ObjectiveTo investigate the molecular mechanism of kaempferol-induced apoptosis in hepatic stellate cells （HSC） via the mitochondrial pathway. MethodsHSC were divided into five groups： blank control， transforming growth factor-β1（TGF-β1） （10 ng/mL） group， and groups treated with different concentrations of kaempferol （8， 16， 32 µmol/L）. Cell counting kit-8（CCK-8） assay was used to evaluate chrysin's effect on HSC proliferation. Transwell assay was used to assess chrysin's impact on HSC migration. Flow cytometry was used to detect apoptosis， reactive oxygen species （ROS） expression， and mitochondrial permeability transition pore （mPTP） opening across groups. 5，5′，6，6′-Tetrachloro-1，1′，3，3′-tetraethylimidacarbocyanine iodide （JC-1） assay was used to test mitochondrial membrane potential. Western blot analysis was performed to determine the expression levels of mitochondrial apoptosis-associated proteins， namely B-cell lymphoma-2 （Bcl-2）， Bcl-2-associated X protein （Bax）， Cleaved-Caspase3， Cleaved-Caspase9， and sirtuin 3 （SIRT3）. Transmission electron microscopy was used to examine mitochondrial structural alterations. Molecular docking and kinetic simulations were used to analyze the targeted interaction between kaempferol and NAD-dependent deacetylase sirtuin-3 （SIRT3）. ResultsCompared with the blank control group： in the TGF-β1 group， HSC proliferation and migration rates increased （P<0.01）， ROS levels and mPTP opening both increased （P<0.05）， the JC-1 red/green fluorescence ratio increased （P<0.01）， and the expression of Cleaved-Caspase-3， Cleaved-Caspase-9 and Bcl-2 increased （P<0.05）， whilst SIRT3 expression decreased （P<0.01）； the number of mitochondria increased （P<0.05）， and mitochondrial length decreased （P<0.01）. Compared with the TGF-β1 group： treatment with all groups of kaempferol reduced HSC proliferation and migration rates （P<0.01）， whilst simultaneously increasing the HSC apoptosis rate （P<0.01）； HSC ROS levels and mPTP opening both increased （P<0.05）； the JC-1 red/green fluorescence ratio decreased （P<0.01）， and the expression levels of Bax， Cleaved-Caspase-3 and Cleaved-Caspase-9 were upregulated （P<0.01）， whilst the expression levels of Bcl-2 and SIRT3 were downregulated （P<0.01）， and the number of mitochondria increased （P<0.05）； mitochondrial length was reduced （P<0.01）. Molecular docking and dynamics simulations revealed that the docking energy for kaempferol with SIRT3 was 108.89 kcal/mol； the RMSD curve stabilized after 20 ns； and RMSF analysis indicated that most residues exhibited minimal fluctuations. ConclusionKaempferol induces HSC apoptosis through the mitochondrial pathway， potentially via targeting SIRT3 and disrupting mitochondrial function.

ObjectiveTo explore the pharmacological mechanism involved in the treatment of allergic cough （AC） by Xiaoer Huatan Zhike granules （XEHT） based on proteomics and network pharmacology. MethodsAfter sensitization by intraperitoneal injection of 1 mL suspension containing 2 mg ovalbumin （OVA） and 100 mg aluminum hydroxide， a guinea pig model of allergic cough was constructed by nebulization with 1% OVA. The modeled guinea pigs were randomized into the model， low-， medium- and high-dose （1， 5， 20 g·kg^-1， respectively） XEHT， and sodium montelukast （1 mg·kg^-1） groups （n=6）， and another 6 guinea pigs were selected as the blank group. The guinea pigs in drug administration groups were administrated with the corresponding drugs by gavage， and those in the blank and model groups received the same volume of normal saline by gavage， 1 time·d^-1. After 10 consecutive days of drug administration， the guinea pigs were stimulated by 1% OVA nebulization， and the coughs were observed. The pathological changes in the lung tissue were observed by hematoxylin-eosin staining. The enzyme-linked immunosorbent assay was performed to measure the levels of C-reactive protein （CRP）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， superoxide dismutase （SOD）， and malondialdehyde （MDA） in the bronchoalveolar lavage fluid （BALF） and immunoglobulin G （IgG） and immunoglobulin A （IgA） in the serum. Immunohistochemistry （IHC） was employed to observe the expression of IL-6 and TNF-α in the lung tissue. Transmission electron microscopy was employed observe the alveolar type Ⅱ epithelial cell ultrastructure. Real-time PCR was employed to determine the mRNA levels of IL-6， interleukin-1β （IL-1β）， and TNF-α in the lung tissue. Label-free proteomics was used to detect the differential proteins among groups. Network pharmacology was used to predict the targets of XEHT in treating AC. The Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analysis was performed to search for the same pathways from the results of proteomics and network pharmacology. ResultsCompared with the blank group， the model group showed increased coughs （P<0.01）， elevated levels of CRP， TNF-α， IL-6， and MDA and lowered level of SOD in the BALF （P<0.05， P<0.01）， elevated levels of IgA and IgG in the serum （P<0.05， P<0.01）， congestion of the lung tissue and infiltration of inflammatory cells， increased expression of IL-6 and TNF-α （P<0.01）， large areas of low electron density edema in type Ⅱ epithelial cells， obvious swelling and vacuolization of the organelles， karyopyknosis or sparse and dissolved chromatin， and up-regulated mRNA levels of IL-6， IL-1β， and TNF-α （P<0.01）. Compared with the model group， the drug administration groups showed reduced coughs （P<0.01）， lowered levels of CRP， TNF-α， IL-6， and MDA and elevated level of SOD in the BALF （P<0.05， P<0.01）， alleviated lung tissue congestion， inflammatory cell infiltration， and type Ⅱ epithelial cell injury， and decreased expression of IL-6 and TNF-α （P<0.01）. In addition， the medium-dose XEHT group and the montelukast sodium group showcased lowered serum levels of IgA and IgG （P<0.05， P<0.01）. The medium- and high-dose XEHT groups and the montelukast sodium showed down-regulated mRNA levels of IL-6， IL-1β， and TNF-α and the low-dose XEHT group showed down-regulated mRNA levels of IL-6 and TNF-α （P<0.05， P<0.01）. Phospholipase D， mammalian target of rapamycin （mTOR）， and epidermal growth factor receptor family of receptor tyrosine kinase （ErbB） signaling pathways were the common pathways predicted by both proteomics and network pharmacology. ConclusionProteomics combined with network pharmacology reveal that XEHT can ameliorate AC by regulating the phospholipase D， mTOR， and ErbB signaling pathways.

Objective To examine the correlation between fetal rectal ampulla diameter and gestational age,and to establish reference value ranges for low-risk fetuses between 18 and 40 weeks of gestation in Yibin region.Methods A total of 1,103 low-risk singleton pregnant women between 18 and 40 weeks of gestation were recruited from five hospitals in Yibin City(the Second People's Hospital,the First People's Hospital,the Fifth People's Hospital,the Maternal and Child Health Hospital of Yibin City,and the Maternal and Child Health Hospital of Cuiping District)for routine level Ⅰ,Ⅱ,and Ⅲ prenatal ultrasound screening from October 2022 to March 2024.Fetal rectal ampulla diameters,including anteroposterior diameter,transverse diameter,and area,were measured using prenatal ultrasound.The normality of these measurements was assessed using the Shapiro-Wilk test.Scatter plots depicting the relationship between fetal rectal ampulla diameter parameters and gestational age were generated using the"Overlap Scatter Plot"function in SPSS.Percentiles were calculated using the"Explore"function in SPSS,with reference value ranges described by P5,P10,P50,P90,and P95.Results The visual-ization rate of the fetal rectal ampulla diameter was 55%at 18～20 weeks of gestation,100%at 21～37 weeks,and 96%at greater than 37 weeks.The fetal rectal ampulla diameter exhibited a significant positive correlation with gestational age(r=0.925～0.949,P<0.01).Conclusions Prenatal ultrasound measurement of fetal rectal ampulla diameter demonstrates a robust correlation with gestational age.The reference intervals for the rectal ampulla diameter of low-risk fetuses between 18 and 40 weeks of gestation,established in this study,may offer valuable theoretical guidance for prenatal diagnosis of fetal rectal and anal abnormalities in Yibin region.

Chronic liver diseases with common causes including viral infections， alcohol abuse， and autoimmune diseases. Alkaloids， as a class of plant-derived compounds， have shown significant potential in regulating chronic liver diseases. Recent studies have shown that alkaloids are able to exert a therapeutic effect on chronic liver diseases through multiple pathways. These compounds have a regulatory effect on key pathological processes such as liver fibrosis， inflammatory response， oxidative stress， and cell apoptosis， and they also regulate the metabolic homeostasis of hepatocytes by modulating multiple signaling pathways， thereby playing a role in regulating chronic liver diseases. This article reviews the role and mechanism of alkaloids in the treatment of chronic liver diseases， in order to provide new ideas and directions for the treatment of chronic liver diseases.

Objective To examine the correlation between fetal rectal ampulla diameter and gestational age,and to establish reference value ranges for low-risk fetuses between 18 and 40 weeks of gestation in Yibin region.Methods A total of 1,103 low-risk singleton pregnant women between 18 and 40 weeks of gestation were recruited from five hospitals in Yibin City(the Second People's Hospital,the First People's Hospital,the Fifth People's Hospital,the Maternal and Child Health Hospital of Yibin City,and the Maternal and Child Health Hospital of Cuiping District)for routine level Ⅰ,Ⅱ,and Ⅲ prenatal ultrasound screening from October 2022 to March 2024.Fetal rectal ampulla diameters,including anteroposterior diameter,transverse diameter,and area,were measured using prenatal ultrasound.The normality of these measurements was assessed using the Shapiro-Wilk test.Scatter plots depicting the relationship between fetal rectal ampulla diameter parameters and gestational age were generated using the"Overlap Scatter Plot"function in SPSS.Percentiles were calculated using the"Explore"function in SPSS,with reference value ranges described by P5,P10,P50,P90,and P95.Results The visual-ization rate of the fetal rectal ampulla diameter was 55%at 18～20 weeks of gestation,100%at 21～37 weeks,and 96%at greater than 37 weeks.The fetal rectal ampulla diameter exhibited a significant positive correlation with gestational age(r=0.925～0.949,P<0.01).Conclusions Prenatal ultrasound measurement of fetal rectal ampulla diameter demonstrates a robust correlation with gestational age.The reference intervals for the rectal ampulla diameter of low-risk fetuses between 18 and 40 weeks of gestation,established in this study,may offer valuable theoretical guidance for prenatal diagnosis of fetal rectal and anal abnormalities in Yibin region.

Objective:To investigate the role of reactive astrocytes expressing aromatase(ARO)in the penumbra during ischemic stroke.Methods:A mouse model of middle cerebral artery occlusion(MCAO/R)was prepared using the suture method.Western blot and immunofluorescence staining were used to observe the expression of ARO in the penumbra after ischemia reperfusion.We generated a glial fibrillary acidic protein promoter-driven aromatase knock-out(GFAP-ARO-KO)mouse model in vivo.Neurologic impairment scores,rotarod test,grip strength test and adhesive removal test on the plantar surface of the paw were performed after MCAO/R modeling.Results:In wild type mice,the expression of ARO was significantly increased in astrocytes in the penumbra after MCAO/R(P<0.01).Compared to the control group,the expression of ARO in the GFAP-ARO-KO group was significantly reduced in astrocytes in the penumbra after MCAO/R.And loss of ARO increased cerebral infarction volume and aggravated sensorimotor impair-ment.Conclusion:After ischemic stroke,reactive astrocytes in the penumbra highly express ARO and play a protective role in post-ischemia reperfusion injury.

Objective:To investigate the role of reactive astrocytes expressing aromatase(ARO)in the penumbra during ischemic stroke.Methods:A mouse model of middle cerebral artery occlusion(MCAO/R)was prepared using the suture method.Western blot and immunofluorescence staining were used to observe the expression of ARO in the penumbra after ischemia reperfusion.We generated a glial fibrillary acidic protein promoter-driven aromatase knock-out(GFAP-ARO-KO)mouse model in vivo.Neurologic impairment scores,rotarod test,grip strength test and adhesive removal test on the plantar surface of the paw were performed after MCAO/R modeling.Results:In wild type mice,the expression of ARO was significantly increased in astrocytes in the penumbra after MCAO/R(P<0.01).Compared to the control group,the expression of ARO in the GFAP-ARO-KO group was significantly reduced in astrocytes in the penumbra after MCAO/R.And loss of ARO increased cerebral infarction volume and aggravated sensorimotor impair-ment.Conclusion:After ischemic stroke,reactive astrocytes in the penumbra highly express ARO and play a protective role in post-ischemia reperfusion injury.

OBJECTIVE To study the interventional effect and mechanism of 1，8-cineole on pancreatic β cell ferroptosis induced by type 2 diabetes. METHODS In vitro ferroptosis model was established in pancreatic β cells of mice by using high glucose. The effects of low-dose and high-dose 1，8-cineole （0.25， 0.5 μmol/L） on the level of Fe2+ in pancreatic β cells were investigated. The effects of 1，8-cineole （0.5 μmol/L） combined with ferroptosis inducer Erastin （20 μmol/L） and ferroptosis inhibitor Ferrostatin-1 （20 μmol/L） on the protein expressions of glutathione peroxidase-4 （GPX4） and cyclooxygenase-2 （COX2） were also detected. The type 2 diabetes model mice were established by feeding high-sugar and high-fat diet combined with intraperitoneal injection of streptozotocin. The effects of low-dose and high-dose 1，8-cineole （50， 200 mg/kg） on the pathological morphology of pancreatic tissue， the content of iron as well as the protein expressions of GPX4 and COX2 were investigated. RESULTS The results of the cell experiment showed that compared with the model group， pretreatment with 1，8-cineole significantly reduced intracellular Fe2+ levels and upregulated GPX4 protein expression， while downregulated COX2 protein expression in pancreatic β cells （P＜0.05）. After combining with Ferrostatin-1， the expression trends of the above two proteins were the same， while there was no statistically significant difference after combining with Erastin. The results of animal experiments showed that compared with the model group， after intervention with 1，8-cineole， the structure of the pancreatic islets in mice recovered intact and their morphology improved； the iron content of pancreatic tissue and protein expression of COX2 were decreased significantly （P＜0.05）， while protein expression of GPX4 was increased significantly （P＜0.05）. CONCLUSIONS 1，8-cineole could ameliorate pancreatic β cell injury induced by diabetes， the mechanism of which may be related to reducing intracellular iron deposition and regulating ferroptosis-related proteins.

Objective:To investigate the clinical effect of drugs combined with hyperbaric oxygen（HBO）on nervous system damage caused by nitrous oxide（N 2O）poisoning. Methods:The clinical data of 12 patients with nerve damage caused by N 2O poisoning admitted to the Department of Neurology，Hyperbaric Oxygen of a certain PLA hospital from February 2020 to April 2021 were reviewed. The changes of neuroelectrophysiological and neurological functions of patients before and after treatment were analyzed using electroneurogram detection，Berg balance scale，and Holden’s functional ambulation categories（FAC）as observation indicators. Results:After drug treatment combined with HBO，the motor conduction velocity，sensory conduction velocity，motor latency，motor evoked potential，and sensory evoked potential of electroneurogram of 12 patients were significantly improved，and the differences were statistically significant（ P < 0.05）.Berg balance scale scores were significantly improved compared with those before treatment，and the differences were statistically significant（ P < 0.05）.FAC scale was improved compared with before treatment，but the difference was not statistically significant（ P > 0.05）. Conclusion:HBO combined with folic acid，vitamin B12 and other neurotrophic drugs has a certain clinical effect in the treatment of nerve damage caused by N 2O poisoning，which is worthy of further study and improvement.

Objective:To investigate the clinical effect of drugs combined with hyperbaric oxygen（HBO）on nervous system damage caused by nitrous oxide（N 2O）poisoning. Methods:The clinical data of 12 patients with nerve damage caused by N 2O poisoning admitted to the Department of Neurology，Hyperbaric Oxygen of a certain PLA hospital from February 2020 to April 2021 were reviewed. The changes of neuroelectrophysiological and neurological functions of patients before and after treatment were analyzed using electroneurogram detection，Berg balance scale，and Holden’s functional ambulation categories（FAC）as observation indicators. Results:After drug treatment combined with HBO，the motor conduction velocity，sensory conduction velocity，motor latency，motor evoked potential，and sensory evoked potential of electroneurogram of 12 patients were significantly improved，and the differences were statistically significant（ P < 0.05）.Berg balance scale scores were significantly improved compared with those before treatment，and the differences were statistically significant（ P < 0.05）.FAC scale was improved compared with before treatment，but the difference was not statistically significant（ P > 0.05）. Conclusion:HBO combined with folic acid，vitamin B12 and other neurotrophic drugs has a certain clinical effect in the treatment of nerve damage caused by N 2O poisoning，which is worthy of further study and improvement.