scholarly journals Conditioned Medium from Adipose-Derived Stem Cell Inhibits Jurkat Cell Proliferation through TGF-β1 and p38/MAPK Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Xiuxia Wang ◽  
Yinmin Wang ◽  
Xianyu Zhou ◽  
Fei Liu
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Conditioned Medium ◽  
Molecular Mechanism ◽  
Western Blotting ◽  
Jurkat Cell ◽  
Jurkat Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Dependent Manner

Background. Since the first report on the immunomodulatory and immunosuppressive properties of Adipose-Derived Stem Cells (ADSCs), many studies have elucidated the underlying molecular mechanism of their suppressive activity on mixed lymphocyte reaction (MLR). However, a gap exists in our understanding of the molecular mechanism of ADSC-conditioned medium (ADSC-CM) on MLR. Methods. ADSCs were isolated from Human Adipose Tissues, and Enzyme-linked Immunosorbent Assay (ELISA) was used to identify the concentration of transforming growth factor β1 (TGF-β1) in ADSC-CM. The transcript abundance of TGF-β1, as well as that of insulin-like growth factor binding protein 3 (IGF-BP3), was evaluated using qRT-PCR on Jurkat cells cultured in ADSC-CM for 24 hours. The proliferation of the Jurkat cells was assessed using cell cycle assay. Western blotting was performed to identify potential signaling molecules involved in the ADSC-CM-induced inhibition of Jurkat cell proliferation. Results. The findings confirm that the isolated ADSCs demonstrate classic ADSC characteristics. The level of TGF-β1 was found to be low in ADSC-CM, as assessed by ELISA. Jurkat cells grown in ADSC-CM show reduced gene expression of TGF-β1 and IGF-BP3 compared with that of the control group. Furthermore, western blotting of ADSC-CM grown Jurkat cells that were blocked at the G0/G1 stage indicates that ADSC-CM decreases the protein expression of pP38 in a dose-dependent manner. Conclusion. ADSC-CM can inhibit Jurkat cell proliferation through the TGF-β1-p38 signaling pathway.

scholarly journals Effects ofAngelicaExtract on Schwann Cell Proliferation and Expressions of Related Proteins

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Xiaowen Jiang ◽  
Lin Liu ◽  
Binqing Zhang ◽  
Ziyin Lu ◽  
Lu Qiao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Schwann Cell ◽  
Nuclear Antigen ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Dependent Manner ◽  
Cell Cycles ◽  
Neural Cell Adhesion ◽  
Related Proteins ◽  
Proliferating Cell

The present study investigated the effects ofAngelicaextract (AE) on Schwann cell proliferation and expressions of related proteins, including brain derived neurotrophic factor (BDNF), neural cell adhesion molecule (NCAM), and proliferating cell nuclear antigen (PCNA). Proliferation activity and cell cycles of SCs were evaluated by MTT assay and flow cytometry methods, respectively, after 12 h treatment of AE at different concentrations (62.5, 125, 250, 1000, 2000, 4000, and 8000 mg/L). SCs were treated by 500, 1000, and 2000 mg/L AE for 24 h or 48 h; the related genes mRNA and proteins expressions in SCs were detected by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) kit. At the concentration range of 125–2000 mg/L, the SC proliferation was induced by AE in a dose-dependent manner, especially 1000 and 2000 mg/L; cells in drug-treated groups showed the most increase.Cells counts were ascended significantly in (G2/M + S) phase compared to control group. BDNF, NCAM, and PCNA protein expressions significantly increased at drug-treated groups. Relative genes mRNA expressions levels were also significantly higher compared to control group. The results indicated that AE facilitated SC proliferation and related genes and proteins expressions, which provided a basic guideline for nerve injury repair in clinic.

scholarly journals Alpha-Ketoglutarate and 5-HMF: A Potential Anti-Tumoral Combination against Leukemia Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1804
Author(s):  
Joachim Greilberger ◽  
Ralf Herwig ◽  
Michaela Greilberger ◽  
Philipp Stiegler ◽  
Reinhold Wintersteiger
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Protein Content ◽  
Jurkat Cell ◽  
Jurkat Cells ◽  
Mitochondrial Activity ◽  
Caspase Activity ◽  
Antioxidative Capacity ◽  
Oxidized Proteins ◽  
Activity Measurements

We have recently shown that a combined solution containing alpha-ketoglutarate (aKG) and 5-hydroxymethyl-furfural (5-HMF) might have anti-tumoral potential due to its antioxidative activities. The question arises if these substances have caspase-3- and apoptosis-activating effects on the cell proliferation in Jurkat and HF-SAR cells. Antioxidative capacity of several combined aKG + 5-HMF solution was estimated by cigarette smoke radical oxidized proteins of fetal calf serum (FCS) using the estimation of carbonylated proteins. The usage of 500 µg/mL aKG + 166.7 µg/mL 5-HMF showed the best antioxidative capacity to inhibit protein modification of more than 50% compared to control measurement. A Jurkat cell line and human fibroblasts (HF-SAR) were cultivated in the absence or presence of combined AKG + 5-HMF solutions between 0 µg/mL aKG + 0 µg/mL 5-HMF and different concentrations of 500 µg/mL aKG + 166.7 µg/mL 5-HMF. Aliquots of Jurkat cells were tested for cell proliferation, mitochondrial activity, caspase activity, apoptotic cells and of the carbonylated protein content as marker of oxidized proteins in cell lysates after 24, 48, and 72 h of incubation. The combined solutions of aKG + 5-HMF were shown to cause a reduction in Jurkat cell growth that was dependent on the dose and incubation time, with the greatest reductions using 500 µg/mL aKG + 166.7 µg/mL 5-HMF after 24 h of incubation compared to 24 h with the control (22,832 cells vs. 32,537 cells), as well as after 48 h (21,243 vs. 52,123 cells) and after 72 h (23,224 cells). Cell growth was totally inhibited by the 500 µg/mL AKG + 166.7 µg/mL solution between 0 and 72 h of incubation compared to 0 h of incubation for the control. The mitochondrial activity measurements supported the data on cell growth in Jurkat cells: The highest concentration of 500 µg/mL aKG + 166.7 µg/mL 5-HMF was able to reduce the mitochondrial activity over 24 h (58.9%), 48 h (28.7%), and 72 h (9.9%) of incubation with Jurkat cells compared not only to the control incubation, but also to the concentrations of 500 µg/mL aKG + 166.7 µg/mL 5-HMF or 375 µg/mL aKG 125 µg/mL 5-HMF, which were able to significantly reduce the mitochondrial activity after 48 h (28.7% or 35.1%) and 72 h (9.9% or 18.2%) compared to 24 h with the control (100%). A slight increase in cell proliferation was found in HF-SAR using the highest concentration (500 µg/mL aKG + 166.7 µg/mL 5-HMF) between 0 h and 72 h incubation of 140%, while no significant differences were found in the mitochondrial activity of HF-SAR in the absence or presence of several combined aKG + 5-HMF solutions. The solutions with 500 µg/mL aKG + 166.7 µg/mL 5-HMF or 250 µg/mL aKG + 83.3 µg/mL 5-HMF showed a significantly higher caspase activity (51.6% or 13.5%) compared to the control (2.9%) in addition to a higher apoptosis rate (63.2% or 31.4% vs. control: 14.9%). Cell lysate carbonylated proteins were significantly higher in Jurkat cells compared to HF-SAR cells (11.10 vs. 2.2 nmol/mg). About 72 h incubation of Jurkat cells with 500 µg/mL aKG + 166.7 µg/mL 5-HMF or 250 µg/mL aKG + 83.3 µg/mL 5-HMF reduced significantly the carbonylated protein content down to 5.55 or 7.44 nmol/mg whereas only the 500 µg/mL aKG + 166.7 µg/mL 5-HMF solution showed a significant reduction of carbonylated proteins of HF-SAR (1.73 nmol/mg).

scholarly journals Suppression of transforming growth factor-β by mesenchymal stem-cells accelerates liver regeneration in liver fibrosis animal model

2021 ◽  
Vol 40 (1) ◽  
pp. 29
Author(s):  
Nur Anna C Sa’dyah ◽  
Agung Putra ◽  
Bayu Tirta Dirja ◽  
Nurul Hidayah ◽  
Salma Yasmine Azzahara ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Transforming Growth Factor ◽  
Healing Process ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Significant Difference ◽  
T1 And T2

Introduction<br />Liver fibrosis (LF) results from the unregulated chronic wound healing process in liver tissue. Transforming growth factor-beta (TGF-β) is the major contributing cytokine of LF promotion through activation of quiescent hepatic stellate cells (HSCs) into myofibroblasts (MFs) and increased extracellular matrix (ECM) deposition such as collagen leading to scar tissue development. Mesenchymal stem cells (MSCs) have an immunomodulatory capability that could be used as a new treatment for repairing and regenerating LF through suppression of TGF-β. This study aimed to examine the role of MSCs in liver fibrosis animal models through suppression of TGF-β levels without scar formation particularly in the proliferation phase.<br /><br />Methods<br />In this study, a completely randomized design was used with sample size of 24. Male Sprague Dawley rats were injected intraperitoneally (IP) with carbon tetrachloride (CCl4), twice weekly, for eight weeks to induce LF. Rats were randomly assigned to four groups: negative control, CCl4 group, and CCL4 + MSC-treated groups T1 and T2, at doses of 1 x 106 and 2x106 cells, respectively. TGF-β levels were analyzed by enzyme-linked immunosorbent assay (ELISA). One-way ANOVA and a least significant difference (LSD) was used to analyse the data. <br /><br />Results<br />The TGF levels of LF rat models decreased on day 7 after MSC administration. The levels of TGF-β in both MSC groups T1 and T2 decreased significantly compared with the control group (p&lt;0.05). The TGF-β suppression capability of T2 was optimal and more significant than that of T1.<br /><br />Conclusion<br />MSCs can suppress TGF levels in liver fibrosis induced rats.

Influence of transforming growth factor beta1 (TGF-beta1) on the behaviour of porcine thyroid epithelial cells in primary culture through thrombospondin-1 synthesis

1999 ◽  
Vol 112 (9) ◽  
pp. 1405-1416
Author(s):  
D. Claisse ◽  
I. Martiny ◽  
B. Chaqour ◽  
Y. Wegrowski ◽  
E. Petitfrere ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Follicle Cells ◽  
Dependent Manner ◽  
Transforming Growth Factor Beta1 ◽  
Thyroid Cells ◽  
Amino Terminal ◽  
Thrombospondin 1 ◽  
Inhibitor Of Protein Synthesis

Transforming growth factor beta1 (TGF-beta1) is a secreted polypeptide that is thought to play a major role in the regulation of folliculogenesis and differentiation of thyroid cells. On porcine thyroid follicular cells cultured on plastic substratum, TGF-beta1, in a concentration-dependent way, promoted the disruption of follicles, cell spreading, migration and confluency by a mechanism that did not involve cell proliferation. TGF-beta1 strongly activated the production of thrombospondin-1 and (alpha)vbeta3 integrin in a concentration-dependent manner whereas the expression of thyroglobulin was unaffected. Anisomycin, an inhibitor of protein synthesis, inhibited the effect of TGF-beta1 on cell organization. Thrombospondin-1 reproduced the effect of TGF-beta1. In the presence of thrombospondin-1 cells did not organize in follicle-like structures but, in contrast, spreaded and reached confluency independently of cell proliferation. This effect is suppressed by an RGD-containing peptide. The adhesive properties of thrombospondin-1 for thyroid cells were shown to be mediated by both the amino-terminal heparin-binding domain and the RGD domain of thrombospondin-1. Adhesion was shown to involve (alpha)vbeta3 integrin. The results show that TGF-beta1 exerted an influence upon function and behaviour of follicle cells partly mediated by the synthesis of thrombospondin-1 and of its receptor (alpha)vbeta3 integrin.

Retinoic acid-induced proliferation of lung alveolar epithelial cells: relation with the IGF system

1998 ◽  
Vol 275 (1) ◽  
pp. L71-L79 ◽  
Author(s):  
Elodie Nabeyrat ◽  
Valérie Besnard ◽  
Sophie Corroyer ◽  
Véronique Cazals ◽  
Annick Clement
Keyword(s):  
Cell Proliferation ◽  
Retinoic Acid ◽  
Growth Factor ◽  
Alveolar Epithelium ◽  
Cell Number ◽  
Dependent Manner ◽  
Alveolar Epithelial ◽  
Igf System ◽  
Tgf Β1

Retinoids, including retinol and retinoic acid (RA) derivatives, are important molecules for lung growth and homeostasis. The presence of RA receptors and of RA-binding proteins in the alveolar epithelium led to suggest a role for RA on alveolar epithelial cell replication. In the present study, we examined the effects of RA on proliferation of the stem cells of the alveolar epithelium, the type 2 cells. We showed that treatment of serum-deprived type 2 cells with RA led to a stimulation of cell proliferation, with an increase in cell number in a dose-dependent manner. To gain some insights into the mechanisms involved, we studied the effects of RA on the expression of several components of the insulin-like growth factor (IGF) system that have been shown to be associated with the growth arrest of type 2 cells, mainly the IGF-binding protein-2 (IGFBP-2), IGF-II, and the type 2 IGF receptor. We documented a marked decrease in the expression of these components upon RA treatment. Using conditioned media from RA-treated cells, we provided evidence that the proliferative response of type 2 cells to RA was mediated through production of growth factor(s) distinct from IGF-I. We also showed that RA was able to reduce the decrease in cell number observed when type 2 cells were treated with transforming growth factor (TGF)-β1. These results together with the known stimulatory effect of TGF-β1 on IGFBP-2 expression led to suggest that RA may be associated with type 2 cell proliferation through mechanisms interfering with the TGF-β1 pathway.

scholarly journals Expression of Notch–Hif-1α signaling pathway in liver regeneration of rats

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052094379
Author(s):  
Yanshan Li ◽  
Yunxiuxiu Xu ◽  
Ruomei Wang ◽  
Wenxin Li ◽  
Wenguang He ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Body Weight ◽  
Protein Expression ◽  
Liver Regeneration ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Saline Control ◽  
Control Group ◽  
Mrna Levels ◽  
Ki 67

Objective To investigate whether the Notch–Hif-1α signaling pathway is involved in liver regeneration. Methods Rats were divided into two groups and treated with daily intraperitoneal injections of saline (control) or the gamma-secretase inhibitor, Fli-06, for 2 days. Two-thirds of the rat livers were resected and rats were later euthanized at specific time points post-resection to analyze the remnant livers. Each group's liver/body weight ratio was calculated, and immunostaining and western blotting were used to determine the cell proliferation marker, PCNA and Ki-67 expression. Real-time PCR and western blotting were used to compare the mRNA expression of Notch homolog-1 ( Notch1), hairy and enhancer of split-1 ( Hes1), and vascular endothelial growth factor ( Vegf), and the protein expression of NICD and HIF-1α, respectively. Results The liver/body weight ratios and number of Ki-67- and PCNA-positive cells were significantly lower in the experimental group than the control group, indicating lower levels of liver regeneration following the disruption of Notch signaling by Fli-06. The Hes1 and Vegf mRNA levels and NICD and HIF-1α protein expression levels were all down-regulated by Fli-06 treatment. Conclusion Notch–Hif-α signaling pathway activation plays an important role in liver regeneration, where it may contribute toward liver cell proliferation.

scholarly journals Amelioration of paraquat-induced pulmonary fibrosis in mice by regulating miR-140-5p expression with the fibrogenic inhibitor Xuebijing

2020 ◽  
Vol 34 ◽  
pp. 205873842092391 ◽  
Author(s):  
Min-na Dong ◽  
Yun Xiao ◽  
Yun-fei Li ◽  
Dong-mei Wang ◽  
Ya-ping Qu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Treatment Group ◽  
Pulmonary Fibrosis ◽  
Transforming Growth Factor ◽  
Lavage Fluid ◽  
Tissue Growth ◽  
Control Treatment ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Tgf Β1

Intravenous Xuebijing (XBJ) therapy suppresses paraquat (PQ)-induced pulmonary fibrosis. However, the mechanism underlying this suppression remains unknown. This work aimed to analyze the miR-140-5p-induced effects of XBJ injection on PQ-induced pulmonary fibrosis in mice. The mice were arbitrarily assigned to four groups. The model group was administered with PQ only. The PQ treatment group was administered with PQ and XBJ. The control group was administered with saline only. The control treatment group was administered with XBJ only. The miR-140-5p and miR-140-5p knockout animal models were overexpressed. The gene expression levels of miR-140-5p, transglutaminase-2 (TG2), β-catenin, Wnt-1, connective tissue growth factor (CTGF), mothers against decapentaplegic homolog (Smad), and transforming growth factor-β1 (TGF-β1) in the lungs were assayed with quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot analysis. The levels of TGF-β1, CTGF, and matrix metalloproteinase-9 (MMP-9) in the bronchoalveolar lavage fluid were assessed by enzyme-linked immunosorbent assay (ELISA). Hydroxyproline (Hyp) levels and pulmonary fibrosis were also scored. After 14 days of PQ induction of pulmonary fibrosis, AdCMV-miR-140-5p, and XBJ upregulated miR-140-5p expression; blocked the expressions of TG2, Wnt-1, and β-catenin; and decreased p-Smad2, p-Smad3, CTGF, MMP-9, and TGF-β1 expressions. In addition, Hyp and pulmonary fibrosis scores in XBJ-treated mice decreased. Histological results confirmed that PQ-induced pulmonary fibrosis in XBJ-treated lungs was attenuated. TG2 expression and the Wnt-1/β-catenin signaling pathway were suppressed by the elevated levels of miR-140-5p expression. This inhibition was pivotal in the protective effect of XBJ against PQ-induced pulmonary fibrosis. Thus, XBJ efficiently alleviated PQ-induced pulmonary fibrosis in mice.

scholarly journals Effect of platelet-rich plasma on implant bone defects in rabbits through the FAK/PI3K/AKT signaling pathway

2019 ◽  
Vol 14 (1) ◽  
pp. 311-317
Author(s):  
Wei Liu ◽  
Ben Chen ◽  
Youyang Zheng ◽  
Yuehua Shi ◽  
Zhuojin Shi
Keyword(s):  
Growth Factor ◽  
Bone Healing ◽  
Alveolar Bone ◽  
Platelet Rich Plasma ◽  
Healing Process ◽  
Bone Defects ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Tissue Healing ◽  
Bone Healing Process

AbstractPlatelet-rich plasma (PRP) has been shown to be a beneficial growth factor for bone tissue healing and is used in implantology. The aim of this study was to investigate the effects of PRP on bone defects in rabbits. Twenty rabbits were used to establish the implant bone defect model in this study. An intrabony defect (5mm × 5mm × 3mm) was created in alveolar bone in the lower jar of each rabbit. The wound was treated with PRP. The expression of platelet-derived growth factor BB (PDGFBB) was assessed by enzyme-linked immunosorbent assay (ELISA). Focal adhesion kinase (FAK) and related phosphatidylinositol 3-kinase (PI3K)/AKT (protein kinase B) levels were measured by Western blot. The results show that PRP could significantly improve the bone healing process when compared with control, and 10% PRP could markedly increase fibroblast proliferation 48-h post treatment. PDGFBB was higher in the PRP group than that in the control group. PRP treatment also could elevate the phosphorylation of FAK and PI3K/AKT, although the inhibitor of PDGFR could reverse this trend. These results suggest that PRP treatment improves the bone healing process through the FAK/PI3K/AKT pathway.

scholarly journals THE TOXICITY OF MAULI BANANA (MUSA ACUMINATA) STEM WATER EXTRACT ON BONE MARROW MESENCHYMAL STEM CELL IN VITRO

2019 ◽  
pp. 184-186
Author(s):  
AMY NINDIA ◽  
DIDIT ASPRIYANTO ◽  
MAHARANI LAILLYZA APRIASARI ◽  
SELVIANA RIZKY
Keyword(s):  
Growth Factor ◽  
Water Extract ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Cell Culture Process ◽  
Control Group Design ◽  
Water Solvent ◽  
Stem Water ◽  
Banana Stem

Objective: Since mesenchymal stem cells (MSC) can differentiate into bone, cementum, and periodontal ligament, they can be used to treat aggressiveperiodontitis. The limited number of MSCs requires replenishment of growth factor in the cell culture process. Since growth factor is quite expensive,an alternative material is needed. Mauli banana stem has antioxidant and immunomodulatory properties. Methanol extract of Mauli banana stem isknown to be toxic toward MSCs; therefore, another solvent with a non-toxic effect is needed, such as a water solvent. We analyzed the toxicity of Maulibanana stem water extract on MSC in vitro.Methods: In this laboratory experimental (true experimental) study with a Post-test Only Control Group Design, MSC cultures were treated withMauli banana stem water extract at 10, 20, 40, 60, 80, and 100 mg/mL dosages. One group without any treatment served as a control group and onewas a media control group. Each group was incubated for 24 h and then was given 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromidereagent and analyzed by an enzyme-linked immunosorbent assay (ELISA) reader.Results: One-way analysis of variance showed a significant difference.Conclusion: Mauli banana stem water extracts at 10, 20, 40, and 60 mg/mL were not toxic toward MSC in vitro, while dosages of 80 and 100 mg/mLdosage were toxic.

scholarly journals Neochamaejasmin A Induces Mitochondrial-Mediated Apoptosis in Human Hepatoma Cells via ROS-Dependent Activation of the ERK1/2/JNK Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Yangfang Ding ◽  
Qi Xie ◽  
Wenjing Liu ◽  
Zhaohai Pan ◽  
Xinmei Fan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Hepg2 Cells ◽  
Morphological Changes ◽  
Control Group ◽  
Dependent Manner ◽  
Human Hepatoma ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway

The botanical constituents of Stellera chamaejasme Linn. exhibit various pharmacological and medicinal activities. Neochamaejasmin A (NCA), one main active constituent of S. chamaejasme, inhibits cell proliferation and induces cell apoptosis in several types of tumor cells. However, the antitumor effect of NCA on hepatocellular carcinoma cells is still unclear. In this study, NCA (36.9, 73.7, and 147.5 μM) significantly inhibited hepatoblastoma-derived HepG2 cell proliferation in a concentration-dependent manner. Hoechst 33258 staining and flow cytometry showed that apoptotic morphological changes were observed and the apoptotic rate was significantly increased in NCA-treated HepG2 cells, respectively. Additionally, the levels of Bax, cleaved caspase-3, and cytoplasmic cytochrome c were increased, while the level of Bcl-2 was decreased in NCA-treated HepG2 cells when compared with the control group. Moreover, we found that the reactive oxygen species (ROS) level was significantly higher and the mitochondrial membrane potential was remarkably lower in NCA-treated HepG2 cells than in the control group. Further studies demonstrated that the levels of p-JNK and p-ERK1/2 were significantly upregulated in NCA-treated HepG2 cells, and pretreatment with JNK and ERK1/2 inhibitors, SP600125 and PD0325901, respectively, suppressed NCA-induced cell apoptosis of HepG2 cells. In addition, NCA also significantly inhibited human hepatoma BEL-7402 cell proliferation and induced cell apoptosis through the ROS-mediated mitochondrial apoptotic pathway. These results implied that NCA induced mitochondrial-mediated cell apoptosis via ROS-dependent activation of the ERK1/2/JNK signaling pathway in HepG2 cells.

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