OBJECTIVES: The neurotoxicity of carbon monoxide (CO) to the central nervous system is a key pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Our previous study found that retinoic acid (RA) can suppress the neurotoxic effects of CO. This study further explores, in vivo and in vitro, the molecular mechanisms by which RA alleviates CO-induced central nervous system damage. METHODS: A cytotoxic model was established using the mouse hippocampal neuronal cell line HT22 and primary oligodendrocytes exposed to CO, and a DEACMP animal model was established in adult Kunming mice. Cell viability and apoptosis of hippocampal neurons and oligodendrocytes were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Annexin V/propidium iodide (PI) double staining. The transcriptional and protein expression of each gene was detected using real-time fluorescence quantitative PCR (RT-qPCR) and Western blotting. Long noncoding RNA (lncRNA) SNHG15 and LINGO-1 were knocked down or overexpressed to observe changes in neurons and oligodendrocytes. In DEACMP mice, SNHG15 or LINGO-1 were knocked down to assess changes in central nervous tissue and downstream protein expression. RESULTS: RA at 10 and 20 μmol/L significantly reversed CO-induced apoptosis of hippocampal neurons and oligodendrocytes, downregulation of SNHG15 and LINGO-1, and upregulation of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB) (all P<0.05). Overexpression of SNHG15 or LINGO-1 weakened the protective effect of RA against CO-induced cytotoxicity (all P<0.05). Knockdown of SNHG15 or LINGO-1 alleviated CO-induced apoptosis of hippocampal neurons and oligodendrocytes and upregulated BDNF and TrkB expression levels (all P<0.05). Experiments in DEACMP model mice showed that knockdown of SNHG15 or LINGO-1 mitigated central nervous system injury in DEACMP (all P<0.05). CONCLUSIONS RA alleviates CO-induced apoptosis of hippocampal neurons and oligodendrocytes, thereby reducing central nervous system injury and exerting neuroprotective effects. LncRNA SNHG15 and LINGO-1 are key molecules mediating RA-induced inhibition of neuronal apoptosis and are associated with the BDNF/TrkB pathway. These findings provide a theoretical framework for optimizing the clinical treatment of DEACMP and lay an experimental foundation for elucidating its molecular mechanisms.
Animals ; RNA, Long Noncoding/physiology* ; Brain-Derived Neurotrophic Factor/genetics* ; Carbon Monoxide Poisoning/complications* ; Mice ; Tretinoin/pharmacology* ; Nerve Tissue Proteins/metabolism* ; Membrane Proteins/metabolism* ; Apoptosis/drug effects* ; Hippocampus/cytology* ; Receptor, trkB/metabolism* ; Neurons/drug effects* ; Male ; Brain Diseases/etiology* ; Oligodendroglia/drug effects* ; Signal Transduction ; Cell Line

Acute carbon monoxide poisoning (ACMP) is one of the most common gas poisonings in the emergency department, with tens of thousands of people seeking medical attention for carbon monoxide (CO) poisoning each year. The severity of poisoning is dependent upon environmental and human factors, with hypoxia and oxidative stress being important mechanisms of cardiac toxicity induced by CO. Myocardial involvement is common in moderate to severe ACMP, including myocardial injury, myocardial infarction, arrhythmia, and sudden death, which are associated with a high risk of death. Ferroptosis is a cell death mechanism caused by iron-dependent lipid peroxidation (LPO), although ferroptosis has been shown to play a critical role in various cardiovascular diseases, the potential mechanism by which it contributes to ACMP-induced myocardial injury is unclear. This review discusses the established link between ferroptosis and cardiovascular disease and summarizes the potential role of ferroptosis in ACMP-induced myocardial injury and the detrimental effects of ACMP on the heart. Elucidating these mechanisms could guide the development of novel therapeutic strategies that target ferroptosis to mitigate ACMP-induced myocardial injury. This review aims to provide a theoretical foundation for future research on the potential use of ferroptosis as a therapeutic target for ACMP-induced myocardial injury.
Humans ; Carbon Monoxide Poisoning/complications* ; Ferroptosis ; Lipid Peroxidation ; Myocardium/pathology* ; Oxidative Stress

OBJECTIVETo compare the efficacy differences on delayed encephalopathy after carbon monoxide poisoning (DEACMP) between acupuncture to restore consciousness combined with hyperbaric oxygen treatment and simple hyperbaric oxygen treatment.

METHODSForty-one patients with DEACMP were randomly divided into an observation group (21 cases) and a control group (20 cases). In the observation group, acupuncture was applied at Neiguan (PC 6), Shuigou (GV 26), Baihui (GV 20), Sishencong (EX-HN 1), Fengchi (GB 20), Hegu (LI 4), Sanyinjiao (SP 6) and Taichong (LR 3), and hyperbaric oxygen treatment was given as well. In the control group, simple hyperbaric oxygen treatment was used. The treatment was adopted once every day, and continuous 5 days' treatment made one session in the two groups. There were two days at the interval between two sessions and 6 sessions in the two groups. The changes of scores of mini mental state examination (MMSE) and Barthel index (BI) for activity of daily life and routine electroencephalogram (EEG) before and after treatment were compared.

RESULTSAfter treatment, the scores of MMSE and BI and EEG were all improved compared with those before treatment (all P<0.01). The raise of the scores of MMSE and BI in the observation group was more obvious than that in the control group (both P<0.05) and the improvement of EEG abnormal condition in the observation group was also superior to that in the control group after treatment (P<0.05).

CONCLUSIONAcupuncture to restore consciousness combined with hyperbaric oxygen could obviously improve the cognitive function, activity of daily life and changes of EEG, and it is better than simple hyperbaric oxygen treatment.

Acupuncture Points ; Acupuncture Therapy ; Adult ; Aged ; Aged, 80 and over ; Brain Diseases ; etiology ; psychology ; therapy ; Carbon Monoxide Poisoning ; complications ; Combined Modality Therapy ; Consciousness ; Female ; Humans ; Hyperbaric Oxygenation ; Male ; Middle Aged ; Treatment Outcome ; Young Adult

OBJECTIVETo explore the diagnostic value of magnetic resonance (MR) diffusion tensor imaging (DTI) in detecting brain white matter (WM) damage of patients with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) and evaluating their cognitive dysfunction.

METHODSThirteen patients with DEACMP and thirteen age- and sex-matched volunteers underwent DTI using 1.5T MR scanner. FA and ADC values of 16 WM regions of interests (ROIs) were measured on DTI by two experienced radiologists independently with double blind methods, cognitive functions were evaluated by another experienced neurologist blinded to patient's medical history using the Montreal cognitive assessment (MoCA). ADC and FA values in DEACMP patients, and their correlations with cognitive dysfunction were analyzed.

RESULTSADC values of DEACMP patients increased significantly in all ROIs (P < 0.05) in comparison with the corresponding ROIs of healthy controls, whereas FA values were significantly decreased in all ROIs (P < 0.05) in comparison with that in controls except the bilateral optic radiations, anterior and posterior internal capsules. MoCA scores were positively correlated with FA values of bilateral lower frontal (r(L) = 0.736, P = 0.011; r(R) = 0.762, P = 0.003) lobe, temporal lobe (r(L) = 0.605, P = 0.016; r(R) = 0.559, P = 0.021) and total average WM (r(A) = 0.688, P = 0.001), however it inversely correlated with ADC values of bilateral lower frontal WM (r(L) = -0.674, P = 0.007; r(R) = -0.681, P = 0.019).

CONCLUSIONDTI can quantitatively reveal WM microstructure damage of DEACMP patients, indicate the severity of cognitive dysfunctions, and provide important information for pathogenesis and pathological study for DEACMP.

Brain ; pathology ; Brain Diseases ; diagnosis ; etiology ; Carbon Monoxide Poisoning ; complications ; Cognition ; Cognition Disorders ; Diffusion Magnetic Resonance Imaging ; Diffusion Tensor Imaging ; Double-Blind Method ; Humans ; White Matter ; pathology

Brain Diseases ; etiology ; Carbon Monoxide Poisoning ; complications ; Humans ; Pulmonary Embolism ; complications

OBJECTIVETo investigate the changes in serum level of high mobility group protein B1 (HMGB1) in patients with delayed encephalopathy after acute carbon monoxide poisoning and the clinical significance of these changes.

METHODSThirty-four patients with delayed encephalopathy after acute carbon monoxide poisoning (delayed encephalopathy group), 30 normal controls (control group), and 32 cases of acute carbon monoxide poisoning without delayed encephalopathy (carbon monoxide poisoning group) were recruited in this study. The serum HMGB1 level was determined by enzyme-linked immunosorbent assay. The correlation between serum HMGB1 level and scores of the activity of daily living scale (ADL), Information-Memory-Concentration Test (IMCT), and Hasegawa dementia scale (HDS) was determined.

RESULTSIn the acute stage of carbon monoxide poisoning, the serum HMGB1 level of delayed encephalopathy group was significantly higher than those of the carbon monoxide poisoning group and the control group (P < 0.01). In the delayed encephalopathy group, serum HMGB1 level in the convalescent stage was significantly lower than that in the acute stage (P < 0.05); ADL score was higher and HDS and IMCT scores were lower in the acute stage than in the convalescent stage (P < 0.01). In the delayed encephalopathy group, serum HMGB1 level was positively correlated with HDS and ADL scores in both acute stage and convalescent stage (correlation coefficients: 0.612, 0.607, 0.609, and 0.612, P < 0.01).

CONCLUSIONHMGB1, as an important late mediator of inflammation, is involved in the inflammatory reaction in delayed encephalopathy, and is positively correlated with HDS and ADL scores, indicating that it can be used as one of the major indicators in monitoring carbon monoxide poisoning.

Adult ; Aged ; Aged, 80 and over ; Brain Diseases ; blood ; etiology ; Carbon Monoxide Poisoning ; blood ; complications ; Female ; HMGB1 Protein ; blood ; Humans ; Male ; Middle Aged

OBJECTIVETo study the MRI-based characteristics of acute carbon monoxide poisoning (ACOP) and delayed encephalopathy after acute carbon monoxide poisoning (DECAMP), and to compare the degree of brain damage.

METHODSA retrospective analysis was performed on the clinical and MRI data of 27 patients diagnosed with ACOP and 35 patients diagnosed with DECAMP. Ten healthy volunteers were recruited in the normal control group. All subjects received both routine MRI and diffusion-weighted MRI. Apparent diffusion coefficient (ADC) was determined with symmetric measurement of region of interest in the bilateral globus pallidus, white matter around lateral ventricle, and centrum semiovale. ADC values were compared afterwards.

RESULTSThirteen of the 27 ACOP cases were found of symmetrical abnormal signal in the bilateral globus pallidus, among whom 8 patients only showed pallidum region involvement, while the other 5 patients showed involvement of other regions. Eight ACOP patients showed cortical and subcortical white matter involvement, and 4 cases showed diffused abnormal signal around the bilateral ventricles and in the bilateral centrum semiovale. Two cases of ACOP presented with multiple region involvement. Thirty-five DECAMP patients showed diffused swelling and symmetric demyelination in multiple regions of the brain parenchyma. The periventricular white matter and centrum semiovale were involved in 33 cases, the deep brain nuclei were involved in 23 cases, and the cerebral cortex was involved in 3 cases. The ACOP and DECAMP groups had significantly lower ADC values in the periventricular white matter and bilateral centrum semiovale than the normal control group (P < 0.05), and the ADC values were significantly lower in the DECAMP group than in the ACOP group (P < 0.05). The ACOP group had a significantly lower ADC value in the globus pallidus than the DECAMP group and normal control group (P < 0.05); the DECAMP group had a significantly higher ADC value in the globus pallidus than the ACOP group and normal control group (P < 0.05).

CONCLUSIONRoutine MRI and ADC value can evaluate the degree of brain damage in ACOP and DECAMP patients based on lesion involvement on a more microscopic scale. It can provide valuable information for therapy selection and prognostic evaluation.

Adult ; Aged ; Brain Diseases ; chemically induced ; diagnosis ; Carbon Monoxide Poisoning ; complications ; diagnosis ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Retrospective Studies ; Young Adult

A 59-year-old man with a history of major depression was found by his wife to be unconscious and foaming at the mouth. On arrival at the emergency department, the patient was noted to be unresponsive. Computed tomography of the brain showed symmetrical ill-defined areas of hypoattenuation involving the medial aspects of both lentiform nuclei, while magnetic resonance images of the brain showed symmetrical increased signal in the bilateral globi pallidi on diffusion weighted, T2-weighted and fluid attenuated inversion recovery sequences. These findings were those of acute carbon monoxide poisoning. Despite aggressive treatment, the patient's condition continued to deteriorate and he eventually passed away. The various imaging findings of carbon monoxide poisoning in the brain and the differential diagnoses are discussed.
Brain ; diagnostic imaging ; Carbon Monoxide Poisoning ; diagnosis ; diagnostic imaging ; Depressive Disorder, Major ; complications ; Diagnostic Imaging ; Fatal Outcome ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Pulmonary Edema ; pathology ; Radiography, Thoracic ; Suicide, Attempted ; Tomography, X-Ray Computed

OBJECTIVEBy explore the role of serum soluble Fas (sFas) in occurrence and progression of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP).

METHODSEnzyme-linked immunosorbent assay (ELISA) was used to detect serum sFas levels in 40 patients with DEACMP in acute stage and convalescent stage, with 36 healthy elderly subjects as the control group.

RESULTSSerum sFas levels of the patients with DEACMP in both the acute and convalescent stages showed no significant difference from those in the control group (P=0.737 and 0.137, respectively), nor was any significant difference found between the patients in acute and exacerbation stages (P=0.059).

CONCLUSIONSerum sFas is not involved in the occurrence and progression of DEACMP.

Adult ; Aged ; Aged, 80 and over ; Brain Diseases ; etiology ; Carbon Monoxide Poisoning ; blood ; complications ; Case-Control Studies ; Female ; Humans ; Male ; Middle Aged ; fas Receptor ; blood

Adult ; Carbon Monoxide Poisoning ; complications ; psychology ; Humans ; Male ; Middle Aged ; Nervous System Diseases ; chemically induced ; diagnosis ; physiopathology ; Suicide, Attempted ; psychology