Protective effect and mechanism of hyperbaric oxygen on delayed encephalopathy after carbon monoxide poisoning via the mitochondrial pathway in mice
10.3760/cma.j.issn.1671-0282.2023.03.008
- VernacularTitle:高压氧通过线粒体途径对一氧化碳中毒迟发性脑病小鼠的保护作用及机制
- Author:
Jinfeng BAO
1
;
Boya HUANG
;
Rongxia NING
;
Xia YUN
;
Shijie GAO
;
Huiqiong JIA
;
Xiaohong HU
;
Zhe LI
;
Zhaoxiao CHEN
Author Information
1. 内蒙古医科大学基础医学院，呼和浩特 010100
- Keywords:
Carbon monoxide poisoning;
Delayed encephalopathy after carbon monoxide poisoning;
Hyperbaric oxygenation;
Mitochondria
- From:
Chinese Journal of Emergency Medicine
2023;32(3):319-326
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the protective effect and underlying mechanism of hyperbaric oxygen (HBO) on delayed encephalopathy after carbon monoxide poisoning (DEACMP) in mice.Methods:Totally 225 adult male Kunming mice were selected to establish CO poisoning model via intraperitoneal injection carbon monoxide (CO), and were randomly divided into the air control group, CO poisoning group, and HBO group. Each group was further divided into five time points group, that was 1, 3, 7, 14 and 21 d. The mice in the air control group were injected intraperitoneally with the same amount of air, and the HBO group received HBO treatment at the same time every day. DEACMP mice model was screened by behaviors using the open field test, new object recognition test and nesting test, and the content of myelin basic protein (MBP) were assayed. The mouse brain tissue and mitochondrial were prepared and malonialdehyde (MDA) and adenosine triphosphate (ATP) content were measured with ultraviolet spectrophotometer. MBP content in brain tissue and cytochrome C (CytC) content in the mitochondrial were measured by ELISA. The mitochondria membrane potential (MMP) was measured by flow cytometry.Results:Compared with the air control group, the content of carboxyhemoglobin (COHB) in blood increased significantly and the content of MBP in brain tissue decreased significantly in CO poisoning mice. CO poisoning mice showed motor ability and cognitive dysfunction. Compared with the air control group, the contents of MMP, CytC and ATP were significantly decreased ( P<0.01) in the CO poisoning group; while the MDA content was significantly increased ( P<0.01). Compared with the CO poisoning group, mice behaviors were improved significantly ( P<0.05), the content of MBP, MMP, CytC and ATP were increased ( P<0.05), while the MDA content decreased significantly ( P<0.01) in the HBO group. Conclusions:The abnormal mitochondrial function might be closely related to the occurrence and development of DEACMP, and HBO therapy plays an effective role in preventing and treating the DEACMP mice model via the mitochondrial pathway.
