ObjectiveTo elucidate the potential mechanisms by which the classic prescription Anmeidan alleviates cognitive impairment in insomnia model rats through metabolic profiling. MethodsA total of 60 SD rats were randomly divided into six groups： blank group， model group， low-， medium-， and high-dose Anmeidan groups， and the Suvorexant group， with 10 rats in each group. Except for the blank group， the insomnia model was established in all other groups via intraperitoneal injection of para-chlorophenylalanine. The Suvorexant group was administered Suvorexant solution （30 mg·kg^-1·d^-1） by gavage， while the low-， medium-， and high-dose Anmeidan groups received Anmeidan decoction （4.55， 9.09， 18.18 g·kg^-1·d^-1） by gavage. The blank group received an equivalent volume of normal saline. The open field test was used to assess spatial exploration and anxiety/depressive-like behaviors in rats. Serum levels of epidermal growth factor （EGF）， brain-derived neurotrophic factor （BDNF）， and vasoactive intestinal peptide （VIP） were measured using enzyme-linked immunosorbent assay （ELISA）. Untargeted metabolomics was employed to identify differential metabolites in rat serum， and systematic biological methods were applied to analyze the potential targets and pathways of Anmeidan. ResultsCompared to the blank group， the model group exhibited significant reductions in total distance traveled， average speed， number of entries into the central area， time spent in the central area， and frequency of upright events （P<0.01）， along with significant decreases in VIP， EGF， and BDNF levels （P<0.05，P<0.01）. A total of 100 differential metabolites were identified between the model and blank groups. Compared to the model group， the low-， medium-， and high-dose Anmeidan groups showed significant increases in total distance traveled， average speed， number of entries into the central area， time spent in the central area， and frequency of upright events （P<0.05，P<0.01）， as well as a significant increase in VIP levels （P<0.05，P<0.01）. Anmeidan significantly reversed abnormal changes in 67 metabolites compared to the model group. A combined analysis identified 134 potential targets of Anmeidan， with network topology analysis suggesting that Caspase-3， B-cell lymphoma 2 （Bcl-2）， nuclear transcription factor-κB （NF-κB）， interleukin-1β （IL-1β）， interleukin-2 （IL-2）， matrix metalloproteinase-9 （MMP-9）， and Toll-like receptor 4 （TLR4）， among others， may serve as key targets of Anmeidan. Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway analysis revealed major enriched pathways， including the cyclic adenosine monophosphate （cAMP） signaling pathway， hypoxia inducible factor-1 （HIF-1） signaling pathway， and IL-17 signaling pathway. ConclusionThis study demonstrates that Anmeidan can recalibrate abnormal metabolic profiles in insomnia model rats to mitigate cognitive impairment， with its mechanisms of action potentially involving the regulation of immune-inflammatory responses， energy metabolism， and apoptosis-related pathways.

Objective:To investigate the changes in the expression of miR-146a-5p and steroidogenic acute regulatory protein (StAR) in the blood vessels of rats with hypertension complicated with sepsis, and to preliminarily evaluate the underlying mechanisms of vascular lesions in hypertension complicated with sepsis.Methods:Twenty-four clean-grade healthy male Wistar rats, aged 12 weeks, weighing 250-270 g, were divided into 4 groups ( n=6 each) using the random number table method: sham operation group, sepsis group, hypertension group, and hypertension complicated with sepsis group. In sham operation group, laparotomy was performed, and sterile normal saline was subcutaneously infused using a micro-osmotic pump for 4 weeks. The sepsis model was established by cecal ligation and perforation after anesthesia in sepsis group. The hypertension model was established by subcutaneously infusing angiotensin Ⅱ at a rate of 500 ng·kg -1·min -1 for 4 weeks using a micro-osmotic pump in hypertension group. In hypertension complicated with sepsis group, angiotensin Ⅱ was subcutaneously infused, and 4 weeks later the sepsis model was established by cecal ligation and perforation. Blood pressure was measured at the end of establishing the model in each group, and blood samples of the abdominal aorta and specimens of aorta were obtained under deep anesthesia, and the serum tumor necrosis factor-alpha (TNF-α) concentration was determined by enzyme-linked immunosorbent assay. The systolic and diastolic functions of the aorta were detected using the aortic vascular ring assay. The collagen volume fraction (CVF) was calculated after Masson staining. The expression of α-smooth muscle actin (α-SMA) and StAR was detected using the immunohistochemical staining assay, and the thickness of the aortic wall was measured. The expression of StAR mRNA and miR-146a-5p was detected using quantitative real-time polymerase chain reaction. Results:Compared with sham operation group, the aortic contraction rate was significantly decreased, the expression of StAR protein and mRNA was up-regulated, the expression of miR-146a-5p was down-regulated, and the serum TNF-α concentration was increased in the other three groups, and the systolic blood pressure and CVF were significantly increased, the thickness of the aortic wall was increased, the expression of α-SMA was up-regulated, and the thickness of the aortic wall was increased in hypertension and hypertension complicated with sepsis groups ( P<0.05). Compared with sepsis group, the systolic pressure was significantly increased, the aortic contraction rate was decreased, CVF was increased, the expression of α-SMA was up-regulated, the thickness of the aortic wall was increased, the expression of StAR protein and mRNA was up-regulated, the expression of miR-146a-5p was down-regulated, and the serum TNF-α concentration was increased in hypertension complicated with sepsis group ( P<0.05). Compared with hypertension group, the aortic contraction rate was significantly decreased, the diastolic rate was increased, the expression of StAR protein and mRNA was up-regulated, the expression of miR-146a-5p was down-regulated, and the serum TNF-α concentration was increased in hypertension complicated with sepsis group ( P<0.05). Conclusions:Down-regulation of miR-146a-5p and up-regulation of StAR in the blood vessels of rats with hypertension complicated with sepsis may be associated with the vascular lesions caused by hypertension complicated with sepsis.

Objective : To investigate the effect of solasonine regulation of the STAT3 signaling pathway on the bio- logical behavior of lung adenocarcinoma cells． Methods : H1299 cells were treated with 0. 125，0. 25，0. 5 and 0. 75 mmol /L solasonine，respectively．The proliferative activity of H1299 cells was detected by CCK-8．The mi- gration and invasion ability of H1299 cells were detected by scratch，Transwell migration and invasion assay．The apoptosis level of H1299 cells was detected by flow cytometry and Hoechest 33258 /PI double staining．The protein expression levels of STAT3，p-STAT3 ，Bcl-2 ，Bax ，Caspase-3 ，Cl-Caspase-3 ，Snail ，Slug ，N-cadherin and E- cadherin in H1299 cells were detected by Western blot assay． Results: Solasonine at different concentrations sig- nificantly reduced the proliferation of H1299 cells (P＜0. 05) ．0. 125 and 0. 25 mmol /L solasonine promoted the apoptosis of H1299 cells (P＜0. 05) and inhibited the migration and invasion of H1299 cells (P＜0. 05) ．Solaso- nine inhibited the expression of STAT3，p-STAT3 and Bcl-2 proteins，enhanced the expression of Bax，Caspase-3 and Cl-Caspase-3 proteins．Solasonine inhibited the activation of STAT3 in cells，reduced Snail and Slug protein expression levels，enhanced E-cadherin，reduced N-cadherin(P＜0. 05) ． Conclusion Solasonine can inhibit the activation of STAT3 ，activate the Bcl-2 /Bax / Caspase3 apoptosis pathway ，inhibit the continuous proliferation of lung adenocarcinoma H1299 cells，and promote the apoptosis of lung adenocarcinoma H1299 cells．Meanwhile，it can inhibit the activation of STAT3，reduce the expression of Snail / Slug protein，affect the EMT transformation of lung adenocarcinoma H1299 cells，and inhibit the migration and invasion of lung adenocarcinoma H1299 cells．

OBJECTIVE To investigate the effects of coptisine on endogenous metabolites in a dextran sulfate sodium(DSS)-in-duced ulcerative colitis(UC)mouse model,and to explore its potential mechanisms of action employing non-targeted metabolomics technology.METHODS SPF-grade male C57BL/6 mice were randomly divided into a control group,a model group,a sulfasalazine group(100 mg·kg-1),and low and high dose groups of coptisine groups(25,50 mg·kg-1).To induce ulcerative colitis(UC),all groups except the control group had free access to a 2.5%DSS solution for 7 days.At the same time,they also received daily intragastric ad-ministration of their corresponding treatments until the 10th day.Body weight changes,stool characteristics,and bloody stool occur-rence were recorded daily,and the disease activity index(DAI)was calculated.After the experiment,colon tissues were collected for pathological examination.Through UPLC-Q-TOF-MS/MS,non-targeted metabolomic analysis was performed to identify differential metabolites,and metabolic pathway enrichment analysis was conducted using the KEGG database.RESULTS Compared to the model group,coptisine significantly ameliorated weight loss,DAI scores,and pathological damage in colon tissues of UC mice(P<0.05,P<0.01).Metabolomic analysis identified 56 differential metabolites,mainly involved in purine metabolism,tryptophan metabo-lism,niacin and nicotinamide metabolism,glutathione metabolism,and the biosynthesis of phenylalanine,tyrosine,and tryptophan.Coptisine intervention significantly reversed the abnormal expression of these metabolites.CONCLUSION Coptisine can markedly improve metabolic disorders in DSS-induced UC mice by modulating multiple key metabolic pathways,thereby exerting a therapeutic effect.

Objective:To investigate the changes in the expression of miR-146a-5p and steroidogenic acute regulatory protein (StAR) in the blood vessels of rats with hypertension complicated with sepsis, and to preliminarily evaluate the underlying mechanisms of vascular lesions in hypertension complicated with sepsis.Methods:Twenty-four clean-grade healthy male Wistar rats, aged 12 weeks, weighing 250-270 g, were divided into 4 groups ( n=6 each) using the random number table method: sham operation group, sepsis group, hypertension group, and hypertension complicated with sepsis group. In sham operation group, laparotomy was performed, and sterile normal saline was subcutaneously infused using a micro-osmotic pump for 4 weeks. The sepsis model was established by cecal ligation and perforation after anesthesia in sepsis group. The hypertension model was established by subcutaneously infusing angiotensin Ⅱ at a rate of 500 ng·kg -1·min -1 for 4 weeks using a micro-osmotic pump in hypertension group. In hypertension complicated with sepsis group, angiotensin Ⅱ was subcutaneously infused, and 4 weeks later the sepsis model was established by cecal ligation and perforation. Blood pressure was measured at the end of establishing the model in each group, and blood samples of the abdominal aorta and specimens of aorta were obtained under deep anesthesia, and the serum tumor necrosis factor-alpha (TNF-α) concentration was determined by enzyme-linked immunosorbent assay. The systolic and diastolic functions of the aorta were detected using the aortic vascular ring assay. The collagen volume fraction (CVF) was calculated after Masson staining. The expression of α-smooth muscle actin (α-SMA) and StAR was detected using the immunohistochemical staining assay, and the thickness of the aortic wall was measured. The expression of StAR mRNA and miR-146a-5p was detected using quantitative real-time polymerase chain reaction. Results:Compared with sham operation group, the aortic contraction rate was significantly decreased, the expression of StAR protein and mRNA was up-regulated, the expression of miR-146a-5p was down-regulated, and the serum TNF-α concentration was increased in the other three groups, and the systolic blood pressure and CVF were significantly increased, the thickness of the aortic wall was increased, the expression of α-SMA was up-regulated, and the thickness of the aortic wall was increased in hypertension and hypertension complicated with sepsis groups ( P<0.05). Compared with sepsis group, the systolic pressure was significantly increased, the aortic contraction rate was decreased, CVF was increased, the expression of α-SMA was up-regulated, the thickness of the aortic wall was increased, the expression of StAR protein and mRNA was up-regulated, the expression of miR-146a-5p was down-regulated, and the serum TNF-α concentration was increased in hypertension complicated with sepsis group ( P<0.05). Compared with hypertension group, the aortic contraction rate was significantly decreased, the diastolic rate was increased, the expression of StAR protein and mRNA was up-regulated, the expression of miR-146a-5p was down-regulated, and the serum TNF-α concentration was increased in hypertension complicated with sepsis group ( P<0.05). Conclusions:Down-regulation of miR-146a-5p and up-regulation of StAR in the blood vessels of rats with hypertension complicated with sepsis may be associated with the vascular lesions caused by hypertension complicated with sepsis.

OBJECTIVE To investigate the effects of coptisine on endogenous metabolites in a dextran sulfate sodium(DSS)-in-duced ulcerative colitis(UC)mouse model,and to explore its potential mechanisms of action employing non-targeted metabolomics technology.METHODS SPF-grade male C57BL/6 mice were randomly divided into a control group,a model group,a sulfasalazine group(100 mg·kg-1),and low and high dose groups of coptisine groups(25,50 mg·kg-1).To induce ulcerative colitis(UC),all groups except the control group had free access to a 2.5%DSS solution for 7 days.At the same time,they also received daily intragastric ad-ministration of their corresponding treatments until the 10th day.Body weight changes,stool characteristics,and bloody stool occur-rence were recorded daily,and the disease activity index(DAI)was calculated.After the experiment,colon tissues were collected for pathological examination.Through UPLC-Q-TOF-MS/MS,non-targeted metabolomic analysis was performed to identify differential metabolites,and metabolic pathway enrichment analysis was conducted using the KEGG database.RESULTS Compared to the model group,coptisine significantly ameliorated weight loss,DAI scores,and pathological damage in colon tissues of UC mice(P<0.05,P<0.01).Metabolomic analysis identified 56 differential metabolites,mainly involved in purine metabolism,tryptophan metabo-lism,niacin and nicotinamide metabolism,glutathione metabolism,and the biosynthesis of phenylalanine,tyrosine,and tryptophan.Coptisine intervention significantly reversed the abnormal expression of these metabolites.CONCLUSION Coptisine can markedly improve metabolic disorders in DSS-induced UC mice by modulating multiple key metabolic pathways,thereby exerting a therapeutic effect.

Objective To analyze the research status,hotspots and trends of TCM in the treatment of attention deficit hyperactivity disorder(ADHD).Methods The literature on the treatment of ADHD by TCM were was retrieved from CNKI,VIP,Wanfang Data,and CBM from the establishment of the databases to 7th,Sep.2023.NoteExpress 3.9 was used to manage and remove weight;Excel 2019 was used to draw a line trend chart for the number of published literature.CiteSpace 6.1R.6 software was used to perform co-occurrence and clustering analysis on authors,institutions and keywords,and a visual graph was drawn.Results A total of 1215 articles were included after screening.800 authors were involved,forming research teams with Han Xinmin,Wang Junhong,Ma Rong and Li Yirui as the cores respectively;Nanjing University of Chinese Medicine,Guangzhou University of Chinese Medicine,Beijing University of Chinese Medicine and so on published more papers.High-frequency keywords included clinical efficacy,acupuncture and moxibustion treatment,clinical experience,Chinese materia medica and so on;research frontiers included clinical efficacy,acupuncture and moxibustion treatment,clinical experience,data mining and attention.Conclusion The main research on the treatment of ADHD by TCM includes clinical efficacy,clinical experience,animal experiments and data mining,and relatively stable research teams have been formed,but there is less cooperation between teams and institutions.

Objective:To evaluate the effect of goal-directed fluid therapy (GDFT) on postoperative acute kidney injury (AKI) in elderly patients undergoing long-time abdominal surgery.Methods:The medical records from elderly patients of both sexes, aged ≥ 65 yr, with a duration of operation ≥ 8 h and American Society of Anesthesiologists Physical Status classification Ⅱ or Ⅲ, undergoing elective first abdominal surgery for gastrointestinal tumors at the Shanxi Provincial People′s Hospital from October 1, 2016 to June 30, 2022, were collected from the electronic medical record database. Patients were divided into conventional fluid therapy group (group C) and GDFT group (group G) according to whether GDFT was employed during operation. In group C, blood pressure was maintained ≥90/60 mmHg or mean arterial pressure≥65 mmHg, and urine output more than 30 ml/h. In group G, the stroke volume variation was maintained ≤13%, and cardiac index ≥2.5 L·min -1·m -2. The patient general characteristics, requirement for fluid, urine output, blood loss, requirement for vasoactive agents and abdominal hyperthermic perfusion, and operation time were recorded during operation. The development of AKI within 72 h after operation and development of other complications (pneumonia, anastomotic leakage, surgical site infection, septic shock, arrhythmia) after operation were recorded. The length of hospital stay and 30-day mortality after operation were recorded. Results:A total of 125 patients were included in this study, with 41 patients in group C and 84 patients in group G. Postoperative AKI occurred in 19 patients, with an incidence of 15.2%. Compared with group C, the requirement for colloid, total volume of fluid infused and urine volume were significantly decreased during operation, the requirement for vasoactive agents was increased during operation ( P<0.05), the risk of postoperative AKI was reduced ( OR=0.23, P<0.05), and no significant change was found in the incidence of other postoperative complications, 30-day mortality, and length of hospital stay in group G ( P>0.05). Conclusions:GDFT can reduce the risk of AKI in the elderly patients undergoing long-time abdominal surgery.

Objective : To investigate the effects of immunoglobulin gene superfamily 10 (IGSF10) on prolifera- tion，migration and invasion of lung adenocarcinoma cells． Methods : ioinformatics was applied to study the ex- pression levels of IGSF10 in tumor tissues and normal tissues． Western blot and quantitative real-time PCR ( qPCR) were used to detect the expression level of IGSF10 in lung adenocarcinoma cell lines and normal lung epi- thelial cells．Knockdown of IGSF10，the effect of knockdown of IGSF10 on proliferation，migration and invasion of lung adenocarcinoma A549 cells was examined using cell counting kit-8 ( CCK-8) ，Transwell migration and inva- sion assay，scratch assay and plate cloning assay．The effects of knockdown of IGSF10 on the expression of invasion and migration-related genes in A549 cells were examined by Western blot and qPCR assays. Results : IGSF10 ex- pression in lung adenocarcinoma tissues was lower than that in normal tissues (P ＜0. 05) ．IGSF10 expression in lung adenocarcinoma cell lines was lower than that in lung epithelial cells (P＜0. 05) ．Knockdown of IGSF10 pro- moted the ability of lung adenocarcinoma A549 cells to proliferate ，proliferation ，migration and invasion ( P < 0. 05) ．Knockdown of IGSF10 promoted the expression of regulatory epithelial-mesenchymal transition marker Neu- ral-cadherin (N-cadherin) and key transcription factors Snail family transcriptional repressor 1 (Snail) and Snail family transcriptional repressor 2 (Slug) (P＜0. 05) and inhibited the expression of Epithelial-cadherin (E-cad- herin) (P＜0. 05) ． Conclusion Knockdown of IGSF10 may promote proliferation，migration and invasion of lung adenocarcinoma cells through activation of Snail，Slug / E-cadherin signaling axis，and this result may provide a po- tential new target for clinical diagnosis and treatment of lung adenocarcinoma.

Objective: To evaluate Magnetic Resonance Imaging (MRI) at 3.0T in differential diagnosis of the origin of adenocarcinoma at the junction of the lower uterine segment and endocervix. Methods: 71 patients with adenocarcinoma at the junction of the lower uterine segment and endocervix were retrospectively collected. Pelvic MR examinations, including diffusion-weighted imaging (DWI) and dynamic contrast-enhanced (DCE) sequences, were performed within 2 weeks before surgery. MR images were analyzed and measured by two radiologists, including the location of the tumor center, the enhancement pattern, the anterior and posterior diameters, the left and right diameters, the upper and lower diameters, and the apparent diffusion coefficient (ADC) of the tumor. Immunohistochemical method was used as gold standard in distinguishing cervical adenocarcinoma and uterine adenocarcinoma. Results: The upper and lower diameters of uterine adenocarcinoma were [(5.80±2.31) cm], significantly larger than those of cervical adenocarcinoma [(4.16±2.17) cm, P=0.009]. Using 4.5cm as the best cutoff point value, the sensitivity and specificity in distinguishing uterine adenocarcinoma and cervical adenocarcinoma were 68.4% and 65.4%, respectively. According to the location of tumor center, the sensitivity and specificity were 84.2% and 73.1%, respectively. Using tumor enhancement pattern as the criterion, the sensitivity and specificity of diagnosing uterine adenocarcinoma and cervical adenocarcinoma were 68.4% and 80.8% respectively. Conclusions MRI has certain clinical value in evaluating the origin of adenocarcinoma at the junction of the lower uterine segment and endocervix. The lesions can be diagnosed according to the main location, the characteristics of dynamic enhancement and the growth pattern of the tumor.