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. 2017 Nov;14(5):5186-5192.
doi: 10.3892/etm.2017.5157. Epub 2017 Sep 21.

A novel effective chemical hemin for the treatment of acute carbon monoxide poisoning in mice

Hui-Min Li  1   2   3 , Ying-Lu Shi  3 , Di Wen  3 , Huan-Min Luo  1 , Xi Lin  1   4 , Fei Xiao  1   4
Affiliations

A novel effective chemical hemin for the treatment of acute carbon monoxide poisoning in mice

Hui-Min Li et al. Exp Ther Med. 2017 Nov.

Abstract

There is no effective drug for the therapy of acute carbon monoxide (CO) poisoning. The purpose of the present study was to investigate the potential preventive and therapeutic effects of hemin on an animal model of acute CO poisoning and to provide a potential therapeutic candidate drug. A total of 80 Kunming mice were randomly divided into four groups, namely the air control, acute CO poisoning, hemin-treatment + CO and hemin-pretreatment + CO groups (n=20 each). Furthermore, the mortality rate of mice, blood carboxyhaemoglobin (HbCO) concentration and serum malondialdehyde (MDA) concentration were measured, and pathological changes of the hippocampal area were determined using histochemical staining. The mice with acute CO poisoning had a 50% mortality rate at 1 h, with an increase in blood HbCO, serum MDA levels and pathological impairments of the hippocampus. Furthermore, the mortality rate, blood HbCO and serum MDA levels of mice with pretreatment and treatment of hemin were decreased. Additionally, the pathological changes of the hippocampal area were improved in the hemin-treatment and hemin-pretreatment groups compared with the mice treated with CO. These results suggest that hemin is a novel effective chemical for the prevention and treatment of acute CO poisoning in mice. Therefore, the present study provides a novel method and experimental basis for the application of hemin in treating patients with acute CO poisoning.

Keywords: acute carbon monoxide poisoning; animal model; carboxyhaemoglobin; hemin; oxidative stress.

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Figures

Figure 1.
Figure 1.
Effect of hemin on the survival rate of acute CO-poisoned mice. *P<0.05 and **P<0.01 vs. the CO poisoning group. CO, carbon monoxide.
Figure 2.
Figure 2.
HbCO level of mice 30 min after acute CO poisoning. **P<0.01 vs. the CO poisoning group. HbCO, carboxyhaemoglobin; CO, carbon monoxide.
Figure 3.
Figure 3.
Changes in serum MDA concentration of the caudal vein after intraperitoneal CO intoxication (nmol/ml). **P<0.01 vs. the CO poisoning group. Data shown are the mean ± standard error of three independent experiments. CO, carbon monoxide; MDA, malondialdehyde.
Figure 4.
Figure 4.
Representative morphological characteristics (hematoxylin and eosin staining) in the hippocampus of mice from (Aa) the control, (Ab) CO poisoning, (Ac) hemin treatment and (Ad) hemin pretreatment (magnification, ×40); and those from (Ba) the control, (Bb) CO poisoning, (Bc) hemin treatment and (Bd) hemin pretreatment, (magnification, ×400). The degeneration or disarrangement of cells is indicated by black arrows. CO, carbon monoxide.
Figure 5.
Figure 5.
Representative images of Nissl staining of the hippocampus in the mice. The effects of hemin on neurons in the hippocampus of mice from (Aa) the control, (Ab) CO poisoning, (Ac) hemin treatment and (Ad) hemin pretreatment, (magnification, ×40); and those from (Ba) control, (Bb) CO poisoning, (Bc) hemin treatment and (Bd) hemin pretreatment, (magnification, ×400). The degeneration or disarrangement of cells is indicated by the arrows. CO, carbon monoxide.
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