scholarly journals Sulforaphane induces p53-deficient SW480 cell apoptosis via the ROS-MAPK signaling pathway

2017 ◽  
Vol 16 (5) ◽  
pp. 7796-7804 ◽  
Author(s):  
Hai Lan ◽  
Hongyin Yuan ◽  
Congyao Lin
Keyword(s):  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Sw480 Cell ◽  
Mapk Signaling Pathway

scholarly journals Protective Effect of Penetratin Analogue-Tagged SOD1 on Cisplatin-Induced Nephrotoxicity through Inhibiting Oxidative Stress and JNK/p38 MAPK Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Xiao-lu Wang ◽  
Liang Wang ◽  
Fo-lan Lin ◽  
Si-si Li ◽  
Ting-xuan Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Membrane ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Tunel Assay ◽  
Mapk Signaling Pathway ◽  
Mapk Activation ◽  
Urea Nitrogen

Copper/zinc superoxide dismutase (SOD1) can clear cisplatin- (CP-) induced excessive reactive oxygen species (ROS), but exogenous SOD1 cannot enter cells because of its low biomembrane permeability. Cell-penetrating peptides (CPPs) can rapidly cross plasma membranes. This study is aimed at identifying an efficient and stable CPP-SOD1 and investigating its effects on CP-induced nephrotoxicity. We recombined SOD1 with 14 different CPPs and purified them using an NTA-Ni2+ column. In in vitro experiments, CPPs-SOD1 cell membrane penetration ability and JNK/p38 MAPK signaling pathway were evaluated using Western blotting. ROS production, mitochondrial membrane potential (MMP), and cell apoptosis were determined using flow cytometry and immunofluorescence staining in VERO and HK-2 cells. For in vivo experiments, mice were administered PSF-SOD1 for 2 h before cotreatment with a single CP injection for an additional 4 days. Blood and kidney samples were collected for renal function assessment (creatinine, urea nitrogen, histopathology, TUNEL assay, and JNK/p38 MAPK signaling pathway). Compared with TAT-SOD1, we found that PSF-SOD1 is more efficient at crossing the cell membrane and is stable after transduction into cells. Pretreatment with PSF-SOD1 inhibited CP-induced apoptosis, ROS generation, and JNK/p38 MAPK activation and restored CP-induced MMP loss in VERO and HK-2 kidney cells. Treatment of mice with PSF-SOD1 inhibited CP-induced serum creatinine, blood urea nitrogen elevation, and JNK/p38 MAPK activation. H&E staining and TUNEL assay indicated that kidney tissue damage was alleviated following PSF-SOD1 pretreatment. Overall, PSF-SOD1 ameliorated CP-induced renal damage by partially reducing oxidative stress and cell apoptosis by regulating JNK/p38 MAPK signaling pathway and might be a better cytoprotective agent than TAT-SOD1.

scholarly journals Protective effects of alfalfa saponins on oxidative stress-induced apoptotic cells

2020 ◽  
Vol 11 (9) ◽  
pp. 8133-8140
Author(s):  
Yalei Cui ◽  
Boshuai Liu ◽  
Xiao Sun ◽  
Zidan Li ◽  
Yanyan Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Antioxidant System ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Apoptotic Cells ◽  
Protective Effects

Alfalfa saponins defend against oxidative stress by enhancing the antioxidant system and further inhibit cell apoptosis by activating the MAPK signaling pathway.

Astragaloside attenuates lipopolysaccharide‐induced cell apoptosis in human gingiva cells via MAPK signaling pathway

2019 ◽  
Vol 120 (8) ◽  
pp. 12273-12279 ◽  
Author(s):  
Xionghu Shen ◽  
Honghua Sun ◽  
Hai Cui ◽  
Yongmin Jin ◽  
Wenbo Jin ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Human Gingiva

scholarly journals MicroRNA-124 inhibits macrophage cell apoptosis via targeting p38/MAPK signaling pathway in atherosclerosis development

Aging ◽  
2020 ◽  
Vol 12 (13) ◽  
pp. 13005-13022
Author(s):  
Xue Liang ◽  
Lijun Wang ◽  
Manman Wang ◽  
Zhaohong Liu ◽  
Xing Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Macrophage Cell ◽  
Microrna 124 ◽  
Atherosclerosis Development

WITHDRAWN: Cinobufagin induced cell apoptosis and protective autophagy through the ROS/MAPK signaling pathway

Life Sciences ◽  
2019 ◽  
pp. 116642 ◽  
Author(s):  
Kaili Wang ◽  
Danxia Chu ◽  
Jie Wu ◽  
Mengling Zhao ◽  
Miaomiao Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway

scholarly journals Rutin Protects against Pirarubicin-Induced Cardiotoxicity through TGF-β1-p38 MAPK Signaling Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Yadi Wang ◽  
Yang Zhang ◽  
Bo Sun ◽  
Qing Tong ◽  
Liqun Ren
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Dose Range ◽  
Mapk Signaling ◽  
Positive Control ◽  
Mapk Signaling Pathway ◽  
Cardioprotective Effect ◽  
Mitogen Activated Protein Kinase ◽  
Ros Generation

We investigated the potential protective effect of rutinum (RUT) against pirarubicin- (THP-) induced cardiotoxicity. THP was used to induce toxicity in rat H9c2 cardiomyoblasts. Positive control cells were pretreated with a cardioprotective agent dexrazoxane (DZR) prior to treatment with THP. Some of the cells were preincubated with RUT and a p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, both individually and in combination, prior to THP exposure. At a dose range of 30–70 μM, RUT significantly prevented THP-induced reduction in cell viability; the best cardioprotective effect was observed at a dose of 50 μM. Administration of RUT and SB203580, both individually as well as in combination, suppressed the elevation of intracellular ROS, inhibited cell apoptosis, and reversed the THP-induced upregulation of TGF-β1, p-p38 MAPK, cleaved Caspase-9, Caspase-7, and Caspase-3. A synergistic effect was observed on coadministration of RUT and SB203580. RUT protected against THP-induced cardiotoxicity by inhibition of ROS generation and suppression of cell apoptosis. The cardioprotective effect of RUT appears to be associated with the modulation of the TGF-β1-p38 MAPK signaling pathway.

scholarly journals Long non-coding RNA H19 contributes to wound healing of diabetic foot ulcer

2020 ◽  
Vol 65 (3) ◽  
pp. 69-84
Author(s):  
Bo Li ◽  
Yue Zhou ◽  
Jing Chen ◽  
Tingting Wang ◽  
Zhijuan Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Signaling Pathway ◽  
Diabetic Foot ◽  
Cell Apoptosis ◽  
Foot Ulcer ◽  
Diabetic Foot Ulcer ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Ecm Remodeling

Diabetic foot ulcer (DFU) is a chronic and non-healing complication of diabetes that leads to high hospital costs and, in extreme cases, to amputation. Recent studies have reported that long non-coding RNAs (lncRNAs) are linked to various diabetes-related symptoms. Thus, we aim to explore the role of lncRNA H19 in the wound healing process following DFU. Fibroblasts were isolated from the ulcer margin tissues of DFU patients, with the expression of lncRNA H19, connective tissue growth factor (CTGF) or serum response factor (SRF) altered by lentivirus infection. Next, rat models of DFU induced by high glucose and lipid diet were established, which was also infected with the corresponding lentivirus. The interaction among lncRNA H19, SRF and CTGF was determined. Afterward, cell proliferation and apoptosis, angiogenesis, ECM remodeling and wound healing in DFU tissues were evaluated to explore the effects of lncRNA H19/SRF/CTGF and MAPK signaling pathway on DFU. CTGF was poorly expressed in ulcer tissues from DFU rats and patients. CTGF overexpression was shown to activate the MAPK signaling pathway to promote cell proliferation, ECM remodeling, angiogenesis and wound healing while inhibiting cell apoptosis. lncRNA H19 was validated to elevate CTGF expression by recruiting SRF to the promoter region of CTGF, thus accelerating cell proliferation, ECM remodeling and wound healing while repressing cell apoptosis. Furthermore, MAPK signaling pathway activation is confirmed to be the underlying mechanism behind lncRNA H19/CTGF/SRF-induced results. Thus, lncRNA H19 accelerated wound healing in DFU through elevation of CTGF and activation of the MAPK signaling pathway.

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