Norcantharidin Enhances High Concentrations of Fetal Bovine Serum-Induced Apoptosis in Human Mesangial Cells by Regulating the Mitogen-Activated Protein Kinase Signaling Pathway

Aim: This study aimed to investigate the effect of norcantharidin (NCTD) on human mesangial cells (HMCs) apoptosis in vitro and further examine its molecular mechanism. Methods: HMCs were divided into 5 groups: control group, 25% fetal bovine serum (FBS)-treated group, and NCTD groups (NCTD [2.5, 5...

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Main Authors: Kun Ye, Qiao-Yu Wei, Teng-Xiang Long, Hong-Guang He, Yun-Feng Huang, Li-Jia Xiong, Jiao Lan, Yi-Yun Huang, Zhi-Feng Gong, Xiao-Mei Peng, Qiu-Xia Wu
Format: Article
Language:English
Published: Karger Publishers 2019-10-01
Series:Kidney & Blood Pressure Research
Subjects:
Online Access:https://www.karger.com/Article/FullText/502524
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author Kun Ye
Qiao-Yu Wei
Teng-Xiang Long
Hong-Guang He
Yun-Feng Huang
Li-Jia Xiong
Jiao Lan
Yi-Yun Huang
Zhi-Feng Gong
Xiao-Mei Peng
Qiu-Xia Wu
author_facet Kun Ye
Qiao-Yu Wei
Teng-Xiang Long
Hong-Guang He
Yun-Feng Huang
Li-Jia Xiong
Jiao Lan
Yi-Yun Huang
Zhi-Feng Gong
Xiao-Mei Peng
Qiu-Xia Wu
author_sort Kun Ye
collection DOAJ
description Aim: This study aimed to investigate the effect of norcantharidin (NCTD) on human mesangial cells (HMCs) apoptosis in vitro and further examine its molecular mechanism. Methods: HMCs were divided into 5 groups: control group, 25% fetal bovine serum (FBS)-treated group, and NCTD groups (NCTD [2.5, 5 and 10 µg/mL] + 25% FBS, respectively). Cell proliferation was determined by MTT assay, while apoptosis was evaluated by Hoechest 33258 staining, the level of cytochrome c, immunohistochemistry, and apoptotic-related proteins/gene expression. Results: Cell viability was inhibited in NCTD-treated HMCs in a dose-dependent manner. The number of apoptotic cells and the content of cytochrome c were significantly increased by NCTD treatment but that of mitochondrial membrane was decreased. Moreover, the expression of bcl-2 and caspase-3 was prompted by NCTD, but the expression of bax, MMP-2, and MMP-9 in 25% FBS-treated HMCs was inhibited. In addition, NCTD markedly unregulated the expression of apoptosis-related gene/protein, including p-Erk1/2, phosphorylated-Jun N-terminal kinase (JNK), p-p38, and p53. Conclusion: NCTD enhances 25% FBS-treated HMC apoptosis in vitro, and this effect may be attributed to the modulation of the ERK, JNK, and p38 mitogen-activated protein kinase signaling pathways.
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spelling doaj.art-a707eae5b1b242a99ed24e098eb2931a2022-12-22T00:12:34ZengKarger PublishersKidney & Blood Pressure Research1420-40961423-01432019-10-0111310.1159/000502524502524Norcantharidin Enhances High Concentrations of Fetal Bovine Serum-Induced Apoptosis in Human Mesangial Cells by Regulating the Mitogen-Activated Protein Kinase Signaling PathwayKun YeQiao-Yu WeiTeng-Xiang LongHong-Guang HeYun-Feng HuangLi-Jia XiongJiao LanYi-Yun HuangZhi-Feng GongXiao-Mei PengQiu-Xia WuAim: This study aimed to investigate the effect of norcantharidin (NCTD) on human mesangial cells (HMCs) apoptosis in vitro and further examine its molecular mechanism. Methods: HMCs were divided into 5 groups: control group, 25% fetal bovine serum (FBS)-treated group, and NCTD groups (NCTD [2.5, 5 and 10 µg/mL] + 25% FBS, respectively). Cell proliferation was determined by MTT assay, while apoptosis was evaluated by Hoechest 33258 staining, the level of cytochrome c, immunohistochemistry, and apoptotic-related proteins/gene expression. Results: Cell viability was inhibited in NCTD-treated HMCs in a dose-dependent manner. The number of apoptotic cells and the content of cytochrome c were significantly increased by NCTD treatment but that of mitochondrial membrane was decreased. Moreover, the expression of bcl-2 and caspase-3 was prompted by NCTD, but the expression of bax, MMP-2, and MMP-9 in 25% FBS-treated HMCs was inhibited. In addition, NCTD markedly unregulated the expression of apoptosis-related gene/protein, including p-Erk1/2, phosphorylated-Jun N-terminal kinase (JNK), p-p38, and p53. Conclusion: NCTD enhances 25% FBS-treated HMC apoptosis in vitro, and this effect may be attributed to the modulation of the ERK, JNK, and p38 mitogen-activated protein kinase signaling pathways.https://www.karger.com/Article/FullText/502524norcantharidinhuman mesangial cellsapoptosismitogen-activated protein kinase pathway
spellingShingle Kun Ye
Qiao-Yu Wei
Teng-Xiang Long
Hong-Guang He
Yun-Feng Huang
Li-Jia Xiong
Jiao Lan
Yi-Yun Huang
Zhi-Feng Gong
Xiao-Mei Peng
Qiu-Xia Wu
Norcantharidin Enhances High Concentrations of Fetal Bovine Serum-Induced Apoptosis in Human Mesangial Cells by Regulating the Mitogen-Activated Protein Kinase Signaling Pathway
Kidney & Blood Pressure Research
norcantharidin
human mesangial cells
apoptosis
mitogen-activated protein kinase pathway
title Norcantharidin Enhances High Concentrations of Fetal Bovine Serum-Induced Apoptosis in Human Mesangial Cells by Regulating the Mitogen-Activated Protein Kinase Signaling Pathway
title_full Norcantharidin Enhances High Concentrations of Fetal Bovine Serum-Induced Apoptosis in Human Mesangial Cells by Regulating the Mitogen-Activated Protein Kinase Signaling Pathway
title_fullStr Norcantharidin Enhances High Concentrations of Fetal Bovine Serum-Induced Apoptosis in Human Mesangial Cells by Regulating the Mitogen-Activated Protein Kinase Signaling Pathway
title_full_unstemmed Norcantharidin Enhances High Concentrations of Fetal Bovine Serum-Induced Apoptosis in Human Mesangial Cells by Regulating the Mitogen-Activated Protein Kinase Signaling Pathway
title_short Norcantharidin Enhances High Concentrations of Fetal Bovine Serum-Induced Apoptosis in Human Mesangial Cells by Regulating the Mitogen-Activated Protein Kinase Signaling Pathway
title_sort norcantharidin enhances high concentrations of fetal bovine serum induced apoptosis in human mesangial cells by regulating the mitogen activated protein kinase signaling pathway
topic norcantharidin
human mesangial cells
apoptosis
mitogen-activated protein kinase pathway
url https://www.karger.com/Article/FullText/502524
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