potent cardiovascular protective functions. Emerging evidence in the past decade has shown that Icariin possesses multiple atheroprotective functions, through multiple mechanisms, including attenuating DNA damage, correcting endothelial dysfunction, inhibiting the proliferation and migration of smooth muscle cells, repressing macrophage-derived foam cell formation and inflammatory responses, as well as preventing platelet activation. All of these protective effects, combined with its lipid-modulatory effects, contribute to the broad atheroprotective effects of Icariin. In this review, we will summarize the anti-atherosclerotic properties of Icariin and highlight future perspectives in developing Icariin as a promising anti-atherosclerotic drug.

“…Icariin is the main constituent of Herba Epimedii. Han et al found that Icariin can inhibit the adipocyte differentiation through downregulation of the adipogenic transcription factors [26]. Zhang et al show that Icariin could inhibit adipogenic differentiation of BMSCs in the osteoblast-osteoclast coculture [27].…”

Section: Discussionmentioning

confidence: 99%

Pingmu Decoction Induces Orbital Preadipocytes Apoptosis In Vitro

Evidence-Based Complementary and Alternative Medicine

Gao

et al. 2017

Pingmu Decoction is the Traditional Chinese Medicine which has treated Graves' Ophthalmopathy (GO) in the inactive stage for more than ten years. This study was to explore the mechanism of Pingmu Decoction of inhibiting preadipocytes in GO patients from differentiating into mature adipocytes. Human orbital preadipocytes were isolated and cultured through tissue explant method. Orbital preadipocytes were induced into mature adipocytes. The medicinal serum was prepared from rats. The cells were treated with medicinal serum which were divided into three groups, low dose group (5%), medium dose group (10%), and high dose group (20%). The cells viabilities were observed by Oil Red O staining, MTT method, and Annexin V/propidium iodide (PI) double staining. Effect of Pingmu Decoction on cell apoptosis rate of orbital matured adipocytes was measured by flow cytometry. The genes Fas and Fas L from cell groups were tested by RT-PCR and Western blotting. The expression of master adipogenic transcription factors, including peroxisome proliferation-activity receptor (PPAR) γ and CCAAT/enhancer binding protein (C/EBP) α, was tested by Western blotting. Pingmu Decoction could reduce orbital preadipocytes viability and induce apoptosis of mature adipocyte via Fas/Fas L signaling pathway. Pingmu Decoction reduced lipid accumulation and downregulated the expression of PPAR γ and C/EBP α. Pingmu Decoction may play a therapeutic effect by reducing the accumulation of orbital adipocytes.