scholarly journals Kirenol inhibits TNF-α-induced proliferation and migration of HaCaT cells by regulating NF-κB pathway

2021 ◽  
Vol 13 (4) ◽  
pp. 44-53
Author(s):  
Jin Li ◽  
Fang Ren ◽  
Wenliang Yan ◽  
Hong Sang
Keyword(s):  
Cell Migration ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Hacat Cells ◽  
Tnf Α

Psoriasis is a common chronic, inflammatory skin disease possessing properties of inflammatory cell infiltration and excessive proliferation of keratinocytes, the occurrence and development of which remain fully elucidated. Therefore, the study was designed to determine the effects of kirenol (50, 100 and 200 μg/mL) on Cultured Human Keratinocytes (cells) (HaCaT) in vitro and reveal its molecular mechanism. The in vitro psoriasis model was established utilizing tumor necrosis factor-α (TNF-α)-stimulated HaCaT cells. Kirenol, a diterpenoid compound, was applied at different concentrations (50, 100 and 200 μg/mL) to HaCaT cells for 24 h. The Cell Counting Kit-8 (CCK-8) and thymidine monobromodeoxyuridine (BrdU) assays were used to assess cell viability and proliferation, followed by assessment of cell migration by Transwell assay. Subsequently, inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA), and Western blot assay was used to evaluate expres-sions of p65, p-p65, IκBα and p-IκBα. Activities of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondialdehyde (MDA) contents were measured spectrophotometrically. The results demonstrated that TNF-α induced a significant increase in cell viability and inflammatory cytokines, including expressions of Interleukin (IL)-6, IL-8, IL-22 and IL-1β in HaCaT cells, which was dose-dependently inhibited by kirenol. Similarly, TNF-α-induced cell migration was also suppressed by kirenol treatment. Furthermore, TNF-α stimuli induced the upregulation of phosphorylation levels of p65 and IκBα as well as p-p65–p65 and p-IκBα–IκBα ratios, whereas kirenol significantly suppressed the activation of cellular nuclear factor-kappa B (NF-κB) signaling pathway. In addition, kirenol significantly decreased the level of MDA but increased the levels of SOD, CAT and GSH in a dose-dependent manner. These results proposed that kirenol could inhibit the proliferation, migration, expression of inflammatory factors, and oxidative stress in HaCaT cells via suppressing NF-κB signaling pathway.

scholarly journals Radiosensitization by CpG ODN7909 in an epidermoid laryngeal carcinoma Hep-2 cell line

2017 ◽  
Vol 45 (6) ◽  
pp. 2009-2022 ◽  
Author(s):  
Shu Wang ◽  
Xiaoqun Liu ◽  
Tiankui Qiao ◽  
Qi Zhang
Keyword(s):  
Cell Viability ◽  
Survival Curve ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cell Cycle Distribution ◽  
Dependent Manner ◽  
Western Blots ◽  
Apoptosis Rate ◽  
Tnf Α

Objective To evaluate the radiosensitivity effect of CpG oligodeoxyribonucleotide (ODN) 7909 on human epidermoid cancer strain-2 (Hep-2) cells in vitro and discuss the potential for improved radiotherapy treatment in patients with laryngeal squamous cell carcinoma. Methods Toll-like receptor ( TLR) 9 expression was assessed in Hep-2 cells using Western blots and reverse transcription polymerase chain reaction. Cell Counting Kit-8 was used to detect Hep-2 cell viability at 24 and 48 h following treatment with different CpG ODN7909 concentrations. Cellular colonization was evaluated using microscopy. Cell cycle distribution and apoptosis rate was determined with flow cytometry. Interleukin (IL)-12 and tumour necrosis factor (TNF)-α concentrations were detected by enzyme-linked immunosorbent assay. Results Hep-2 cells were found to express TLR9, and CpG ODN7909 treatment suppressed Hep-2 cell viability in a dose- and time-dependent manner. Cell survival curve analyses revealed a sensitivity enhancement ratio of the mean death dose of 1.225 for CpG ODN7909 plus irradiation versus irradiation alone. Furthermore, the population of Gap 2/mitotic-phase cells, apoptosis rate and secreted IL-12 and TNF-α levels were significantly increased in Hep-2 cells treated with CpG ODN7909 plus irradiation versus IR alone. Conclusion CpG ODN7909 enhanced the radiosensitivity of Hep-2 cells in vitro.

scholarly journals MiR-200a-3p Accelerated Hypoxia/Reoxygenation Injury in HCM Cells by Enhancing IGF2R via Wnt/β-catenin Signalling Pathway

2021 ◽  
Vol 21 (02) ◽  
Author(s):  
Yaolei Ge
Keyword(s):  
Cell Viability ◽  
Inflammatory Cytokines ◽  
Caspase 3 ◽  
Signalling Pathway ◽  
Dependent Manner ◽  
Tnf Α ◽  
Reoxygenation Injury ◽  
Pro Inflammatory Cytokines ◽  
Hypoxia Reoxygenation

ABSTRACT The present study examined functions of miR-200a-3p accelerated progressions of HCM cells via IGF2R and Wnt/β-catenin signalling pathway after hypoxia/reoxygenation treatment in vitro. CCK-8 showed that cell viability of HCM was inhibited while apoptosis rates detected by flow cytometry were promoted in a time dependent manner after H/R (12 hours and 24 hours). Beyond that, Bcl-2 and c-IAP1 were decreased but Bax and caspase-3 were upregulated by H/R treatment. IL-1β, IL-6, TNF-α and NLRP3 were also increased after treatment. RT-qPCR showed increased expressions of miR-200a-3p by H/R treatment while its inhibitor elevated cell viability but depressed apoptosis rate and pro-inflammatory cytokines’ expressions. IGF2R was upregulated after H/R treatment and its downregulation magnified effects of suppressed miR-200a-3p. HIF-1α/Wnt/β -catenin signalling pathway was activated by miR-200a-3p and IGF2R while IWP-2 treatment abolished the activation of Wnt3a andβ -catenin, causing decreased apoptosis and pro-inflammatory cytokines’ expressions but accelerated the cell viability.

scholarly journals Schizandrin A Alleviates LPS-Induced Injury in Human Keratinocyte Cell Hacat Through a MicroRNA-127-Dependent Regulation

2018 ◽  
Vol 49 (6) ◽  
pp. 2229-2239 ◽  
Author(s):  
Shujie Li ◽  
Ruijin Xie ◽  
Chengrui Jiang ◽  
Mei Liu
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Skin Diseases ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Hacat Cells ◽  
Protective Effects ◽  
Human Keratinocyte ◽  
Tnf Α ◽  
Keratinocyte Cell

Background/Aims: Inflammatory skin diseases are the most common problems in dermatology. Schizandrin A (SchA) has been reported to have anti-inflammatory properties. Herein, we aimed to investigate the protective effects of SchA on lipopolysaccharide (LPS)-induced injury in keratinocyte HaCaT cells. Methods: Inflammation injury in HaCaT cells was induced by LPS treatment. Cell viability, apoptotic cell rate, and apoptosis-related proteins were analyzed by cell counting kit-8 (CCK-8) assay, Annexin V-(fluorescein isothiocyanate (FITC)/ Propidium Iodide (PI) double staining method, and western blot, respectively. The pro-inflammatory factors were analyzed by western blot and quantified by enzyme linked immunosorbent assay (ELISA). Expression of miR-127 in SchA-treated cells was analyzed by qRT-PCR. The effects of SchA on activations of p38MAPK/ERK and JNK pathways were analyzed by western blot. Results: SchA protected HaCaT cells from LPS-induced inflammation damage via promoting cell viability, suppressing apoptosis. Meanwhile, SchA inhibited IL-1β, IL-6, and TNF-α expression. miR-127 expression was up-regulated in LPS-treated HaCaT cells but down-regulated after SchA treatment. Overexpression of miR-127 inhibited cell growth and induced expression of IL-1β, IL-6 and TNF-α. Additionally, miR-127 overexpression impaired the protective effects of SchA, implying miR-127 might be correlated to the anti-inflammation property of SchA and also involved in inactivation of p38MAPK/ERK and JNK pathways by SchA. Conclusion: miR-127 is involved in the protective functions of SchA on LPS-induced inflammation injury in human keratinocyte cell HaCaT, which might inactivates of p38MAPK/ERK and JNK signaling pathways in HaCaT cells.

scholarly journals MiR-103a-3p antagonism attenuates pneumonia via inactivating the PI3K/AKT/NF-κB signaling pathway by targeting PTEN

2020 ◽  
Author(s):  
Lin Xu ◽  
Qingying Song ◽  
Zhanghong Ouyang ◽  
Xiangyan Zhang ◽  
Cheng Zhang
Keyword(s):  
Cell Viability ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Expression Levels ◽  
Tensin Homolog ◽  
Factor Α

Abstract Pneumonia accounts for approximately 15% mortalities in adolescents worldwide. MicroRNAs (miRNAs) regulate numerous diseases including pneumonia. miRNA and mRNA expression levels were detected by real time polymerase chain reaction (RT-qPCR). Protein expression levels were determined by enzyme-linked immunosorbent assay (ELISA) and western blot. The interaction between phosphatase and tensin homolog on chromosome ten (PTEN) and miR-103a-3p was explored by dual luciferase reporter assay. Cell viability and cell apoptosis were detected by cell Counting Kit-8 (CCK-8) and flow cytometry. Herein, we discovered that PTEN was decreased and miR-103a-3p was overexpressed in Ana-1 cells of in vitro pneumonia model. miR-103a-3p downregulated the expression levels of PTEN. AntagomiR-103a-3p reversed the increased cell apoptosis and decreased cell viability and inflammatory cytokine expression levels (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6) induced by LPS in Ana-1 cells by PTEN. AntagomiR-103a-3p inhibited the activation of PTEN/PI3K/AKT/NF-κB signaling pathway induced by LPS in Ana-1 cells. Taken together, our findings exhibited that miR-103a-3p attenuated LPS induced pneumonia by blocking the activation of PTEN/PI3K/AKT/NF-κB signaling pathway and the following cell apoptosis as well as release of proinflammatory cytokines, suggesting that miR-103a-3p might serve as a novel therapeutic target for the treatment of pneumonia.

scholarly journals Glycyrrhizin improves the pathogenesis of psoriasis partially through IL-17A and the SIRT1-STAT3 axis

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Huang Qiong ◽  
Ling Han ◽  
Nanxue Zhang ◽  
Huyan Chen ◽  
Kexiang Yan ◽  
...  
Keyword(s):  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Pathological State ◽  
Hacat Cells ◽  
Skin Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Interfering Rna

Abstract Background The anti-inflammatory effect of glycyrrhizin has been widely recognized, while the specific mechanism of glycyrrhizin in psoriasis remains poorly understood. Results In the imiquimod-induced mouse model of psoriasis (IMD), we found that glycyrrhizin can substantially improve the adverse symptoms in mice. The hematoxylin-eosin staining results showed that glycyrrhizin can also improve the pathological state of skin cells in IMD mice. Using enzyme-linked immunosorbent assay (ELISA), we found that glycyrrhizin substantially inhibited the expression of IL-17A and IFN-γ in the serum of IMD mice. In order to simulate the effect of IL-17A on keratinocytes in psoriasis, we treated HaCaT cells with 100 ng/mL IL-17A (IL-17A-HaCaT cells) for 48 h. Then, using cell-counting kit-8 (CCK-8) and ELISA assays, we found that glycyrrhizin inhibited the proliferation of IL-17A-HaCaT cells and reversed the promotion of IL-6, CCL20, and TNF-α induced by IL-17A. Further, western blotting (WB) results indicated that glycyrrhizin promoted the expression of SIRT1 and inhibited the expression of STAT3 and phosphorylated STAT3 (p-STAT3). By treating IL-17A-HaCaT cells with EX-527 (a potent and selective inhibitor of SIRT1), combined with CCK-8 and WB experiments, we initially found that EX-527 inhibited the proliferation of IL-17A-HaCaT cells and promoted the expression of STAT3, p-STAT3, and acetylated STAT3 (a-STAT3). However, when glycyrrhizin was added at the same time, the proliferation of IL-17A-HaCaT cells increased, and the expression of STAT3, p-STAT3, and a-STAT3 reduced. We then knocked down the expression of SIRT1 via small interfering RNA in IL-17A-HaCaT cells, and the results were consistent with those of EX-527. Conclusions Together, these results indicated that glycyrrhizin improved psoriasis by inhibiting the expression of IL-17A and IFN-γ in vivo and suppressed the proliferation of IL-17A-HaCaT cells and the expression of STAT3, p-STAT3, and a-STAT3 by upregulating SIRT1 in vitro.

scholarly journals Glycyrrhizin improves the pathogenesis of psoriasis through IL-17A and the SIRT1-STAT3 axis

2020 ◽  
Author(s):  
Huang Qiong ◽  
Ling Han ◽  
Nan Zhang ◽  
Hu Chen ◽  
Ke Yan ◽  
...  
Keyword(s):  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Pathological State ◽  
Hacat Cells ◽  
Skin Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Interfering Rna

Abstract Background: The anti-inflammatory effect of glycyrrhizin has been widely recognized, while the specific mechanism of glycyrrhizin in psoriasis remains poorly understood. Results: Here, in an imiquimd-induced mouse model of psoriasis (IMD), we found that glycyrrhizin can substantially improve the adverse symptoms in mice. The hematoxylin-eosin staining results showed that glycyrrhizin can also improve the pathological state of skin cells in IMD mice. Using enzyme-linked immunosorbent assay (ELISA), we found that glycyrrhizin substantially inhibited the expression of IL-17A and IFN-γ in the serum of IMD mice. In order to simulate the effect of IL-17A on keratinocytes in psoriasis, we treated HaCaT cells with 100 ng/mL IL-17A (IL-17A-HaCaT cells) for 48 h. Then, using cell-counting kit-8 (CCK-8) and ELISA assays, we found that glycyrrhizin inhibited the proliferation of IL-17A-HaCaT cells and reversed the promotion of IL-6, CCL20, and TNF-α induced by IL-17A. Further, western blotting (WB) results indicated that glycyrrhizin promoted the expression of SIRT1 and inhibited the expression of STAT3 and phosphorylated STAT3 (p-STAT3). By treating IL-17A-HaCaT cells with EX-527 (a potent and selective inhibitor of SIRT1), combined with CCK-8 and WB experiments, we initially found that EX-527 inhibited the proliferation of IL-17A-HaCaT cells and promoted the expression of STAT3, p-STAT3, and acetylated STAT3 (a-STAT3). However, when glycyrrhizin was added at the same time, the proliferation of IL-17A-HaCaT cells increased, and the expression of STAT3, p-STAT3, and a-STAT3 reduced. We then knocked down the expression of SIRT1 via small interfering RNA in IL-17A-HaCaT cells, and the results were consistent with those of EX-527. Conclusions: Together, these results indicated that glycyrrhizin improved psoriasis by inhibiting the expression of IL-17A and IFN-γ in vivo and suppressed the proliferation of IL-17A-HaCaT cells and the expression of STAT3, p-STAT3, and a-STAT3 by upregulating SIRT1 in vitro.

ALK7 Inhibition Protects Osteoblast Cells Against High Glucose-induced ROS Production via Nrf2/HO-1 Signaling Pathway

2021 ◽  
Vol 21 ◽  
Author(s):  
Zhen Zhao ◽  
Yu Lu ◽  
Huan Wang ◽  
Xiang Gu ◽  
Luting Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Signaling Pathway ◽  
High Glucose ◽  
Collagen I ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Heme Oxygenase 1 ◽  
Ros Production ◽  
Alizarin Red

Background: Some studies demonstrated that under high-glucose (HG) condition, osteoblasts develop oxidative stress, which will impair their normal functions. The effects of activin receptor-like kinase 7 (ALK7) silencing on HG-induced osteoblasts remained unclear. Objective: The aim of this study was to explore the effect of ALK7 on HG-induced osteoblasts. Methods: MC3T3-E1 cells were treated with different concentrations of HG (0, 50, 100, 200 and 300mg/dL), and the cell viability was detected using cell counting kit-8 (CCK-8). HG-treated MC3T3-E1 cells were transfected with siALK7 or ALK7 overexpression plasmid or siNrf2, and then the viability and apoptosis were detected by CCK-8 and flow cytometry. The levels of reactive oxygen species (ROS), collagen I and calcification nodule were determined by oxidative stress kits, Enzyme-linked immunosorbent assay and Alizarin red staining. The expressions of NF-E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and osteoblast-associated genes were determined by quantitative real-time PCR (qRT-PCR) and Western blot. Results: Cell viability was reduced with HG treatment. Silencing ALK7 inhibited the effect of HG on increasing cell apoptosis and ROS production, reduced cell viability, mineralized nodules, and downregulated collagen I and osteoblast-associated genes expression in MC3T3-E1 cells. ALK7 silencing activated the Nrf2/HO-1 signaling pathway by affecting expressions of HO-1 and Nrf2. ALK7 overexpression had the opposite effects. In addition, siNrf2 partially reversed the effects of ALK7 silencing on HG-induced MC3T3-E1 cells. Conclusion: ALK7 silencing protected osteoblasts under HG condition possibly through activating the Nrf2/HO-1 pathway.

Glia Maturation Factor-Gamma Negatively Modulates Fatty Acid-Induced Inflammation in Macrophages Via PI3K/AKT Pathway

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1096-1096
Author(s):  
Wulin Aerbajinai ◽  
Kyung Chin ◽  
Jianqiong Zhu ◽  
Griffin P Rodgers
Keyword(s):  
Insulin Resistance ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Mapk Signaling ◽  
Negative Regulator ◽  
Enzyme Linked Immunosorbent Assay ◽  
Glia Maturation Factor ◽  
Endogenous Expression ◽  
Maturation Factor ◽  
Tnf Α

Abstract Abstract 1096 The macrophage-mediated inflammatory response plays a critical role in the development of obesity-related tissue inflammation and insulin resistance. Free-fatty acids (FFAs) are well-characterized factors causing production of inflammatory factors and insulin resistance. Glia maturation factor-gamma (GMFG), a member of the ADF/cofilin family of proteins that regulate actin cytoskeleton reorganization, is preferentially expressed in inflammatory cells, but its function in the macrophages immune response remains unclear. In this study, we investigated whether GMFG may affect FFAs-induced inflammatory reaction in macrophages. We show here that silencing of GMFG (80% inhibition of the endogenous expression levels) by transfected with GMFG siRNA significantly enhanced FFAs-induced production of proinflammatory cytokines and chemokines, including TNF-α, IL-6 and IL-8 compared to transfected non-targeting silencing siRNA in human peripheral blood monocytes-derived macrophage (1.2 × 104 ± 224.2 vs. 4.6 × 103 ± 98.4 molecules/ng, P < 0.001; 1.2 × 103 ± 56.1 vs. 2.3 × 102 ± 8.4 molecules/ng, P =0.001; 1.3 × 107 ± 5.8 × 105 vs. 4.9 × 106 ± 2.8 × 105 molecules/ng, P < 0.001) as determined by quantitative real time-PCR and confirmed by enzyme-linked immunosorbent assay (TNF-α: 9.4 × 102 ± 38.6 vs. 5.6 × 102 ± 31.1 ng/mL, P < 0.01; IL-6: 4.5 × 102 ± 31.3 vs. 2.2 × 102 ± 22.7 ng/mL, P < 0.01; IL-8: 2.2 × 103 ± 205.5 vs. 1.3 × 103 ± 113.9 ng/mL, P < 0.01). These increased inflammatory cytokines resulted from an increased activation of NF-κB and the ERK1/2 MAPK signaling pathway (based on increased NF-κB p65 phosphorylation, IκBα loss and enhanced phosphorylation of ERK1/2 in Western blot analysis) and a reduced phosphorylation of the PI3K/Akt/GSK3-β pathway following FFAs stimulation. Overexpression of GFP-GMFG in GMFG-silenced cells abrogated enhanced phosphorylation of NF-κB p65, ERK1/2 MAPK and reduced phosphorylation of Akt and GSK3-β. Furthermore, in cells in which GMFG was knockdown, FFAs induced an increase in the expression of SHIP1, a phosphatase that negatively regulates the PI3K signaling pathway, suggesting increased SHIP1 expression may be responsible for the augmentation of inflammatory cytokines following FFAs stimulation. We also show that silencing of GMFG enhances the oxidized low density lipoprotein (oxLDL) induced expression of TNF-α and IL-6 (2.9 × 104 ± 204.8 vs. 1.3 × 104 ± 153.9 molecules/ng, P < 0.01; 2.5 × 103 ± 31.3 vs. 9.2 × 102 ± 22.7 ng/mL, P < 0.01) in MDM. Taking together with the data that GMFG is constitutively expressed in macrophages and its expression is down-regulated by FFAs stimulation, GMFG might function as a novel negative regulator through participating in the PI3K/Akt signaling pathway, suggesting that macrophage-specific modulation of GMFG may be beneficial in the treatment of FFAs induced inflammation. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Berberine Protects against TNF-α-Induced Injury of Human Umbilical Vein Endothelial Cells via the AMPK/NF-κB/YY1 Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Li Chen ◽  
Xiao-Di Fan ◽  
Hua Qu ◽  
Rui-Na Bai ◽  
Da-Zhuo Shi
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Proinflammatory Cytokines ◽  
Antioxidant Activities ◽  
Umbilical Vein ◽  
Endothelial Injury ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Compound C ◽  
Tnf Α

Endothelial injury, characterized by an inflammatory response and increased permeability, is an initial stage of atherosclerosis (AS). Adenosine 5′-monophosphate (AMP), activated protein kinase (AMPK), and Nuclear Factor kappa B (NF-κB)/Yin Yang 1(YY1) signaling pathways play important roles in the process of endothelial injury. Berberine (BBR), a bioactive alkaloid isolated from several herbal substances, possesses multiple pharmacological effects, including anti-inflammatory, antimicrobial, antidiabetic, anticancer, and antioxidant activities. Previous studies showed a protective effect of berberine against endothelial injury. However, the underlying mechanism remains unclear. We explored the potential effect of BBR on TNF- (tumor necrosis factor-) α-induced injury of human umbilical endothelial cells (HUVECs) and studied its possible molecular mechanism. In the present study, HUVECs were divided into three groups. HUVEC viability was measured with Cell Counting Kit-8 assay. Extracellular lactic dehydrogenase (LDH) concentration was measured with LDH leakage assay. Endothelial microparticle (EMP) numbers were evaluated by flow cytometry analysis assay. The expression of proinflammatory cytokines was evaluated by Enzyme-Linked Immunosorbent Assay (ELISA). The mRNA expression of NF-κB and YY1 was detected by Real-Time PCR (RT-PCR). The protein expression of NF-κB, YY1, and AMPK was detected by immunofluorescence microscopy assay or western blot analysis. The results showed that LDH concentration, EMPs numbers, and the expression of proinflammatory cytokines (IL-6, IL-8, and IL-1β) increased in TNF-α-induced injured HUVECs, but ameliorated by BBR pretreatment. BBR pretreatment upregulated the expression of phosphorylated AMPK and downregulated the expressions of NF-κB and YY1 in injured HUVECs induced by TNF-α, which were offset by the AMPK inhibitor Compound C (CC). The results indicated that BBR protected against TNF-α-induced endothelial injury via the AMPK/NF-κB/YY1 signaling pathway.

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