scholarly journals Aspirin enhances the sensitivity of hepatocellular carcinoma side population cells to doxorubicin via miR-491/ABCG2

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Zheng-Yuan Xie ◽  
Mao-Sheng Liu ◽  
Cong Zhang ◽  
Peng-Cheng Cai ◽  
Zhi-Hua Xiao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Viability ◽  
Colony Formation ◽  
Side Population ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Flow Cytometry Analysis ◽  
Side Population Cells ◽  
Concentration Dependent Manner

Objective: To explore whether aspirin (ASA) enhances the sensitivity of hepatocellular carcinoma (HCC) side population (SP) cells to doxorubicin (Doxo) via miR-491/ATP-binding cassette sub-family G member 2 (ABCG2).Methods: Non-SP and SP cells were isolated from MHCC-97L cell line using flow cytometry analysis and fluorescence-activated cell sorting. Colony formation assay was performed to determine the colony-formation ability of cells. Cell viability of SP cells was determined with the MTT assay. Luciferase reporter assay was applied in confirming the binding between miR-491 and ABCG2.Results: Although the Doxo treatment lowered the colony-formation ability of both non-SP and SP cells, the colony-formation ability of SP cells was 2-fold higher than that of non-SP cells (P<0.05). Doxo slightly inhibited the cell viability of SP cells in a concentration-dependent manner; the addition of ASA dramatically enhanced the inhibitory effect of Doxo on SP cell viability in a concentration-dependent manner (P<0.05). Compared with non-SP cells, the miR-491 expression was significantly decreased in SP cells, which was significantly reversed by ASA (P<0.05). miR-491 directly controlled the ABCG2 expression. In the presence of Doxo, miR-491 inhibitor reduced the inhibitory effect of ASA on the cell viability of SP cells, which was significantly reversed by knockdown of ABCG2 (P<0.05).Conclusion: ASA enhanced the sensitivity of SP cells to Doxo via regulating the miR-491/ABCG2 signaling pathway.

scholarly journals MicroRNA-518-3p suppresses cell proliferation, invasiveness, and migration in colorectal cancer via targeting TRIP4

2020 ◽  
Vol 98 (5) ◽  
pp. 575-582
Author(s):  
Heng Yang ◽  
Jia Ren ◽  
Yu Bai ◽  
Jielin Jiang ◽  
Shiyao Xiao
Keyword(s):  
Colorectal Cancer ◽  
Cell Viability ◽  
Colony Formation ◽  
Thyroid Hormone Receptor ◽  
Formation Rate ◽  
Negative Control ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Closure Rate ◽  
Normal Tissues

MicroRNA (miR)-518-3p has been shown to function as a tumor suppressor. This study was conducted to investigate the effects of miR-518-3p in colorectal cancer (CRC). The miR-518-3p mimic, mimic negative control (NC), miR-518-3p inhibitor, inhibitor-NC, ShRNA-TRIP4, and ShRNA-NC vectors were transfected into SW480 cells using Lipofectamine 2000. Cell viability was detected using CCK-8. Colony formation, cell invasiveness, and cell migration were assessed by plate colony formation, Transwell assays, and wound healing assays, respectively. Relative mRNA and protein levels were detected using RT–qPCR and Western blot, respectively. The target gene thyroid hormone receptor interactor 4 (TRIP4) of miR-518-3p was identified and further verified using dual-luciferase reporter assay. Compared with normal tissues, levels of miR-518-3p were decreased and TRIP4 was significantly increased in the tissues from patients with CRC. Following transfection with a miR-518-3p mimic or ShRNA-TRIP4, cell viability decreased in a time-dependent manner, and colony formation rate, wound closure rate, and the number of invasive cells were much lower for the transfected cells than in the corresponding NC and control groups. miR-518-3p overexpression or silencing of TRIP4 significantly down-regulated the expression of MMP-2 and MMP-9. Knockdown of miR-518-3p had the opposite effects, and TRIP4 was identified as a target of miR-518-3p. The inhibitory effects of miR-518-3p on the progressions of CRC are associated with TRIP4.

scholarly journals LINC00665 Targets miR-214-3p/MAPK1 Axis to Accelerate Hepatocellular Carcinoma Growth and Warburg Effect

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Hongyu Wan ◽  
Yi Tian ◽  
Juan Zhao ◽  
Xiao Su
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Viability ◽  
Colony Formation ◽  
Warburg Effect ◽  
Aerobic Glycolysis ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Tumor Formation ◽  
Luciferase Reporter

Inhibition of aerobic glycolysis is a hopeful method for cancer treatment. In this study, we aimed to explore LINC00665/miR-214-3p/MAPK1 role in regulating cell viability and aerobic glycolysis in hepatocellular carcinoma (HCC). The expressions of LINC00665 in 50 paired HCC tissues and normal tissues were determined by qRT-PCR. Pearson analysis was applied to evaluate the association between the expression levels of miR-214-3p, LINC00665, and MAPK1 in HCC tissues. The interactions between miR-214-3p and LINC00665 or MAPK1 were determined by luciferase reporter assay and RNA immunoprecipitation. CCK-8 and colony formation assays were used for cell viability evaluation. Lactate production, glucose consumption, and ATP levels were measured to assess Warburg effect. The results showed that LINC00665 was overexpressed in HCC, which positively associated with MAPK1 level and negatively associated with miR-214-3p level in HCC tissues. Overexpression of LINC00665 led to significant enhancements in cell viability and colony formation, whereas this effect was weakened when miR-214-3p was overexpressed or MAPK1 was downregulated. In addition, deletion of LINC00665 expression repressed tumor formation in vivo. Mechanically, LINC00665 increased MAPK1 expression through binding to miR-214-3p. Collectively, this study revealed that LINC00665 accelerated cell growth and Warburg effect through sponging miR-214-3p to increase MAPK1 expression in HCC.

scholarly journals Circ_0015756 aggravates hepatocellular carcinoma development by regulating FGFR1 via sponging miR-610

2020 ◽  
Author(s):  
Weisheng Guo ◽  
Lin Zhao ◽  
Yaguang Wei ◽  
Peng Liu ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Viability ◽  
Colony Formation ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Therapeutic Effects

Abstract Background: Hepatocellular carcinoma (HCC) is the leading threat of cancer-related death in humans with poor therapeutic effects. Circular RNAs (circRNAs) are important indicators in cancer diagnosis and prognosis. This study intended to explore the function and mechanism of circ_0015756 in HCC, providing the additional opinion for HCC treatment.Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to detect the expression of circ_0015756 and miR-610. Cell viability was assessed by cell counting kit-8 (CCK-8) assay, and colony formation capacity was ascertained by colony formation assay. Cell proliferation and invasion were monitored by transwell assay. Cell cycle progression and apoptosis were analyzed by flow cytometry assay. Circ_0015756 oncogenicity was determined by Xenograft models. The prediction of targets was performed using the bioinformatics tools, and the verification of targeted relationship was conducted using RNA pull-down, RNA immunoprecipitation (RIP) and dual-luciferase reporter assays. The expression level of fibroblast growth factor receptor 1 (FGFR1) was measured by western blot.Result: The expression of circ_0015756 was increased in HCC tissues, serums and cells. Circ_0015756 downregulation impaired HCC cell viability, colony formation capacity, invasion and migration, induced cell cycle arrest and apoptosis, and inhibited tumor growth in vivo. MiR-610 was ensured as a target of circ_0015756, and miR-610 absence reversed the effects of circ_0015756 downregulation. Further, FGFR1 was interacted by miR-610, and FGFR1 overexpression overturned the effects of miR-610 restoration in vitro. Circ_0015756 could regulate FGFR1 expression by targeting miR-610.Conclusion: Circ_0015756 played its tumorigenic properties in HCC by activating FGFR1 and sponging miR-610, and circ_0015756 was expected to be a vital indicator in HCC diagnosis and treatment.

scholarly journals Circular RNA circ-PAN3 (hsa_circ_0100181) Promotes Hepatocellular Carcinoma Growth Through Sponging miR-153 to Elevate Cyclin D1 Expression

2020 ◽  
Author(s):  
Shuo Yu ◽  
Min Wang ◽  
Xu Li ◽  
Xingjun Guo ◽  
Renyi Qin
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Cyclin D1 ◽  
Colony Formation ◽  
Xenograft Model ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Circular Rnas

Abstract Background: Circular RNAs (circRNAs) are engaged in hepatocellular carcinoma (HCC) progression, but the mechanisms remain to be elucidated. This study aimed to unveil the expression pattern and potential biological mechanisms of a newly indentified circRNA, circ-PAN3, in HCC. Methods: Cell Counting Kit-8 (CCK‐8) assay and colony formation assay were used to assess cell proliferation. Transcription-quantitative PCR (RT-qPCR) analysis and western blot analysis were used to determine the relative expression level of mRNA and protein, respectively. Cell apoptosis assay was used to evaluate the apoptosis rate of transfected cells. CircInteractome and Targetscan were utilized to predict the possible targets of circRNAs and miRNAs, respectively. Luciferase reporter assay and RNA pull-down assay were used to assess the direct interaction of RNAs. HCC cancer xenograft model was used to evaluate the biological process of circ-PAN3 in vivo. Student’s t test, χ2 test or one-way ANOVA was adopted appropriately.Results: Circ-PAN3 was elevated in HCC tissues, and patients with high Circ-PAN3 expression had a poor survival outcome. Knockdown of circ-PAN3 expression suppressed cell viability, colony formation and cell proliferation in vitro and in vivo. Circ-PAN3 elevates cyclin D1 expression to promote HCC progression. Subsequently, using CircInteractome, miR-153 were confirmed to interact with circ-PAN3 and was downregulated by circ-PAN3. Further, using Targetscan, cyclin D1 was validated to interact with miR-153 and was downregulated by miR-153. Addition of miR-153 expression with corresponsive mimics significantly reduced the expression of cyclin D1. Notably, the inhibition of cell viability, colony formation and proliferation induced by knockdown of circ-PAN3 were recovered following the combination with miR-153 inhibitor, cyclin D1, respectively. Conclusion: Together, this study demonstrated that a novel circ-PAN3/miR-153/cyclin D1 axis regulatory axis that promoted HCC progression.

4-Acetylantrocamol LT3, a New Ubiquinone from Antrodia cinnamomea, Inhibits Hepatocellular Carcinoma HepG2 Cell Growth by Targeting YAP/TAZ, mTOR, and WNT/β-Catenin Signaling

2020 ◽  
Vol 48 (05) ◽  
pp. 1243-1261 ◽  
Author(s):  
Yen-Lin Chen ◽  
I-Chuan Yen ◽  
Kuen-Tze Lin ◽  
Feng-Yi Lai ◽  
Shih-Yu Lee
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
Cell Viability ◽  
Signaling Pathways ◽  
Hepg2 Cell ◽  
Colony Formation ◽  
Molecular Mechanisms ◽  
Binding Motif ◽  
Dependent Manner ◽  
Antrodia Cinnamomea

4-acetylantrocamol LT3 (4AALT3), a new ubiquinone from the mycelium of Antrodia cinnamomea (Polyporaceae), has been recently shown to possess anticancer activity. However, the detailed mechanisms of such action remain unclear. In this study, the molecular mechanisms of 4AALT3 on hepatocellular carcinoma cells (HCC) were investigated. Human hepatocellular carcinoma cell line HepG2 cells were treated with concentrations of 4AALT3. Cell viability, colony formation, and the underlying mechanisms were then analyzed by CCK-8, colony formation, qPCR, and Western blotting assays. We found that 4AALT3 significantly decreased cell viability and colony formation in a dose-dependent manner. Accordingly, 4AALT3 significantly decreased protein levels of cyclin B, E1, D1, and D3, thereby facilitating cell cycle arrest. In addition, 4AALT3 significantly suppressed the nuclear localization of Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ), mammalian target of rapamycin (mTOR), and WNT/[Formula: see text]-catenin signaling pathways, all of which are well-known signaling pathways that contribute to the malignant properties of HCC. These effects are associated with activation of 5′ AMP-activated protein kinase (AMPK) and autophagy. Our findings indicate that 4AALT3 exerts inhibitory effects on HepG2 cell growth via multiple signaling pathways and may be a potential agent for HCC therapy.

Chalcone-thiosemicarbazone Hybrids as Inhibitors of Human Hepatocellular Carcinoma HepG2 Cells Viability and Oxygen Consumption

2022 ◽  
Vol 18 ◽  
Author(s):  
Vivian Cordeiro Rodrigues ◽  
William Queiroz Felippe ◽  
Carla Marins Goulart ◽  
Aurea Echevarria ◽  
Ana Paula Pereira da Silva
Keyword(s):  
Hepatocellular Carcinoma ◽  
Oxygen Consumption ◽  
Cell Viability ◽  
Hepg2 Cells ◽  
Atp Synthesis ◽  
Human Hepatocellular Carcinoma ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Open Chain

Background: Chalcones are open-chain flavonoids especially attractive to medicinal chemistry due to their easy synthesis and the possibility of structural modifications. Objective: Evaluate the in vitro anticancer activity of a series of hybrids chalcones-thiosemicarbazones against the human hepatocellular carcinoma cell line, HepG2. Methods: Seven hybrid chalcones-thiosemicarbazones (CTs), 3-(4’-X-phenyl)-1-phenylprop-2-en-1-one thiosemicarbazone, where X=H (CT-H), CH3 (CT-CH3), NO2 (CT-NO2), Cl (CT-Cl), CN (CT-CN), F (CT-F) and Br (CT-Br), were synthesized and their effects on cells viability and mitochondrial oxygen consumption were accessed. Results: Incubation with CTs caused a decrease in HepG2 cells viability in a time-concentration-dependent manner. The most effective compounds in inhibiting cell viability, after 24 hours of treatment, were CT-Cl and CT-CH3 (IC50 20.9 and 23.63 μM, respectively). In addition, using 10 M and only 1 hour of pre-incubation, CT-CH3 caused a reduction in basal respiration (-37%), oxygen consumption coupled with ATP synthesis (-60%) and maximum oxygen consumption (-54%). These alterations in respiratory parameters may be involved with the inhibitory effects of CT-CH3, since significant changes in oxygen consumption rates were observed in a condition that anticipates more significant losses of cell viability. The ADME parameters and the no violation of Lipinski Rule of Five showed that all compounds are safe. Conclusion: These results may contribute to the knowledge about the effects of CTs on these cells and the development of new treatments against HCCs.

scholarly journals The miR-200b-3p/ERG/PTHrP Axis Mediates the Inhibitory Effect of Ethanol on the Differentiation of Rat Fetal Chondrocytes into Articular Cartilage

2021 ◽  
Author(s):  
Qubo Ni ◽  
Haitao Chen ◽  
Bin Li ◽  
Hangyuan He ◽  
Huasong Shi ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Inhibitory Effect ◽  
Ethanol Exposure ◽  
Luciferase Reporter ◽  
Marker Genes ◽  
Dependent Manner ◽  
Prenatal Ethanol Exposure ◽  
Concentration Dependent Manner ◽  
Marrow Mesenchymal Stem Cells

Abstract Background This study aims to further explore cartilage development in prenatal ethanol exposure (PEE) offspring at different times to explore the specific time points and mechanism of ethanol-induced fetal cartilage dysplasia. Methods On gestational day (GD)14, GD17, and GD20, PEE fetal cartilage was evaluated by morphological analysis. RT-qPCR, immunohistochemistry, and immunofluorescence were used to detect the expression of cartilage marker genes and their regulatory factors. Bone marrow mesenchymal stem cells (BMSCs) were used to explore the effect of ethanol on the differentiation of chondrocytes. Additionally, we used inhibitors, overexpression plasmids and a luciferase reporter assay on GD17 chondrocytes to verify the mechanism. Findings: PEE significantly reduced cartilage matrix content and the expression of marker genes on GD17 and GD20 but had no effect on GD14. The inhibition of chondrogenic differentiation by PEE mainly occurred on GD14-17. Furthermore, the expression of miR-200b-3p was increased, while that of ERG and PTHrP was markedly reduced in PEE fetal cartilage. In vitro, ethanol (30–120 mM) inhibited the differentiation of BMSCs into chondrocytes in a concentration-dependent manner, accompanied by strong expression of miR-200b-3p and low expression of ERG and PTHrP. Moreover, PTHLH and ERG overexpressed, as well as a miR-200b-3p inhibitor reversed the inhibitory effect of ethanol on the differentiation of fetal chondrocytes. Furthermore, miR-200b-3p could target and negatively regulate ERG. Interpretation: PEE can significantly inhibit the development of articular cartilage, especially during articular cartilage formation. The mechanism is related to the decreased differentiation of fetal cartilage into articular cartilage mediated by the miR-200b-3p/ERG/PTHrP axis.

The role of 70-kDa heat shock protein in dDAVP-induced AQP2 trafficking in kidney collecting duct cells

2013 ◽  
Vol 304 (7) ◽  
pp. F958-F971 ◽  
Author(s):  
Eui-Jung Park ◽  
Jung-Suk Lim ◽  
Hyun Jun Jung ◽  
Eunjung Kim ◽  
Ki-Hwan Han ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Cell Viability ◽  
Collecting Duct ◽  
In Silico Analysis ◽  
Luciferase Reporter ◽  
Apical Plasma Membrane ◽  
Dependent Manner ◽  
Concentration Dependent Manner

It has been reported that several proteins [heat shock protein 70 (Hsp70 and Hsc70), annexin II, and tropomyosin 5b] interact with the Ser256 residue on the COOH terminus of aquaporin-2 (AQP2), where vasopressin-induced phosphorylation occurs for mediating AQP2 trafficking. However, it remains unknown whether these proteins, particularly Hsp70, play a role in AQP2 trafficking. Semiquantitative immunoblotting revealed that renal expression of AQP2 and Hsp70 was significantly increased in water-restricted or dDAVP-infused rats. In silico analysis of the 5′-flanking regions of AQP2, Hsp70-1, and Hsp70-2 genes revealed that transcriptional regulator binding elements associated with cAMP response were identified at both the Hsp70-1 and Hsp70-2 promoter regions, in addition to AQP2. Luciferase reporter assay demonstrated the significant increase of luminescence after dDAVP stimulation (10−8 M, 6 h) in the LLC-PK1 cells transfected with luciferase vector containing 1 kb of the 5′-flanking region of Hsp70-2 gene. Hsp70-2 protein expression was also increased in mpkCCDc14 cells treated by dDAVP in a concentration-dependent manner. Cell surface biotinylation analysis demonstrated that forskolin (10−5 M, 15 min)-induced AQP2 targeting to the apical plasma membrane was significantly attenuated in the mpkCCDc14 cells with Hsp70-2 knockdown. Moreover, forskolin-induced AQP2 phosphorylation (Ser256) was not significantly induced in the mpkCCDc14 cells with Hsp70-2 knockdown. In contrast, Hsp70-2 knockdown did not affect the dDAVP-induced AQP2 abundance. In addition, siRNA-directed knockdown of Hsp70 significantly decreased cell viability. The results suggest that Hsp70 is likely to play a role in AQP2 trafficking to the apical plasma membrane, partly through affecting AQP2 phosphorylation at Ser256 and cell viability.

scholarly journals Novel Biphenyl Amines Inhibit Oestrogen Receptor (ER)-α in ER-Positive Mammary Carcinoma Cells

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 783
Author(s):  
Basappa Basappa ◽  
Baburajeev Chumadathil Pookunoth ◽  
Mamatha Shinduvalli Kempasiddegowda ◽  
Rangappa Knchugarakoppal Subbegowda ◽  
Peter E. Lobie ◽  
...  
Keyword(s):  
Cell Viability ◽  
Mammary Carcinoma ◽  
Oestrogen Receptor ◽  
Three Dimensional ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Structural Basis ◽  
Dependent Manner ◽  
Luciferase Reporter Construct ◽  
Ic50 Value

Herein, the activity of adamantanyl-tethered-biphenyl amines (ATBAs) as oestrogen receptor alpha (ERα) modulating ligands is reported. Using an ERα competitor assay it was demonstrated that ATBA compound 3-(adamantan-1-yl)-4-methoxy-N-(4-(trifluoromethyl) phenyl) aniline (AMTA) exhibited an inhibitory concentration 50% (IC50) value of 62.84 nM and demonstrated better binding affinity compared to tamoxifen (IC50 = 79.48 nM). Treatment of ERα positive (ER+) mammary carcinoma (MC) cells (Michigan Cancer Foundation-7 (MCF7)) with AMTA significantly decreased cell viability at an IC50 value of 6.4 μM. AMTA treatment of MC cell-generated three-dimensional (3D) spheroids resulted in significantly decreased cell viability. AMTA demonstrated a superior inhibitory effect compared to tamoxifen-treated MC cell spheroids. Subsequently, by use of an oestrogen response element (ERE) luciferase reporter construct, it was demonstrated that AMTA treatment significantly deceased ERE transcriptional activity in MC cells. Concordantly, AMTA treatment of MC cells also significantly decreased protein levels of oestrogen-regulated CCND1 in a dose-dependent manner. In silico molecular docking analysis suggested that AMTA compounds interact with the ligand-binding domain of ERα compared to the co-crystal ligand, 5-(4-hydroxyphenoxy)-6-(3-hydroxyphenyl)-7- methylnaphthalen-2-ol. Therefore, an analogue of AMTA may provide a structural basis to develop a newer class of ERα partial agonists.

The Anti-Atherogenic Properties of Sesamin are Mediated via Improved Macrophage Cholesterol Efflux Through PPARγ1-LXRα and MAPK Signaling

2014 ◽  
Vol 84 (1-2) ◽  
pp. 79-91 ◽  
Author(s):  
Amin F. Majdalawieh ◽  
Hyo-Sung Ro
Keyword(s):  
Cholesterol Efflux ◽  
Transcriptional Activity ◽  
Molecular Mechanisms ◽  
Foam Cell ◽  
Mapk Signaling ◽  
Luciferase Reporter ◽  
Foam Cell Formation ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Macrophage Cholesterol Efflux

Background: Foam cell formation resulting from disrupted macrophage cholesterol efflux, which is triggered by PPARγ1 and LXRα, is a hallmark of atherosclerosis. Sesamin and sesame oil exert anti-atherogenic effects in vivo. However, the exact molecular mechanisms underlying such effects are not fully understood. Aim: This study examines the potential effects of sesamin (0, 25, 50, 75, 100 μM) on PPARγ1 and LXRα expression and transcriptional activity as well as macrophage cholesterol efflux. Methods: PPARγ1 and LXRα expression and transcriptional activity are assessed by luciferase reporter assays. Macrophage cholesterol efflux is evaluated by ApoAI-specific cholesterol efflux assays. Results: The 50 μM, 75 μM, and 100 μM concentrations of sesamin up-regulated the expression of PPARγ1 (p< 0.001, p < 0.001, p < 0.001, respectively) and LXRα (p = 0.002, p < 0.001, p < 0.001, respectively) in a concentration-dependent manner. Moreover, 75 μM and 100 μM concentrations of sesamin led to 5.2-fold (p < 0.001) and 6.0-fold (p<0.001) increases in PPAR transcriptional activity and 3.9-fold (p< 0.001) and 4.2-fold (p < 0.001) increases in LXR transcriptional activity, respectively, in a concentration- and time-dependent manner via MAPK signaling. Consistently, 50 μM, 75 μM, and 100 μM concentrations of sesamin improved macrophage cholesterol efflux by 2.7-fold (p < 0.001), 4.2-fold (p < 0.001), and 4.2-fold (p < 0.001), respectively, via MAPK signaling. Conclusion: Our findings shed light on the molecular mechanism(s) underlying sesamin’s anti-atherogenic effects, which seem to be due, at least in part, to its ability to up-regulate PPARγ1 and LXRα expression and transcriptional activity, improving macrophage cholesterol efflux. We anticipate that sesamin may be used as a therapeutic agent for treating atherosclerosis.

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