OBJECTIVE To investigate the effect of astragaloside Ⅳ（AST） on the injury of arterial endothelial tissue in rats with intracranial aneurysms （IA）， and to explore its mechanism of action based on the nuclear factor κB （NF-κB）/nucleotide- binding domain leucine-rich repeat and pyrin domain-containing protein 3 （NLRP3） signaling pathway. METHODS Rats were divided into Sham group （intragastric administration and intraperitoneal injection of the same volume of normal saline）， IA group （intragastric administration and intraperitoneal injection of the same volume of normal saline）， AST low-dose group （AST-L group， intragastric administration of 40 mg/kg AST）， AST high-dose group （AST-H group， intragastric administration of 80 mg/kg AST）， AST-H+HY-N2485 group [intragastric administration of 80 mg/kg AST and intraperitoneal injection of 25 mg/kg HY-N2485 （activator of NF-κB/NLRP3 signaling pathway）]. They were given relevant medicine， once a day， for 8 consecutive weeks. After last medication， the levels of inflammatory factors [serum tumor necrosis factor-α （TNF-α）， interleukin-18 （IL-18）， IL-6] and vascular endothelial growth factor （VEGF） and endothelin （ET） were detected； the morphology of IA was observed； the expressions of von Willebrand factor （vWF）， vascular cell adhesion molecule-1 （VCAM-1）， endothelial nitric oxide synthase （eNOS）， and NF-κB/NLRP3 pathway related proteins in vascular tissue were also determined. RESULTS Compared with the Sham group， the basilar arterial ring of rats in the IA group had obvious protrusions， and the arterial vascular endothelial cells were significantly damaged. The levels of inflammatory factors， VEGF and ET in serum， as well as the expression levels of vWF， VCAM-1 and NLRP3 proteins and the phosphorylation level of NF-κB protein in vascular tissues were increased significantly （P＜ 0.05）. Aneurysms and ruptures of the internal elastic layer were significantly increased （P＜0.05）， while the expression level of eNOS protein was significantly decreased （P＜0.05）. Compared with IA group， the morphology of IA and the levels of above indexes were all improved significantly in AST-L and AST-H groups （P＜0.05），and the improvement in the AST-H group was more significant than that in the AST-L group （P＜0.05）； HY-N2485 could attenuate the improvement effect of AST on vascular endothelial tissue damage in IA rats （P＜0.05）. CONCLUSIONS AST may inhibit the expression of inflammatory factors， alleviate inflammation and vascular endothelial tissue damage in IA rats by inhibiting NF- κB/NLRP3 signaling pathway，thereby inhibiting the formation of IA. active_999@sina.com

Since the introduction of monoamine oxidase and monoamine neurotransmitter reuptake inhibitors for the treatment of major depression in the 1950s, their strengths and limitations have been fully and accurately determined. Therefore, the development of novel drugs for the treatment of depression has become a priority for researchers who aim to address treatment resistance and improve patient outcomes. Panax ginseng C. A. Mey (P. ginseng, Ren Shen) is a Chinese medicine used to treat neurological and psychiatric disorders. Numerous studies have shown that ginsenosides, the primary active constituents of P. ginseng, exert a wide range of effects on the central nervous system. Recent studies have demonstrated that ginsenosides possess significant antidepressant properties in animal models. Ginsenosides, such as Rb1 and Rg1, are steroidal molecules, and steroid derivatives have been successfully used in anesthesia, epilepsy, and more recently, postpartum depression treatment. Based on these findings, ginsenosides are promising candidates for the treatment of depression. This raises the following question: What are the prospects of using ginsenosides to treat depression? To gain a clearer understanding, this review provides a comprehensive analysis of recent research on the antidepressant potential of ginsenosides, along with insights and suggestions for future development in this field.

BackgroundIn schizophrenia， a subset of patients may progress to treatment-resistant schizophrenia owing to inadequate response to standard antipsychotic therapies， resulting in profound impairments in cognitive and social functioning alongside a cumulative burden of adverse drug reactions during the prolonged treatment. Currently， evidence supporting the use of blonanserin for treatment-resistant schizophrenia remains limited. ObjectiveTo investigate the efficacy and safety of blonanserin in the treatment of treatment-resistant schizophrenia， so as to provide references for clinical management of this condition. MethodsA total of 43 inpatients fulfilling the International Classification of Diseases， tenth edition （ICD-10） diagnostic criteria for treatment-resistant schizophrenia were consecutively recruited from Taiyuan Psychiatric Hospital from September 2024 to January 2025. Subjects were assigned to either the study group （n=21） or the control group （n=22） using the random number table method. The study group received blonanserin at a daily dosage ranging from 8 to 24 mg， while the control group was administered amisulpride at a daily dosage from 400 to 1 200 mg. At baseline and at the end of the 4^th and 8^th week of treatment， the Positive and Negative Symptom Scale （PANSS） and the Personal and Social Performance scale （PSP） were used to access patients' psychotic symptoms and social functioning， respectively. Cognitive function was evaluated using the Hopkins Verbal Learning Test （HVLT）， the Stroop Color-Word Test （SCWT）， the Trail Making Test （TMT）， the Digit Span Test （DST）， and the Digit Symbol Substitution Test （DSST）. During the treatment process， treatment-related adverse reactions were recorded between two groups. ResultsSignificant time effects were found in PANSS total scores， as well as its positive symptom， negative symptom， and general psychopathological subscale scores （F=186.505， 149.318， 135.671， 416.744， P<0.01）. The group-by-time interaction effect was significant in PANSS total scores and general psychopathological subscale scores （F=3.483， 4.318， P<0.05）. At the end of the 8^th week， the study group exhibited lower general psychopathological subscale scores and the PANSS total scores compared to the control group， with statistically significant differences （t=-2.106， -2.429， P<0.05）. Significant group effects were detected in HVLT scores， Stroop word scores and Stroop color scores （F=6.720， 7.921， 11.383， P<0.05 or 0.01）. The group-by-time interaction effect for Stroop word scores， Stroop interference scores， TMT scores and DSST scores were statistically significant （F=3.571， 4.095， 3.463， 37.000， P<0.05 or 0.01）. At the end of the 8^th week， the DSST score of the study group was higher than that of the control group （t=2.074， P<0.05）. For PSP scores， significant time effect， group effect and group-by-time interaction effect were all observed （F=433.710， 4.463， 10.491， P<0.05 or 0.01）. At the end of the 8^th week， the study group reported higher PSP score compared to the control group， with a statistically significant difference （t=3.451， P<0.05）. No significant difference in the incidence of adverse reactions was exhibited between the two groups （P>0.05）. ConclusionBlonanserin demonstrates efficacy comparable to amisulpride in ameliorating positive and negative symptoms in patients with treatment-resistant schizophrenia. Notably， blonanserin exhibits a superior efficacy to amisulpride in improving general psychopathological symptoms， cognitive and social functioning， while both agents show comparable safety profiles. （www.chictr.org.cn number： ChiCTR2400094222）

OBJECTIVE To establish HPLC fingerprint of Shuangdong capsules， and to study the spectral effect relationship of its anti-inflammatory effect. METHODS The fingerprints of 15 batches of Shuangdong capsules were established by HPLC，and the similarity evaluation was carried out； the foot swelling model was established to investigate the anti-inflammatory activity of Shuangdong capsules. The gray correlation analysis method was used to construct the spectral effect relationship for the anti- inflammatory effect of Shuangdong capsules using the swelling rate of rat foot and the levels of malondialdehyde （MDA）， superoxide dismutase （SOD）， prostaglandin E2 （PGE2）， interleukin-6 （IL-6）， IL-8， IL-1β and tumor necrosis factor-α （TNF-α） in right hindfoot tissues as the pharmacodynamic indexes of anti-inflammatory effects. RESULTS Overall 15 batches of Shuangdong capsules identified 20 common peaks， the similarities were all greater than 0.97， and a total of 8 chromatographic peaks were identified. According to the gray correlation analysis， the correlation degrees between the peak area and the foot swelling rate and the levels of MDA， SOD， PGE2， IL-6， IL-8， IL-1β and TNF-α in 15 batches of Shuangdong capsules were 0.621 1- 0.783 5， 0.564 3-0.827 9， 0.581 0-0.845 3， 0.564 9-0.855 0， 0.583 1-0.856 4， 0.576 5-0.863 5， 0.564 1-0.838 0 and 0.572 5- 0.851 3， respectively. Among them， the chemical components represented by peak 4 （geniposidic acid）， peak 10 （chlorogenic acid） and the chemical composition represented by peak 2 were strongly correlated with anti-inflammatory efficacy indicators. CONCLUSIONS In this study， HPLC fingerprints of 15 batches of Shuangdong capsules were successfully established. Among them， geniposidic acid， chlorogenic acid may be its anti-inflammatory ingredients.

Objectives: To investigate whether the protective actions of ginsenoside Rb1 (Rb1) on astrocytes are mediated through the Gs-type G-protein-coupled receptor (GPCR-Gs). Methods: Primary astrocyte cultures derived from neonatal mouse brain were used. Astrocyte injury was induced via oxygen-glucose deprivation/re-oxygenation (OGD/R). Cell morphology, viability, lactate dehydrogenase (LDH) leakage, apoptosis, glutamate uptake, and brain-derived neurotrophic factor (BDNF) secretion were assessed to gauge cell survival and functionality. Western blot was used to investigate the cyclic adenosine monophosphate (cAMP) and protein kinase B (Akt) signaling pathways. GPCR-Gs-specific inhibitors and molecular docking were used to identify target receptors. Results: Rb1 at concentrations ranging from 0.8 to 5 μM did not significantly affect the viability, glutamate uptake, or BDNF secretion in normal astrocytes. OGD/R reduced astrocyte viability, increasing their LDH leakage and apoptosis rate. It also decreased glutamate uptake and BDNF secretion by these cells. Rb1 had protective effects of astrocytes challenged by OGD/R, by improving viability, reducing apoptosis, and enhancing glutamate uptake and BDNF secretion. Additionally, Rb1 activated the cAMP and Akt pathways in these cells. When the GPCR-Gs inhibitor NF449 was introduced, the protective effects of Rb1 completely disappeared, and its activation of cAMP and Akt signaling pathways was significantly inhibited. Conclusion Rb1 protects against astrocytes from OGD/R-induced injury through GPCR-Gs mediation.

ObjectiveTo observe the neuroprotective effects of ginsenoside Rb₁ on lipopolysaccharide （LPS）-induced neuroinflammation in mice and to preliminarily investigate its mechanism of action. MethodSeventy ICR mice were randomly divided into blank group， model group， dexamethasone sodium phosphate injection group， and low-dose， high-dose ginsenoside Rb₁ groups， with 14 mice in each group. A mouse brain neuroinflammation model was prepared using the LPS dose escalation method， starting with a dose of 1 mg·kg^-1 and administered via intraperitoneal injection every 48 h （every other morning）. Each subsequent dose increased by 2 mg·kg^-1， for a total of 7 injections， culminating in a final dose of 13 mg·kg^-1. The dexamethasone sodium phosphate injection group received an intraperitoneal injection at 5 mg·kg^-1·d^-1. The low-dose and high-dose ginsenoside Rb₁ groups were given intraperitoneal injections at 10 mg·kg^-1·d^-1 and 20 mg·kg^-1·d^-1， respectively， while the blank and model groups received the same volume of normal saline for 14 days. The behavioral activity of LPS mice was observed， anxiety-like behavior was assessed using the Y-maze and elevated plus maze， and brain levels of monocyte chemoattractant protein-1 （MCP-1）， tumor necrosis factor-α （TNF-α）， and interleukin-1β （IL-1β） were measured by enzyme-linked immunosorbent assay （ELISA）. Neuronal damage of microglia， and the activation status of microglia and astrocytes in the brain were assessed using immunofluorescence staining. The protein expression of phosphatidylinositol-3-kinase （PI3K）， protein kinase B （Akt）， and nuclear factor-κB （NF-κB） in mouse brain were detected by Western blot. ResultCompared with the blank group， the model group showed significantly increased anxiety-like behavior in the Y-maze and elevated plus maze （P<0.05， P<0.01）， significantly elevated levels of MCP-1， TNF-α， and IL-1β in the brain （P<0.01）， a significant decrease in the number of neuronal positive cells in the somatosensory cortex and hippocampus CA1 region （P<0.01）， significant activation of microglia and astrocytes （P<0.01）， and a significant increase in the expression of phosphorylated PI3K， Akt， and NF-κB proteins （P<0.01）. Compared with the model group， the ginsenoside Rb₁ low-dose and high-dose groups showed significantly reduced anxiety-like behavior in the Y-maze and elevated plus maze （P<0.05， P<0.01）， significantly decreased levels of MCP-1， TNF-α， and IL-1β in the brain （P<0.01）， a significant increase in the number of neuronal positive cells in the somatosensory cortex and hippocampus CA1 region （P<0.01）， significant inhibition of microglia and astrocyte activation （P<0.05， P<0.01）， and a significant decrease in the expression of phosphorylated PI3K， Akt， and NF-κB proteins （P<0.05， P<0.01）. ConclusionGinsenoside Rb₁ has neuroprotective effects on LPS-induced inflammation in mice， which may involve the regulation of the PI3K/Akt signaling pathway.

Objective:To design a fully integrated multi-channel implantable brain-computer interface electrical stimulation system.Methods:The human-computer interaction interface of the upper computer was set by users, and the data was packaged via a self-built protocol. When parameters were transmitted to the field programmable gate array (FPGA) chip through the Bluetooth module, the stimulation chip was controlled after the parameter analysis was completed. Eventually the user-set current stimulation was output. To verify the system feasibility, the accuracy of the single-channel stimulation waveform, the multi-channel output capability, and the adjustable range of the parameter were tested separately.Results:It realized 16 channels of time-sharing differential stimulation current output, the output stimulation current waveform was dual-phase equal-width pulse, the amplitude ranged within 4~1 000 μA, the pulse single-phase width range was 10~1 000 μs, the cycle time was 1~1 000 ms, thus the current parameters could be accurately adjusted.Conclusions:A fully integrated multi-channel implantable brain-computer interface electrical stimulation system was completed.

Objective:To explore influencing factors of poor prognosis in patients with severe trauma,and to analyze distribu-tion characteristics of adverse prognostic factors in patients with different early peripheral blood lymphocyte levels based on potential categories.Methods:A total of 174 patients with severe trauma treated in Mianyang Central Hospital from September 2020 to Septem-ber 2022 were selected.According to condition of massive blood transfusion or death within 24 hours after admission,patients were divided into:good prognosis group(n=136)and poor prognosis group(n=38).Clinical data of two groups were compared,multivariate Logistic regression analysis was used to analyze factors affecting poor prognosis,and cluster analysis and potential classification were used to analyze distribution characteristics of adverse prognostic factors in patients with different early peripheral blood lymphocyte levels.Results:Multivariate Logistic regression analysis results showed decrease of Glasgow coma scale(GCS),prolongation of acti-vated partial thromboplastin time(APTT),increase of D-dimer(D-D),decrease of fibrinogen(Fib),increase of fibrinogen degrada-tion products(FDP),increase of neutrophil/lymphocyte ratio(NLR)and decrease of lymphocyte level were factors influencing poor prognosis(P<0.05).Cluster analysis results showed that risk of poor prognosis was obviously clustered,and patients could be divided into poor prognosis high risk group(lymphocyte level≤0.90×109 L-1,n=72)and low risk group(lymphocyte level>0.90×109 L-1,n=102).Incidence of poor prognosis in high risk group[33.33%(24/72)]was significantly higher than that in low risk group[13.73%(14/102)](P<0.05).Potential category analysis results showed that there were three potential category distribution patterns in poor prognosis high risk group and low risk group.Proportion of"unelevated distribution of D-D in patients with low GCS score"in high risk group was significantly higher than that in low risk group,and proportion of"distribution of less risk factors"in high risk group was sig-nificantly lower than that in low risk group(P<0.05).There was no significant difference in proportion of elevated D-D distribution in patients with low GCS score between two groups(P>0.05).Conclusion:Decrease of GCS score,prolongation of APTT and increase of D-D are all associated with poor prognosis in patients with severe trauma.Patients with lymphocyte level≤0.90×109 L-1 have a higher risk of poor prognosis,and main influencing factors are"non-elevated distribution of D-D in patients with low GCS score".

Objective To investigate the longitudinal changes in left ventricular(LV)structure and function after bariatric surgery in obese individuals and their relationship with preoperative left ventricular ejection fraction(LVEF)by cardiac magnetic resonance(CMR)imaging.Methods We prospectively enrolled 75 obese subjects scheduled for laparoscopic sleeve gastrectomy and 46 age and sex-matched healthy controls(the control group).All subjects underwent CMR examination to obtain LV structural parameters,LVEF,and strain parameters.According to their preoperative LVEF,the obese subjects were divided into two obesity groups,including the group of patients with LVEF≥60％(n=43)and the group of patients with 50％≤LVEF＜60％(n=32).LV structural and functional differences between the control group and the two obesity groups were compared.Eventually,38 obese subjects completed the CMR follow-up at 1 month and 12 months after bariatric surgery.The longitudinal changes in LV structure and function after surgery in the LVEF ≥ 60％(n=20)group and the 50％≤LVEF＜60％group(n=18)were compared.Results Before bariatric surgery,the global longitudinal strain was significantly lower in the LVEF ≥ 60％group than that in the control group([-18.36±1.86]％vs.[-19.50±1.53]％,P＜0.05).The global radial([27.70±3.52]％vs.[34.44±4.11]％,P＜0.05),circumferential([-17.35±1.46]％vs.[-19.85±1.42]％,P＜0.05),and longitudinal([-16.22±1.81]％vs.[-19.50±1.53]％,P＜0.05)strain in the 50％≤ LVEF＜60％group was significantly lower than that in the control group.At 12 months after bariatric surgery,the global radial([32.52±7.84]％vs.[30.92±4.27]％,P＞0.05),circumferential([-19.02±2.42]％vs.[-18.63±1.49]％,P＞0.05),and longitudinal([-18.18±2.06]％vs.[-17.78±1.66]％,P＞0.05)strain in the LVEF≥60％group showed no significant difference compared with the baseline findings.In the 50％≤ LVEF＜60％group,the global radial([32.73±5.86]％vs.[26.83±4.85]％,P＜0.05)and circumferential([-19.10±2.00]％vs.[-16.91±2.09]％,P＜0.05)strain was significantly higher than that before surgery.Conclusion LV remodeling is reversed after bariatric surgery in obese subjects,and the longitudinal changes in LV structure and function vary with the preoperative LVEF.

BACKGROUND: Weather conditions are a possible contributing factor to age-related macular degeneration (AMD), a leading cause of irreversible loss of vision. The present study evaluated the joint effects of meteorological factors and fine particulate matter (PM_2.5) on AMD. METHODS: Data was extracted from a national cross-sectional survey conducted across 10 provinces in rural China. A total of 36,081 participants aged 40 and older were recruited. AMD was diagnosed clinically by slit-lamp ophthalmoscopy, fundus photography, and spectral domain optical coherence tomography (OCT). Meteorological data were calculated by European Centre for Medium-Range Weather Forecasts (ECMWF) reanalysis and were matched to participants' home addresses by latitude and longitude. Participants' individual PM_2.5 exposure concentrations were calculated by a satellite-based model at a 1-km resolution level. Multivariable-adjusted logistic regression models paired with interaction analysis were performed to investigate the joint effects of meteorological factors and PM_2.5 on AMD. RESULTS: The prevalence of AMD in the study population was 2.6% (95% CI 2.42-2.76%). The average annual PM_2.5 level during the study period was 63.1 ± 15.3 µg/m³. A significant positive association was detected between AMD and PM_2.5 level, temperature (T), and relative humidity (RH), in both the independent and the combined effect models. For PM_2.5, compared with the lowest quartile, the odds ratios (ORs) with 95% confidence intervals (CIs) across increasing quartiles were 0.828 (0.674,1.018), 1.105 (0.799,1.528), and 2.602 (1.516,4.468). Positive associations were observed between AMD and temperature, with ORs (95% CI) of 1.625 (1.059,2.494), 1.619 (1.026,2.553), and 3.276 (1.841,5.830), across increasing quartiles. In the interaction analysis, the estimated relative excess risk due to interaction (RERI) and the attributable proportion (AP) for combined atmospheric pressure and PM_2.5 was 0.864 (0.586,1.141) and 1.180 (0.768,1.592), respectively, indicating a synergistic effect between PM_2.5 and atmospheric pressure. CONCLUSIONS This study is among the first to characterize the coordinated effects of meteorological factors and PM_2.5 on AMD. The findings warrant further investigation to elucidate the relationship between ambient environment and AMD.
Humans ; Adult ; Middle Aged ; Cross-Sectional Studies ; Air Pollutants/analysis* ; Particulate Matter/analysis* ; China/epidemiology* ; Macular Degeneration/etiology* ; Meteorological Concepts