The Inhibitory Role of Hydrogen Sulfide in Airway Hyperresponsiveness and Inflammation in a Mouse Model of Asthma

2013 ◽  
Vol 182 (4) ◽  
pp. 1188-1195 ◽  
Author(s):  
Gensheng Zhang ◽  
Peipei Wang ◽  
Guangdong Yang ◽  
Qiuhui Cao ◽  
Rui Wang
Keyword(s):  
Hydrogen Sulfide ◽  
Mouse Model ◽  
Airway Hyperresponsiveness ◽  
Inhibitory Role

scholarly journals Reductions in Hydrogen Sulfide Precede Onset of Mitochondrial Quality Control in the Corneal Kindled Mouse Model of Epilepsy

2021 ◽  
Author(s):  
Christi Cho ◽  
Maxwell Zeigler ◽  
Stephanie Mizuno ◽  
Richard S. Morrison ◽  
Rheem Totah ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Mouse Model ◽  
Membrane Integrity ◽  
Brain Homogenate ◽  
Maximal Electroshock ◽  
Maximal Electroshock Seizure ◽  
Mitochondrial Stress ◽  
Acute Seizures ◽  
Related Proteins

Epilepsy is a heterogenous neurological disorder characterized by recurrent unprovoked seizures, mitochondrial stress, and neurodegeneration. Hydrogen sulfide (H2S), a gasotransmitter, promotes mitochondrial function and biogenesis, elicits neuromodulation and neuroprotection, and may acutely suppress seizures. A major gap in knowledge remains in understanding the role of mitochondrial dysfunction and progressive changes in H2S levels following acute seizures and during epileptogenesis. We thus sought to quantify changes in H2S and its methylated metabolite (MeSH) via LC-MS/MS subsequent to acute maximal electroshock and 6 Hz 44 mA seizures in mice, as well as in the corneal kindled mouse model of chronic seizures. Plasma H2S was acutely reduced after a maximal electroshock seizure. H2S or MeSH levels in whole brain homogenate and expression of related genes in corneal kindled mice were not altered. However, plasma H2S and MeSH levels were significantly lower during kindling, but not after established kindling. Morever, we demonstrated a time-dependent increase in expression of mitochondrial membrane integrity-related proteins, Opa1, Mfn2, Drp1, and Mff during kindling, which did not correlate with gene expression. Taken together, short-term reductions in plasma H2S could be a novel biomarker for seizures. Future studies should further define the role of H2S and mitochondrial stress in epilepsy.

scholarly journals Hydrogen Sulfide Protects against Chronic Unpredictable Mild Stress-Induced Oxidative Stress in Hippocampus by Upregulation of BDNF-TrkB Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Min Hu ◽  
Wei Zou ◽  
Chun-Yan Wang ◽  
Xi Chen ◽  
Hui-Ying Tan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Hydrogen Sulfide ◽  
Protein Expression ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Inhibitory Role ◽  
Bdnf Signaling ◽  
Antioxidant Effects

Chronic unpredictable mild stress (CUMS) induces hippocampal oxidative stress. H2S functions as a neuroprotectant against oxidative stress in brain. We have previously shown the upregulatory effect of H2S on BDNF protein expression in the hippocampus of rats. Therefore, we hypothesized that H2S prevents CUMS-generated oxidative stress by upregulation of BDNF-TrkB pathway. We showed that NaHS (0.03 or 0.1 mmol/kg/day) ameliorates the level of hippocampal oxidative stress, including reduced levels of malondialdehyde (MDA) and 4-hydroxy-2-trans-nonenal (4-HNE), as well as increased level of glutathione (GSH) and activity of superoxide dismutase (SOD) in the hippocampus of CUMS-treated rats. We also found that H2S upregulated the level of BDNF and p-TrkB protein in the hippocampus of CUMS rats. Furthermore, inhibition of BDNF signaling by K252a, an inhibitor of the BDNF receptor TrkB, blocked the antioxidant effects of H2S on CUMS-induced hippocampal oxidative stress. These results reveal the inhibitory role of H2S in CUMS-induced hippocampal oxidative stress, which is through upregulation of BDNF/TrkB pathway.

scholarly journals The importance of leukotrienes in airway inflammation in a mouse model of asthma.

1996 ◽  
Vol 184 (4) ◽  
pp. 1483-1494 ◽  
Author(s):  
W R Henderson ◽  
D B Lewis ◽  
R K Albert ◽  
Y Zhang ◽  
W J Lamm ◽  
...  
Keyword(s):  
Mouse Model ◽  
Murine Model ◽  
Airway Hyperresponsiveness ◽  
Pulmonary Inflammation ◽  
Late Phase ◽  
Lavage Fluid ◽  
Bronchial Hyperreactivity ◽  
Leukocytic Infiltration ◽  
Specific Inhibitors

Inhalation of antigen in immunized mice induces an infiltration of eosinophils into the airways and increased bronchial hyperreactivity as are observed in human asthma. We employed a model of late-phase allergic pulmonary inflammation in mice to address the role of leukotrienes (LT) in mediating airway eosinophilia and hyperreactivity to methacholine. Allergen intranasal challenge in OVA-sensitized mice induced LTB4 and LTC4 release into the airspace, widespread mucus occlusion of the airways, leukocytic infiltration of the airway tissue and broncho-alveolar lavage fluid that was predominantly eosinophils, and bronchial hyperreactivity to methacholine. Specific inhibitors of 5-lipoxygenase and 5-lipoxygenase-activating protein (FLAP) blocked airway mucus release and infiltration by eosinophils indicating a key role for leukotrienes in these features of allergic pulmonary inflammation. The role of leukotrienes or eosinophils in mediating airway hyperresponsiveness to aeroallergen could not be established, however, in this murine model.

Complement halts angiogenesis gone wild

Blood ◽  
2010 ◽  
Vol 116 (22) ◽  
pp. 4393-4394 ◽  
Author(s):  
Walter H. A. Kahr
Keyword(s):  
Mouse Model ◽  
Complement System ◽  
Retinopathy Of Prematurity ◽  
Inhibitory Role ◽  
Culture Model ◽  
Matrigel Culture ◽  
The Complement System

In this issue of Blood, Langer and colleagues demonstrate the inhibitory role of the complement system during neovascularization, which is mediated by complement-stimulated macrophages in both a mouse model of retinopathy of prematurity and in a Matrigel culture model.1

The role of tachykinin 1 in a mouse model of trait anxiety

2007 ◽  
Vol 40 (05) ◽  
Author(s):  
L Czibere ◽  
LA Baur-Jaronowski ◽  
P Weber ◽  
B Pütz ◽  
M Panhuysen ◽  
...  
Keyword(s):  
Mouse Model ◽  
Trait Anxiety
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