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

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.

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Protective effect of peptide DR8 on bleomycin-induced pulmonary fibrosis by regulating the TGF-β/MAPK signaling pathway and oxidative stress

Toxicology and Applied Pharmacology ◽

10.1016/j.taap.2019.114703 ◽

2019 ◽

Vol 382 ◽

pp. 114703 ◽

Cited By ~ 4

Author(s):

Dan Wang ◽

Zhibin Yan ◽

Lili Bu ◽

Chunmei An ◽

Bochuan Deng ◽

...

Keyword(s):

Oxidative Stress ◽

Pulmonary Fibrosis ◽

Protective Effect ◽

Signaling Pathway ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

And Oxidative Stress

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

Aging ◽

10.18632/aging.103301 ◽

2020 ◽

Vol 12 (11) ◽

pp. 10873-10895

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

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Umbelliferone ameliorates ulcerative colitis induced by acetic acid via modulation of TLR4/NF-κB-p65/iNOS and PPARγ/SIRT1 signaling pathways in rats

10.21203/rs.3.rs-619327/v1 ◽

2021 ◽

Author(s):

Basel A Abdel-Wahab ◽

Saad A Alkahtani ◽

Abdulsalam A Alqahtani ◽

Emad H.M. Hassanein

Keyword(s):

Ulcerative Colitis ◽

Acetic Acid ◽

Inflammatory Response ◽

Signaling Pathways ◽

Signaling Pathway ◽

Therapeutic Potential ◽

Tissue Injury ◽

Oxidative Injury ◽

Control Group ◽

Anti Inflammatory

Abstract Ulcerative colitis (UC) is a common chronic, idiopathic inflammatory bowel disease associated with inflammatory perturbation and oxidative stress. Umbelliferone (UMB) is a potent anti-inflammatory and antioxidant coumarin derivative. Depending on the possible mechanisms, we aimed to explore and elucidate the therapeutic potential of UMB on UC-inflammatory response and oxidative injury-induced via intrarectal administration of acetic acid (AA). Rats were assigned into four groups: control group, UMB (30 mg/kg) treated group, colitis model group (2 ml of AA; 3% v/v), and colitis treated with UMB groups. Our results exhibited that UMB improved macroscopic and histological tissue injury caused by the AA. Mechanistically, UMB reduced the elevated TNF-α, IL-6, MPO and VCAM-1 via effective downregulation of TLR-4, NF-κB and iNOS signaling pathway, thereby mediated potent anti-inflammatory effects. Moreover, UMB administration resulted in effective up-regulation of both PPARγ and SIRT1 signaling pathways, thereby inhibited both oxidative injury and inflammatory response. Conclusively, UMB protected against AA-induced UC in rats through suppressing of the TLR4/NF-κB-p65/iNOS signaling pathway and promoting the PPARγ/SIRT1 signaling. Indeed, our data proved the effectiveness of UMB in UC and introduced it as a potential therapeutic beneficial applicant for clinical application.

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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 ◽

10.18632/aging.202509 ◽

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

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Total flavones of fermentation broth by co-culture of Coprinus comatus and Morchella esculenta induces an anti-inflammatory effect on LPS-stimulated RAW264.7 macrophages cells via the MAPK signaling pathway

Microbial Pathogenesis ◽

10.1016/j.micpath.2018.10.008 ◽

2018 ◽

Vol 125 ◽

pp. 431-437 ◽

Cited By ~ 6

Author(s):

Xiaohong Zhao ◽

Xianwei Zou ◽

Qian Li ◽

Xu Cai ◽

Liya Li ◽

...

Keyword(s):

Signaling Pathway ◽

Fermentation Broth ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Coprinus Comatus ◽

Raw264.7 Macrophages ◽

Morchella Esculenta ◽

Anti Inflammatory ◽

Inflammatory Effect

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

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/5526053 ◽

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.

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