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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.
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Objective To detect the expressions of two protein factors hypoxia-inducible factor (HIF)-1α and Helicobacter pylori (Hp) in gastric cancer in Mongolian and Han two nationalities respectively,and to explore the relationship of HIF-1α and Hp in the development of gastric cancer.Methods A modified Warthin-Starry (W-S) silver staining method was used to detect Hp infection in 27 Mongolian patients with gastric cancer and 30 Han patients with gastric cancer.Immunohistochemical (S-P) method and reverse transcription polymerase chain reaction (RT-PCR) method were used to detect protein and mRNA expressions of HIF-1α in cancer tissue,paracancerous tissue and normal tissue samples.The relationship of HIF-1α protein and Hp expression was analyzed between gastric carcinoma tissue samples of Mongolian patient group and Han patient group.Results Hp infection rates were 81.5％ (22/27) and 66.7％ (20/30) in Mongolian and Han patients with gastric cancer.The difference in infection rate was not statistically significant between two groups of patients (~=1.608,P ＞ 0.05).The positive expression levels of HIF-1α protein were 62.96％ (17/27) and 70.00％ (21/30) in gastric cancer tissue samples of Mongolian and Han groups.The relative expression levels of HIF-1α mRNA were 0.891 4±0.075 0 and 0.907 4±0.065 5.There was no significant difference in the HIF-1 α mRNA expression between the two nationalities.No positive expressions of HIF-1α protein and mRNA were found in paracancerous tissue and normal tissue samples.There was a positive correlation in the positive expression of HIF-1α protein and Hp infection in gastric cancer tissue samples of Mongolian and Han patient groups (r,=0.424 and 0.617,P ＜ 0.05).Conclusion HIF-1α and Hp are pathogenic factors of gastric cancer.Hp and HIF-1α may promote the occurrence of gastric cancer together.The pathogenic mechanism of HIF-1α and Hp in gastric cancer may be the same for Mongolian and Han patients.