Objective:s To investigate the risk factors for delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) in patients with acute carbon monoxide poisoning (ACOP) and to develop predictive models based on machine learning algorithms.Methods:Patients with ACOP hospitalized at the First Affiliated Hospital of Zhengzhou University from August 2019 to October 2024 were included, with the occurrence of DEACMP as the outcome measure. The dataset was randomly divided into training and validation sets at a ratio of 7:3. Lasso regression was used to select features influencing the outcome in training sets. Nine machine learning models—including Random Forest (RF), Extreme Gradient Boosting (XGBoost), and Support Vector Machine (SVM)—were constructed. Receiver operating characteristic (ROC) curves were plotted and the area under the curve (AUC) calculated for each model. Calibration curves were used to assess accuracy, and decision curve analysis (DCA) was applied to evaluate clinical utility. The SHapley Additive exPlanations (SHAP) method was employed to visualize and interpret the best-performing model.Results:A total of 264 ACOP patients were included, of whom 54 (20.5%) developed DEACMP. Lasso regression identified eight key feature variables. Based on these factors, predictive models were constructed, showing good AUC stability across the nine machine learning models in both training (0.92–0.99) and validation sets (0.85–0.91). The RF model performed best, with an AUC of 0.99 in the training set and 0.90 in the validation set; its calibration curve and DCA curve also demonstrated excellent performance. SHAP analysis of the RF model revealed the importance ranking of factors from highest to lowest as follows: Glasgow Coma Scale (GCS) score, duration of coma, age, history of coronary heart disease, CK-MB level, monocyte count, diastolic blood pressure (DBP), and drinking history.Conclusions:The RF model exhibited the highest predictive performance for DEACMP occurrence in ACOP patients. The influencing factors, ranked in order of importance from highest to lowest, are as follows: GCS score, duration of coma, age, history of coronary heart disease, CK-MB level, monocyte count, DBP, and drinking history.

AIM: To investigate the effect of gastrodin on the expression of brain-derived neurotrophic factor (BDNF) and interleukin-6 (IL-6) in the striatum of cerebral ischemia rats, and to explore the potential mechanism of gastrodin in treating cerebral ischemia. METHODS: The rats were randomly divided into four groups: normal, sham, model, and gastrodin groups, each consisting of 10 rats. After successful modeling using middle cerebral artery occlusion (MCAO), the gastrodin group received intraperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days. Pathological changes in striatal neurons were observed using Nissl staining. Immunohistochemistry was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum. Additionally, immunoblot analysis was performed to determine the expression levels of BDNF and IL-6 proteins in the striatum. RESULTS: Nissl staining revealed clear and intact structures of striatal neurons in the normal and sham groups, with tightly arranged cells. In the model group, the number of cells was significantly reduced compared to the sham group (P<0.01), and there was a noticeable cytosolic atrophy and loose cell arrangement. The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group (P<0.01), and there was also a significant improvement in cell morphology. The results of immunohistochemistry and immunoblot were consistent, and there was no statistically significant difference in BDNF and IL-6 protein expression between the normal group and the sham group (P>0.05). Compared to the sham group, the model group showed a decrease in the protein expression level of BDNF in the striatum on the ischemic side (P<0.01) and an increase in the protein expression level of IL-6 (P<0.05, P<0.01). In contrast, the gastrodin group showed an increase in the protein expression level of BDNF in the striatum on the ischemic side (P<0.05, P<0.01) and a decrease in the protein expression level of IL-6 (P< 0.05, P<0.01) compared to the model group. CONCLUSION: Gastrodin has a significant protective effect on striatal injury caused by cerebral ischemia, and its mechanism may be related to the up-regulation of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

Objective Mitochondrial reactive oxygen species(mtROS)could cause damage to pancreatic β-cells,rendering them susceptible to oxidative damage.Hence,investigating the potential of the mitochondria-targeted antioxidant(Mito-TEMPO)to protect pancreatic β-cells from ferroptosis by mitigating lipid peroxidation becomes crucial. Methods MIN6 cells were cultured in vitro with 100 μmol/L sodium palmitate(SP)to simulate diabetes.FerroOrange was utilized for the detection of Fe2+fluorescence staining,BODIPY581/591C11 for lipid reactive oxygen species,and MitoSox-Red for mtROS.Alterations in mitophagy levels were assessed through the co-localization of lysosomal and mitochondrial fluorescence.Western blotting was employed to quantify protein levels of Acsl4,GPX4,FSP1,FE,PINK1,Parkin,TOMM20,P62,and LC3.Subsequently,interventions were implemented using Mito-TEMPO and Carbonyl cyanide 3-chlorophenylhydrazone(CCCP)to observe changes in ferroptosis and mitophagy within MIN6 cells. Results We found that SP induced a dose-dependent increase in Fe2+and lipid ROS in MIN6 cells while decreasing the expression levels of GPX4 and FSP1 proteins.Through bioinformatics analysis,it has been uncovered that mitophagy assumes a crucial role within the ferroptosis pathway associated with diabetes.Additionally,SP decreased the expression of mitophagy-related proteins PINK1 and Parkin,leading to mtROS overproduction.Conversely,Mito-TEMPO effectively eliminated mtROS while activating the mitophagy pathways involving PINK1 and Parkin,thereby reducing the occurrence of ferroptosis in MIN6 cells.CCCP also demonstrated efficacy in reducing ferroptosis in MIN6 cells. Conclusion In summary,Mito-TEMPO proved effective in attenuating mtROS production and initiating mitophagy pathways mediated by PINK1 and Parkin in MIN6 cells.Consequently,this decreased iron overload and lipid peroxidation,ultimately safeguarding the cells from ferroptosis.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.