scholarly journals Correction for: miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke

Aging ◽  
2021 ◽  
Author(s):  
Runhui Tian ◽  
Bo Wu ◽  
Cong Fu ◽  
Kaimin Guo
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Cognitive Impairment ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Neuronal Injury ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway

scholarly journals Protective Effect of Methane-Rich Saline on Acetic Acid-Induced Ulcerative Colitis via Blocking the TLR4/NF-κB/MAPK Pathway and Promoting IL-10/JAK1/STAT3-Mediated Anti-inflammatory Response

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Guanghui Wang ◽  
Bing Xu ◽  
Feiyu Shi ◽  
Mengfan Du ◽  
Yaguang Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ulcerative Colitis ◽  
Acetic Acid ◽  
Inflammatory Response ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Tissue Damage ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Anti Inflammatory

Ulcerative colitis (UC) is an inflammation-related disease involved in uncontrolled inflammation and oxidative stress and is characterized by high recurrence and relapse risk. As a rising star in gas medicine, methane owns the properties of anti-inflammation, antioxidation, and antiapoptosis. Based on the possible mechanism, we aimed to investigate the effect of methane on UC. Methane-rich saline (MRS) was introduced here, and UC was induced by acetic acid. All the C57BL/6 mice were allocated into groups as follows: control group, colitis model group, colitis treated with salazosulfapyridine (SASP) group, and colitis treated with MRS (1 or 10 ml/kg) groups. Tissue damage, the degree of inflammation, oxidative stress, and apoptosis were evaluated in the study, as well as the TLR4/NF-κB/MAPK and IL-10/JAK1/STAT3 signaling pathways for further exploration of the potential mechanism. The results showed that MRS (1) alleviated tissue damage caused by acetic acid, (2) controlled acetic acid-induced inflammation, (3) inhibited acetic acid-caused oxidative stress, (4) reduced colonic cell apoptosis due to acetic acid, (5) suppressed the TLR-4/NF-κB/MAPK signaling pathway, and (6) activated IL-10/JAK1/STAT3 anti-inflammatory response to improve the injury induced by acetic acid. We conclude that MRS has a protective effect on acetic acid-induced ulcerative colitis in mice via blocking the TLR4/NF-κB/MAPK signaling pathway and promoting the IL-10/JAK1/STAT3-mediated anti-inflammatory response.

MAPK: A Key Player in the Development and Progression of Stroke

2020 ◽  
Vol 19 (4) ◽  
pp. 248-256
Author(s):  
Yangmin Zheng ◽  
Ziping Han ◽  
Haiping Zhao ◽  
Yumin Luo
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Complex Disease ◽  
Therapeutic Targets ◽  
Cell Types ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Effective Prevention ◽  
Prevention And Treatment ◽  
Different Cell Types

Conclusion: Stroke is a complex disease caused by genetic and environmental factors, and its etiological mechanism has not been fully clarified yet, which brings great challenges to its effective prevention and treatment. MAPK signaling pathway regulates gene expression of eukaryotic cells and basic cellular processes such as cell proliferation, differentiation, migration, metabolism and apoptosis, which are considered as therapeutic targets for many diseases. Up to now, mounting evidence has shown that MAPK signaling pathway is involved in the pathogenesis and development of ischemic stroke. However, the upstream kinase and downstream kinase of MAPK signaling pathway are complex and the influencing factors are numerous, the exact role of MAPK signaling pathway in the pathogenesis of ischemic stroke has not been fully elucidated. MAPK signaling molecules in different cell types in the brain respond variously after stroke injury, therefore, the present review article is committed to summarizing the pathological process of different cell types participating in stroke, discussed the mechanism of MAPK participating in stroke. We further elucidated that MAPK signaling pathway molecules can be used as therapeutic targets for stroke, thus promoting the prevention and treatment of stroke.

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.

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