The time dependant protective effect of hyperbaric oxygen on neuronal cell apoptosis in carbon monoxide poisoning

2009 ◽  
Vol 189 ◽  
pp. S253
Author(s):  
Miran Brvar ◽  
Bostjan Luzar ◽  
Zarko Finderle ◽  
Dusan Suput ◽  
Matjaz Bunc
2010 ◽  
Vol 22 (12) ◽  
pp. 1026-1031 ◽  
Author(s):  
Miran Brvar ◽  
Boštjan Luzar ◽  
Žarko Finderle ◽  
Dušan Šuput ◽  
Matjaž Bunc

2021 ◽  
Vol 13 (7) ◽  
pp. 1383-1390
Author(s):  
Guangcong Li ◽  
Dan Li

ABSTRACTThis study aimed to explore the mechanism of perfluorooctylbromide (PFOB) nanoparticles (NPs) combined with ulinastatin (UTI) on early brain injury (EBI) caused by carbon monoxide poisoning (CMP). Firstly, PFOB NPs were prepared by high-speed dispersion and high-speed homogenization. The physicochemical characteristics of the particle size distribution and Zeta potential distribution of the NPs were analyzed using a laser particle size analyzer. The thermal and photoinduced phase transition characteristics of the NPs were analyzed under heating and laser irradiation conditions. Then, 50 Sprague Dawley (SD) rats were deemed as the research objects to establish the CMP rat models using hyperbaric oxygen chambers. According to different treatment methods, they were rolled into a healthy control group, a carbon monoxide (CO) model group, a PTOB treatment group, an UTI treatment group, and a PTOB + UTI treatment group. The brain tissues of each group of rats were collected 3 days after treatment. The neuronal cell apoptosis, expression of Caspase-3, messenger ribonucleic acid (mRNA) of inflammatory factors interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in rat brain tissue were detected through immunohistochemical staining, in situ cell apoptosis detection, Reverse transcription-polymerase chain reaction (RT-PCR), and Western blotting, so did the relative expression of target proteins B-cell lymphoma-2 (Bcl-2), Bcl2-Associated X (Bax) and myelin basic protein (MBP). As a result, the average particle size and the average Zeta potential of the prepared PFOB NPs was 103±31 nm and −23 ± 15 mV, respectively. When the PFOB NPs were heated to 80 °C, the particle size increased greatly and cracks appeared. The particle size of PFOB NPs also increased obviously after laser irradiation, and the PFOB inside the particles changed into gas phase. Compared to CO group, expression of Caspase-3, neuronal cell apoptosis rate, mRNA expression of IL-1β and TNF-α, and protein expression of Bax and Bcl-2 in the brain tissue of PTOB group, UTI group, and PFOB + UTI group were notably decreased (P < 0.05), while the MBP protein expression increased considerably (P < 0.05). Changes in PFOB + UTI group were more obvious than those in PTOB group and UTI group, and those indicators weren’t considerably different from the controls. In summary, PFOB NPs were successfully prepared with favorable phase transition characteristics. Moreover, PFOB NPs combined with UTI could reduce the apoptosis of brain neurons after CMP, improve the inflammatory response, and play a protective effect on EBI of CMP.


2018 ◽  
Vol 45 (1) ◽  
pp. 83-87 ◽  
Author(s):  
Lon W. Keim ◽  
◽  
Sreekanth Koneru ◽  
Vesper Fe Marie Ramos ◽  
Najib Murr ◽  
...  

2020 ◽  
pp. 607-619
Author(s):  
Ya’nan Qi ◽  
◽  
Zhibao Guo ◽  
Huijun Hu ◽  
Xiang’en Meng ◽  
...  

Neuroinflammation plays an important role in brain damage after acute carbon monoxide poisoning (ACOP). The nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing (NLRP) 3 inflammasome triggers the activation of inflammatory caspases and maturation of interleukin (IL)-1β and -18, and has been linked to various human autoinflammatory and autoimmune diseases. In this study we investigated the effects of hyperbaric oxygen (HBO2) on NLRP3 inflammasome activation after ACOP. Mice were randomly divided into four groups: sham group (exposure to normobaric air – i.e., 21% O2 at 1 atmosphere absolute); HBO2-only group; CO + normobaric air group; and CO + HBO2 group. Cognitive function was evaluated with the Morris water maze; myelin injury was assessed by Fluoro-Myelin GreenTM fluorescent myelin staining and myelin basic protein (MBP) immunostaining; and mRNA and protein levels of NLRP3 inflammasome complex proteins were measured by quantitative real-time PCR and Western blot, respectively. Additionally, serum and brain levels of IL-1β and -18 and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase were determined by enzyme-linked immunosorbent assay. It was found that HBO2 improved learning and memory, and alleviated myelin injury in mice subjected to acute CO exposure. Furthermore, HBO2 decreased NLRP3, absent in melanoma 2 (AIM2), caspase-1, and apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain mRNA and protein levels, and reduced brain and serum concentrations of IL-1β and -18 and NADPH oxidase. These results indicate that HBO2 suppresses the inflammatory response after ACOP by blocking NLRP3 inflammasome activation, thereby alleviating cognitive deficits.


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