Objective To establish and evaluate a mouse model of chronic obstructive pulmonary disease(COPD)induced by cigarette smoke(CS).Methods Forty BALB/c mice were divided randomly into a control group and a CS group.Mice in the CS group were subjected to passive smoking for 20 weeks and a COPD model was established.Morphological changes in the organs and lung,heart,liver,and kidney fibrosis were observed by hematoxylin-eosin(HE)and Masson staining.Lung,cardiac,and brain cognitive function were evaluated by pulmonary function testing,small-animal ultrasound,and Morris water maze trials.Tumor necrosis factor-α(TNF-α),interleukin(IL)-6 and IL-1β levels in lung and brain tissues were detected by ELISA.Liver and renal functions were measured by biochemical method.Results The alveolar septum was narrowed or broken in mice in the CS group,and the adjacent alveolar cavity was enlarged and fused,consistent with the pathological changes of COPD.Neuronal degeneration and necrosis were observed in the hippocampus,but there were no significant morphological changes in other organs.Masson staining showed no obvious fibrosis in the lung,heart,liver,or kidney in CS-group mice.The result of pulmonary function tests showed that the forced expiratory volume in 0.1 second/forced vital capacity(FEV 0.1/FVC)and dynamic compliance were significantly decreased in the CS group compared with the control group,while airway resistance was obviously increased.Cognitive impairment in mice in the CS group was confirmed in the Morris water maze trial.TNF-α,IL-6,and IL-1β levels in lung and brain tissues were higher in the CS group compared with the control group.There were no significant differences in cardiac,liver,and renal functions between the groups.Conclusions A mouse model of COPD can be established by CS exposure for 20 weeks.Lung histomorphology,lung function,brain cognitive function,and levels of inflammatory factors can be used as indicators to evaluate the success of the model.

ObjectiveTo investigate the antidepressant effects and mechanisms of total flavonoids from Cuscutae Semen （TFCC） in the mouse model of chronic unpredictable mild stress （CUMS）. MethodsFifty male 4-week-old ICR mice were randomized into five groups （n=10 per group）： blank control， model， Cuscutae Semen decoction （10.2 g·kg^-1·d^-1）， paroxetine （2.6 mg·kg^-1·d^-1）， and TFCC （173.2 mg·kg^-1·d^-1）. The other groups except the blank control group underwent chronic unpredictable mild stress （CUMS） for 4 weeks. Behavioral assessments were conducted post-modeling. Then， the model group received distilled water （10 mL·kg^-1·d^-1）， while treatment groups were administrated with respective agents via oral gavage （10 mL·kg^-1） for 4 weeks. Depression-like behaviors were evaluated by the sucrose preference test （SPT）， forced swimming test （FST）， and tail suspension test （TST）. Hippocampal neuronal morphology was observed via hematoxylin-eosin staining， and apoptosis in the brain tissue was assessed via terminal- deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling （TUNEL）. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the hippocampal levels of inflammatory cytokines ［interleukin （IL）-1β， IL-6， and TNF-α）］ and neurotransmitters ［5-hydroxytryptamine （5-HT）， dopamine （DA）， and brain-derived neurotrophic factor （BDNF）］， while the reactive oxygen species （ROS） levels were quantified via the DCFH-DA probe. Real-time PCR was performed to measure the mRNA levels of NOD-like receptor protein 3 （NLRP3）， apoptosis-associated Speck-like protein containing a CARD （ASC）， cysteinyl aspartate-specific proteinase-1 （Caspase-1）， IL-1β， and inducible nitric oxide synthase （iNOS）. Western blot was employed to evaluate the protein levels of NLRP3， ASC， Caspase-1， uncoupling protein 2 （UCP2）， and thioredoxin-interacting protein （TXNIP）. ResultsCompared with the blank control group， the model group exhibited weight loss （P<0.01）， reduced sucrose preference （P<0.01）， prolonged immobility time in FST and TST （P<0.01）， neuron disarrangement with nuclear pyknosis in hippocampal CA3 region， increased apoptosis in the brain tissue， elevated levels of IL-1β， IL-6， and TNF-α （P<0.01）， declined levels of 5-HT， DA， and BDNF （P<0.01）， increased ROS accumulation （P<0.01）， upregulated mRNA levels of NLRP3， ASC， Caspase-1， IL-1β， and iNOS （P<0.01）， down-regulated protein level of UCP2 （P<0.01）， and up-regulated protein levels of NLRP3， ASC， Caspase-1， and TXNIP （P<0.01）. Compared with the model group， the interventions restored sucrose preference （P<0.01）， shortened immobility time （P<0.01）， repaired hippocampal neuronal structure， reduced apoptosis， lowered the levels of inflammatory cytokines （P<0.01）， restored the levels of neurotransmitters （P<0.01）， alleviated ROS accumulation （P<0.01）， downregulated the mRNA levels of NLRP3， ASC， Caspase-1， IL-1β， and iNOS （P<0.01）， upregulated the protein level of UCP2 （P<0.01）， and reduced the protein levels of NLRP3， ASC， Caspase-1， and TXNIP （P<0.01）. Moreover， TFCC outperformed Cuscutae Semen decoction in ameliorating depressive behaviors. TFCC excelled in neuronal repair， neurotransmitter regulation， anti-inflammatory effects， and modulation of the UCP2/TXNIP/NLRP3 pathway （P<0.05）. ConclusionTFCC modulates the hippocampal UCP2/TXNIP/NLRP3 pathway to inhibit inflammasome activation， reduce oxidative stress， restore neurotransmitters， thus suppressing neuronal apoptosis and promoting the rearrangement and morphology recovery of hippocampal cells. It outperforms Cuscutae Semen decoction in the antidepressant efficacy.

ObjectiveTo investigate the antidepressant effects and mechanisms of total flavonoids from Cuscutae Semen （TFCC） in the mouse model of chronic unpredictable mild stress （CUMS）. MethodsFifty male 4-week-old ICR mice were randomized into five groups （n=10 per group）： blank control， model， Cuscutae Semen decoction （10.2 g·kg^-1·d^-1）， paroxetine （2.6 mg·kg^-1·d^-1）， and TFCC （173.2 mg·kg^-1·d^-1）. The other groups except the blank control group underwent chronic unpredictable mild stress （CUMS） for 4 weeks. Behavioral assessments were conducted post-modeling. Then， the model group received distilled water （10 mL·kg^-1·d^-1）， while treatment groups were administrated with respective agents via oral gavage （10 mL·kg^-1） for 4 weeks. Depression-like behaviors were evaluated by the sucrose preference test （SPT）， forced swimming test （FST）， and tail suspension test （TST）. Hippocampal neuronal morphology was observed via hematoxylin-eosin staining， and apoptosis in the brain tissue was assessed via terminal- deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling （TUNEL）. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the hippocampal levels of inflammatory cytokines ［interleukin （IL）-1β， IL-6， and TNF-α）］ and neurotransmitters ［5-hydroxytryptamine （5-HT）， dopamine （DA）， and brain-derived neurotrophic factor （BDNF）］， while the reactive oxygen species （ROS） levels were quantified via the DCFH-DA probe. Real-time PCR was performed to measure the mRNA levels of NOD-like receptor protein 3 （NLRP3）， apoptosis-associated Speck-like protein containing a CARD （ASC）， cysteinyl aspartate-specific proteinase-1 （Caspase-1）， IL-1β， and inducible nitric oxide synthase （iNOS）. Western blot was employed to evaluate the protein levels of NLRP3， ASC， Caspase-1， uncoupling protein 2 （UCP2）， and thioredoxin-interacting protein （TXNIP）. ResultsCompared with the blank control group， the model group exhibited weight loss （P<0.01）， reduced sucrose preference （P<0.01）， prolonged immobility time in FST and TST （P<0.01）， neuron disarrangement with nuclear pyknosis in hippocampal CA3 region， increased apoptosis in the brain tissue， elevated levels of IL-1β， IL-6， and TNF-α （P<0.01）， declined levels of 5-HT， DA， and BDNF （P<0.01）， increased ROS accumulation （P<0.01）， upregulated mRNA levels of NLRP3， ASC， Caspase-1， IL-1β， and iNOS （P<0.01）， down-regulated protein level of UCP2 （P<0.01）， and up-regulated protein levels of NLRP3， ASC， Caspase-1， and TXNIP （P<0.01）. Compared with the model group， the interventions restored sucrose preference （P<0.01）， shortened immobility time （P<0.01）， repaired hippocampal neuronal structure， reduced apoptosis， lowered the levels of inflammatory cytokines （P<0.01）， restored the levels of neurotransmitters （P<0.01）， alleviated ROS accumulation （P<0.01）， downregulated the mRNA levels of NLRP3， ASC， Caspase-1， IL-1β， and iNOS （P<0.01）， upregulated the protein level of UCP2 （P<0.01）， and reduced the protein levels of NLRP3， ASC， Caspase-1， and TXNIP （P<0.01）. Moreover， TFCC outperformed Cuscutae Semen decoction in ameliorating depressive behaviors. TFCC excelled in neuronal repair， neurotransmitter regulation， anti-inflammatory effects， and modulation of the UCP2/TXNIP/NLRP3 pathway （P<0.05）. ConclusionTFCC modulates the hippocampal UCP2/TXNIP/NLRP3 pathway to inhibit inflammasome activation， reduce oxidative stress， restore neurotransmitters， thus suppressing neuronal apoptosis and promoting the rearrangement and morphology recovery of hippocampal cells. It outperforms Cuscutae Semen decoction in the antidepressant efficacy.

Objective:To investigate the key technical aspects of laparoscopic anti-reflux surgery (LARS) in complex gastroesophageal reflux disease (GERD) with hiatal hernia (HH) and evaluate the feasibility and efficacy of reoperation.Methods:A retrospective analysis was conducted on 28 patients with complex GERD treated at Zhejiang Provincial People's Hospital from Feb 2020 to May 2024. Preoperative examinations were recorded, and surgical videos were reviewed to reconstruct operative time, critical intraoperative steps, complications, and management techniques. Postoperative follow-up via telephone and outpatient visits assessed symptom relief, complications, and medication use.Results:All 28 patients (4 robotic-assisted and 24 conventional laparoscopic surgeries) successfully underwent LARS, with an operative duration of (152.6±10.3) minutes and a postoperative hospital stay of (4.0±1.9) days. Large HH 9 cases, intraoperative bleeding 6 cases, pleural rupture 3 case, and esophageal perforation 1 case, preoperative diagnoses included short esophagus 2 cases and 7 redo surgeries. The overall recurrence rate was 11%. Postoperative complications occurred in 14%. The redo surgeries group achieved 71% symptom resolution. At 1-12 months of follow-up, 82% of patients were asymptomatic, and 82% discontinued proton pump inhibitor therapy.Conclusions:Complex scenarios requiring specialized techniques in LARS increase surgical difficulty and risks. Standardized management of the hernia sac, hiatal repair, neurovascular protection, identification of anatomical landmarks in reoperations, selection of biological mesh, and adhesiolysis may reduce recurrence rates and complication risks.

Objective:To investigate the effects of budesonide/formoterol versus budesonide on lung volume and serum miR-146 and interleukin-4 levels in patients with bronchiectasis and asthma. Methods:This study adopted a prospective design. A total of 102 patients with bronchiectasis and asthma who received treatment at the People's Hospital of Tongchuan from October 2021 to August 2024 were included. The patients were randomly divided into a conventional group and an observation group using an envelope method ( n = 51 per group). The conventional group received budesonide inhalation treatment, while the observation group was given budesonide/formoterol inhalation powder. All patients were treated for 15 days. The lung function, lung volume, miR-146 mRNA, interleukin-4 (IL-4), interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and eosinophil percentage (EOS%) levels of both groups were measured before and after treatment, and the incidence of adverse reactions in the two groups was statistically analyzed. Results:Before treatment, there was no statistically significant difference in lung function and lung volume between the two groups (both P > 0.05). After treatment, the forced vital capacity (FVC), peak expiratory flow (PEF), and forced expiratory volume in the first second (FEV 1) /FVC of both groups were significantly higher than those before treatment ( t = 2.54, 16.22, 9.67, 5.75, 29.25, and 16.91, all P < 0.05). Residual volume (RV) and the ratio of RV to total lung capacity (TLC) were significantly lower in both groups after treatment compared with before treatment ( t = 2.24, -2.98, -3.51, -6.79, all P < 0.05). There was no statistically significant difference in TLC in both groups between before and after treatment ( P > 0.05). The observation group had significantly higher FVC [(2.96 ± 0.65) L], PEF [(75.96 ± 6.54) mL/s], and FEV 1/FVC (85.45 ± 6.03) than the conventional group [(2.57 ± 0.61) L, (67.85 ± 6.06) mL/s, (70.86 ± 5.16), t = -3.12, -6.50, -13.13, all P < 0.05]. After treatment, the RV [(2.81 ± 0.32) L] and RV/TLC [(49.13 ± 3.94)] in the observation group were significantly lower than those in the conventional group [(2.95 ± 0.37) L, (52.03 ± 4.16), t = 2.04, 3.62, both P < 0.05]. The difference in TLC between the two groups was not statistically significant ( P > 0.05). Before treatment, there was also no statistically significant difference in miR-146 mRNA levels between the two groups ( P > 0.05). After treatment, miR-146a and miR-146b mRNA levels in both groups were significantly lower compared to their levels before treatment ( t = -9.21, -4.14, -11.02, -7.58, all P < 0.05). In the observation group, the levels of miR-146a mRNA [(1.41 ± 0.26)] and miR-146b mRNA [(1.15 ± 0.26)] after treatment were significantly lower than those in the conventional group [(1.66 ± 0.34), (1.32 ± 0.34), t = 4.17, 2.84, both P < 0.05]. Before treatment, there were no statistically significant differences in IL-4, IFN-γ, TNF-α, and EOS% between the two groups (all P > 0.05). After treatment, IL-4, IFN-γ, TNF-α, and EOS% levels were significantly lower in both groups compared with before treatment ( t = -6.13, -2.56, -18.57, -23.67, -11.20, -3.83, -20.56, -30.00, all P < 0.05). In the observation group, IL-4 [(234.51 ± 34.03) ng/L], IFN-γ [(214.41 ± 31.54) ng/L], TNF-α [(23.65 ± 10.47) ng/L], and EOS% (2.03 ± 0.33) were significantly lower than those in the conventional group [(265.63 ± 37.51) ng/L], (230.12 ± 36.95) ng/L, (39.69 ± 13.41) ng/L, (2.57 ± 0.51), t = 0.49, 12.39, 6.73, 6.35, all P < 0.05]. There was no significant difference in the incidence of adverse reactions between the observation and conventional groups [13.73% (7/51) vs. 7.84% (4/51), χ2 = 0.92, P > 0.05]. Conclusions:Both budesonide/formoterol and budesonide alone can improve lung function and lung volume in patients with bronchiectasis and asthma while reducing levels of miR-146 and IL-4. However, budesonide/formoterol shows superior efficacy.

Objective To establish and evaluate a mouse model of chronic obstructive pulmonary disease(COPD)induced by cigarette smoke(CS).Methods Forty BALB/c mice were divided randomly into a control group and a CS group.Mice in the CS group were subjected to passive smoking for 20 weeks and a COPD model was established.Morphological changes in the organs and lung,heart,liver,and kidney fibrosis were observed by hematoxylin-eosin(HE)and Masson staining.Lung,cardiac,and brain cognitive function were evaluated by pulmonary function testing,small-animal ultrasound,and Morris water maze trials.Tumor necrosis factor-α(TNF-α),interleukin(IL)-6 and IL-1β levels in lung and brain tissues were detected by ELISA.Liver and renal functions were measured by biochemical method.Results The alveolar septum was narrowed or broken in mice in the CS group,and the adjacent alveolar cavity was enlarged and fused,consistent with the pathological changes of COPD.Neuronal degeneration and necrosis were observed in the hippocampus,but there were no significant morphological changes in other organs.Masson staining showed no obvious fibrosis in the lung,heart,liver,or kidney in CS-group mice.The result of pulmonary function tests showed that the forced expiratory volume in 0.1 second/forced vital capacity(FEV 0.1/FVC)and dynamic compliance were significantly decreased in the CS group compared with the control group,while airway resistance was obviously increased.Cognitive impairment in mice in the CS group was confirmed in the Morris water maze trial.TNF-α,IL-6,and IL-1β levels in lung and brain tissues were higher in the CS group compared with the control group.There were no significant differences in cardiac,liver,and renal functions between the groups.Conclusions A mouse model of COPD can be established by CS exposure for 20 weeks.Lung histomorphology,lung function,brain cognitive function,and levels of inflammatory factors can be used as indicators to evaluate the success of the model.

Objective:To investigate the effects of budesonide/formoterol versus budesonide on lung volume and serum miR-146 and interleukin-4 levels in patients with bronchiectasis and asthma. Methods:This study adopted a prospective design. A total of 102 patients with bronchiectasis and asthma who received treatment at the People's Hospital of Tongchuan from October 2021 to August 2024 were included. The patients were randomly divided into a conventional group and an observation group using an envelope method ( n = 51 per group). The conventional group received budesonide inhalation treatment, while the observation group was given budesonide/formoterol inhalation powder. All patients were treated for 15 days. The lung function, lung volume, miR-146 mRNA, interleukin-4 (IL-4), interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and eosinophil percentage (EOS%) levels of both groups were measured before and after treatment, and the incidence of adverse reactions in the two groups was statistically analyzed. Results:Before treatment, there was no statistically significant difference in lung function and lung volume between the two groups (both P > 0.05). After treatment, the forced vital capacity (FVC), peak expiratory flow (PEF), and forced expiratory volume in the first second (FEV 1) /FVC of both groups were significantly higher than those before treatment ( t = 2.54, 16.22, 9.67, 5.75, 29.25, and 16.91, all P < 0.05). Residual volume (RV) and the ratio of RV to total lung capacity (TLC) were significantly lower in both groups after treatment compared with before treatment ( t = 2.24, -2.98, -3.51, -6.79, all P < 0.05). There was no statistically significant difference in TLC in both groups between before and after treatment ( P > 0.05). The observation group had significantly higher FVC [(2.96 ± 0.65) L], PEF [(75.96 ± 6.54) mL/s], and FEV 1/FVC (85.45 ± 6.03) than the conventional group [(2.57 ± 0.61) L, (67.85 ± 6.06) mL/s, (70.86 ± 5.16), t = -3.12, -6.50, -13.13, all P < 0.05]. After treatment, the RV [(2.81 ± 0.32) L] and RV/TLC [(49.13 ± 3.94)] in the observation group were significantly lower than those in the conventional group [(2.95 ± 0.37) L, (52.03 ± 4.16), t = 2.04, 3.62, both P < 0.05]. The difference in TLC between the two groups was not statistically significant ( P > 0.05). Before treatment, there was also no statistically significant difference in miR-146 mRNA levels between the two groups ( P > 0.05). After treatment, miR-146a and miR-146b mRNA levels in both groups were significantly lower compared to their levels before treatment ( t = -9.21, -4.14, -11.02, -7.58, all P < 0.05). In the observation group, the levels of miR-146a mRNA [(1.41 ± 0.26)] and miR-146b mRNA [(1.15 ± 0.26)] after treatment were significantly lower than those in the conventional group [(1.66 ± 0.34), (1.32 ± 0.34), t = 4.17, 2.84, both P < 0.05]. Before treatment, there were no statistically significant differences in IL-4, IFN-γ, TNF-α, and EOS% between the two groups (all P > 0.05). After treatment, IL-4, IFN-γ, TNF-α, and EOS% levels were significantly lower in both groups compared with before treatment ( t = -6.13, -2.56, -18.57, -23.67, -11.20, -3.83, -20.56, -30.00, all P < 0.05). In the observation group, IL-4 [(234.51 ± 34.03) ng/L], IFN-γ [(214.41 ± 31.54) ng/L], TNF-α [(23.65 ± 10.47) ng/L], and EOS% (2.03 ± 0.33) were significantly lower than those in the conventional group [(265.63 ± 37.51) ng/L], (230.12 ± 36.95) ng/L, (39.69 ± 13.41) ng/L, (2.57 ± 0.51), t = 0.49, 12.39, 6.73, 6.35, all P < 0.05]. There was no significant difference in the incidence of adverse reactions between the observation and conventional groups [13.73% (7/51) vs. 7.84% (4/51), χ2 = 0.92, P > 0.05]. Conclusions:Both budesonide/formoterol and budesonide alone can improve lung function and lung volume in patients with bronchiectasis and asthma while reducing levels of miR-146 and IL-4. However, budesonide/formoterol shows superior efficacy.

Objective:To investigate the key technical aspects of laparoscopic anti-reflux surgery (LARS) in complex gastroesophageal reflux disease (GERD) with hiatal hernia (HH) and evaluate the feasibility and efficacy of reoperation.Methods:A retrospective analysis was conducted on 28 patients with complex GERD treated at Zhejiang Provincial People's Hospital from Feb 2020 to May 2024. Preoperative examinations were recorded, and surgical videos were reviewed to reconstruct operative time, critical intraoperative steps, complications, and management techniques. Postoperative follow-up via telephone and outpatient visits assessed symptom relief, complications, and medication use.Results:All 28 patients (4 robotic-assisted and 24 conventional laparoscopic surgeries) successfully underwent LARS, with an operative duration of (152.6±10.3) minutes and a postoperative hospital stay of (4.0±1.9) days. Large HH 9 cases, intraoperative bleeding 6 cases, pleural rupture 3 case, and esophageal perforation 1 case, preoperative diagnoses included short esophagus 2 cases and 7 redo surgeries. The overall recurrence rate was 11%. Postoperative complications occurred in 14%. The redo surgeries group achieved 71% symptom resolution. At 1-12 months of follow-up, 82% of patients were asymptomatic, and 82% discontinued proton pump inhibitor therapy.Conclusions:Complex scenarios requiring specialized techniques in LARS increase surgical difficulty and risks. Standardized management of the hernia sac, hiatal repair, neurovascular protection, identification of anatomical landmarks in reoperations, selection of biological mesh, and adhesiolysis may reduce recurrence rates and complication risks.

BACKGROUND:Croton cream can activate ERK pathways and have anti-apoptotic effects on neuronal cells.It is not clear whether it synergistically exerts anti-apoptotic effects by inhibiting the activation of JNK and p38 pathways. OBJECTIVE:To explore the effects and mechanisms of croton cream on neuronal damage and apoptosis in the ischemic cortex of rats with cerebral ischemia-reperfusion injury. METHODS:(1)Ninety Sprague-Dawley rats were randomly divided into sham operation group,model group,croton cream low-dose group,croton cream medium-dose group,croton cream high-dose group and nimodipine group,with 15 rats in each group.Except for the sham operation group,animal models of middle cerebral artery occlusion were prepared in rats by the thread method.Rats in the three croton cream groups were given 20,40,and 60 mg/kg croton cream,respectively.Rats in the sham operation and model groups were given the same amount of normal saline,once a day,for 7 consecutive days.The optimal concentration of croton cream,namely the high dose of croton cream,was selected based on neurological deficit score,TTC staining,brain tissue water content,hematoxylin-eosin staining and Nissl staining.(2)Another 120 Sprague-Dawley rats were randomly divided into sham operation group,model group,croton cream group,JNK inhibitor group,croton cream+JNK inhibitor group,p38 MAPK inhibitor group,croton cream+p38 MAPK inhibitor group,and nimodipine group,with 15 rats in each group.Animal models of middle cerebral artery occlusion were prepared using the thread method in all the groups except in the sham operation group.Thirty minutes before modeling,10 μL of SP600125(JNK inhibitor)and 10 μL of SB203580(p38 MAPK inhibitor)were injected into the lateral ventricle of the rats,respectively.Rats in croton cream groups were intragastrically given 60 mg/kg croton cream.Seven days later,the JNK/p38 MAPK signaling pathway,apoptosis-related proteins and cell apoptosis were detected by western blot,TUNEL staining and flow cytometry,respectively. RESULTS AND CONCLUSION:(1)Compared with the sham operation group,neurological deficit score,cerebral water content,cerebral infarction volume and apoptosis rate were significantly increased in the model group(P<0.05),where nerve cells showed scattered distribution.Compared with the model group,neurological deficit score,water content of brain tissue and cerebral infarction volume were significantly decreased in the croton cream medium-dose group,high-dose group and nimodipine group(P<0.05),and the pathological morphology of nerve cells was significantly improved.(2)Compared with the JNK inhibitor group,p-JNK/JNK,p-p38/p38 and Bax expressions in rat brain tissue and the apoptotic rate were significantly decreased in the croton cream+inhibitor groups(P<0.05),while the expression of and Bcl-2 was significantly increased(P<0.05).To conclude,croton cream may inhibit the activation of JNK/p38 MAPK signaling pathway and reduce neuronal apoptosis to achieve neuroprotective effects in rats with cerebral ischemia-reperfusion injury.

Objective:To investigate the application value of 3D printed model in hemostasis training for laparoscopic sleeve gastrectomy.Methods:The retrospective and descriptive study was conducted. Data were collected from six surgeons who participated in hemostasis training for laparoscopic sleeve gastrectomy using 3D printed model at Zhejiang Provincial People′s Hospital in July 2023. All participants were male, aged (33.5±9.9)years. A 3D printed model simulating bleeding during laparoscopic sleeve gastrectomy was created using hydrogel. Videos were recorded to document the surgeons′ hemostasis techniques and outcomes during laparoscopic sleeve gastrectomy. Two external expert reviewers blindly assessed the training videos using the objective structured assess-ment of technical skills (OSATS) scoring system to evaluate mesentery mobilization, vessel exposure, vessel clipping and bleeding after vessel clipping. Observation indicators: (1) face validity and content validity of the 3D printed model; (2) validity verification of the 3D printed model. Measurement data with normal distribution were represented as Mean± SD. Comparison between groups was conducted using the t test. Results:(1) Face validity and content validity of the 3D printed model. The surgeons′ scores for overall impression, fidelity, texture, appearance, workspace and tactile similarity of the 3D printed model were 4.5±0.6, 4.0±0.6, 3.7±0.5, 4.2±0.8, 3.8±0.8 and 4.2±0.4, respectively. The surgeons′ scores for similarity to real scenarios, operation convenience, learning curve shortening and operation skills improving, patient risk reduction, trainee′s interest enhancing, confidence increasing and recommendation for promotion were 4.0±0.6, 4.2±0.8, 4.3±0.8, 4.3±0.5, 4.3±0.5, 4.0±0.6 and 4.8±0.4, respectively. (2) Validity verification of the 3D printed model. The OSATS scores and operation time to treat bleeding during laparoscopic sleeve gastrectomy for expert surgeons were 18.7±0.6 and (125±12)seconds, respectively, versus 13.7±1.5 and (212±51)seconds for junior doctors, showing significant differences between the two groups ( t=5.30, -2.89, P<0.05). Conclusion:The 3D printed model effectively simulates bleeding scenarios during laparoscopic sleeve gastrectomy and distinguishes between different technical levels of expertise.