In recent years， traditional Chinese medicine （TCM） has achieved significant progress in the treatment of inflammatory bowel disease （IBD）. A comprehensive literature search was conducted covering the period from January 1， 2010， to December 30， 2024， across Chinese databases including China National Knowledge Infrastructure （CNKI）， Wanfang Data， VIP China Science and Technology Journal Database， and the Chinese Biomedical Literature Service System， as well as international databases such as PubMed， Web of Science， and Embase. The clinical applications and mechanistic studies of TCM in IBD were systematically reviewed. The current status of TCM research on the etiology and pathogenesis of IBD， innovative clinical practices， and multimodal therapeutic approaches， including Chinese herbal formulas， single herbs or active compounds， acupuncture， herbal retention enema， and acupoint application， were summarized， together with their synergistic effects when combined with western medical treatments. The development and application of Chinese patent medicines for IBD are undergoing a profound transition from efficacy validation to mechanistic exploration. Mechanistic studies on the effects of TCM in IBD mainly focus on regulating gut microbiota homeostasis， repairing the intestinal mucosal barrier， and modulating intestinal immune balance. Furthermore， future research directions for TCM-based IBD management are proposed， including the establishment of TCM diagnostic and treatment models， expanding integrated applications of external and internal TCM therapies， innovating personalized treatment strategies， and advancing drug development. These efforts aim to provide insights for the standardized and precision-oriented development of TCM in the diagnosis and treatment of IBD.

The personalized patient preference predictor proposed in 2024 has sparked widespread discussion. It mainly integrates machine learning with fine-tuning large language models to extract patients’ medical preferences by training and analyzing patients’ personalized sample data， to achieve better treatment. Combined with the current research situation， this paper pointed out its application dilemma： that is， the risks of inductive and analogical reasoning trigger its technical dilemma in accurate prediction， process explanation， and functional evaluation， ultimately leading to the ethical dilemma of the reduction of subject autonomy. Its solution paths were also clarified， including introducing substantive induction theory and substantive analogy theory to ensure the validity of sample data； implementing technology integration， perspective change， and evaluation system construction to improve the accuracy of prediction； as well as clarifying the priority of human subject status to protect the patient’s subjective autonomy. These showed that the personalized patient preference predictor has important social value and practical significance.

Dendritic cells (DCs) serve as the primary antigen-presenting cells in autoimmune diseases, like rheumatoid arthritis (RA), and exhibit distinct signaling profiles due to antigenic diversity. Type II collagen (CII) has been recognized as an RA-specific antigen; however, little is known about CII-stimulated DCs, limiting the development of RA-specific therapeutic interventions. In this study, we show that CII-stimulated DCs display a preferential gene expression profile associated with migration, offering a new perspective for targeting DC migration in RA treatment. Then, saikosaponin D (SSD) was identified as a compound capable of blocking CII-induced DC migration and effectively ameliorating arthritis. Optineurin (OPTN) is further revealed as a potential SSD target, with Optn deletion impairing CII-pulsed DC migration without affecting maturation. Function analyses uncover that OPTN prevents the proteasomal transport and ubiquitin-dependent degradation of C-C chemokine receptor 7 (CCR7), a pivotal chemokine receptor in DC migration. Optn-deficient DCs exhibit reduced CCR7 expression, leading to slower migration in CII-surrounded environment, thus alleviating arthritis progression. Our findings underscore the significance of antigen-specific DC activation in RA and suggest OPTN is a crucial regulator of CII-specific DC migration. OPTN emerges as a promising drug target for RA, potentially offering significant value for the therapeutic management of RA.

ObjectiveMetabolomics was utilized to investigate the preventive effect of notoginseng total saponins（NTS） on aspirin（acetyl salicylic acid， ASA）-induced small bowel injury in rats. MethodFifty male SD rats were randomly divided into normal and model groups， NTS high-dose and low-dose groups（62.5， 31.25 mg·kg^-1）， and positive drug group（omeprazole 2.08 mg·kg^-1+rebamipide 31.25 mg·kg^-1）， with 10 rats in each group. Except for the normal group， rats in other groups were given ASA enteric-coated pellets 10.41 mg·kg^-1 daily to establish a small intestine injury model. On this basis， each medication group was gavaged daily with the corresponding dose of drug， and the normal group and the model group were gavaged with an equal amount of drinking water. Changes in body mass and fecal characteristics of rats were recorded and scored during the period. After 14 weeks of administration， small intestinal tissues of each group were taken for hematoxylin-eosin（HE） staining， scanning electron microscopy to observe the damage， and the apparent damage of small intestine was scored. Serum from rats in the normal group， the model group， and the NTS high-dose group was taken and analyzed for metabolomics by ultra-performance liquid chromatography-quadrupole-electrostatic field orbitrap high-resolution mass spectrometry（UPLC-Q-Exactive Orbitrap MS）， and the data were processed by multivariate statistical analysis， the potential biomarkers were screened by variable importance in the projection（VIP） value≥1.0， fold change（FC）≥1.5 or ≤0.6 and t-test P<0.05， and pathway enrichment analysis of differential metabolites was performed in conjunction with Human Metabolome Database（HMDB） and Kyoto Encyclopedia of Genes and Genomes（KEGG）. ResultAfter 14 weeks of administration， the average body mass gain of the model group was lower than that of the normal group， and the NTS high-dose group was close to that of the normal group. Compared with the normal group， the fecal character score of rats in the model group was significantly increased（P<0.05）， and compared with the model group， the scores of the positive drug group and the NTS high-dose group were reduced， but the difference was not statistically significant. HE staining and scanning electron microscopy results showed that NTS could significantly improve ASA-induced small intestinal injury， compared with the normal group， the small bowel injury score of the model group was significantly increased（P<0.01）， compared with the model group， the small bowel injury scores of the NTS low and high dose groups were significantly reduced（P<0.05， P<0.01）. Serum metabolomics screened a total of 75 differential metabolites between the normal group and the model group， of which 55 were up-regulated and 20 were down-regulated， 76 differential metabolites between the model group and the NTS groups， of which 14 were up-regulated and 62 were down-regulated. NTS could modulate three differential metabolites（salicylic acid， 3-hydroxybenzoic acid and 4-hydroxybenzoic acid）， which were involved in 3 metabolic pathways， namely， the bile secretion， the biosynthesis of folic acid， and the biosynthesis of phenylalanine， tyrosine and tryptophan. ConclusionNTS can prevent ASA-induced small bowel injury， and the underlying mechanism may be related to the regulation of bile secretion and amino acid metabolic pathways in rats.

Objective: To explore the clinical efficacy of Xiaoshuan enteric-coated capsule (XSECC) in treating cerebral infarction and its potential mechanism of action. Methods: Patients with acute ischemic stroke (AIS) of the qi deficiency and blood stasis type were randomly assigned to the control and observation groups. They were evaluated using the National Institutes of Health Stroke Scale (NIHSS), Activities of Daily Living (ADL), Hachinskilnchemic Scale (HIS), Barthel Index (BI), clinical efficacy scores, and TCM syndrome scores on days 0, 14, 30, and 90. Furthermore, VEGF and BDNF levels were measured on days 30 and 90. Finally, we analyzed the changes in each scale score and vascular neurological factor in both groups. Results: After 14 days of treatment, the difference values in NIHSS, ADL, and BI were higher, and TCM syndrome and clinical efficacy scores were increased in the observation group compared with those of the control group (all P < .05). After 30 days, the NIHSS, ADL, HIS, and TCM syndrome scores were decreased compared with those of the control group, while BI and clinical efficacy scores were increased (all P < .05). After 90 days, the difference value in ADL was higher, and TCM syndrome score was increased in the observation group compared with that of the control group (P = .047, P = .005, respectively). The levels of VEGF and BDNF were higher in the observation group than in the control group on days 14, 30, and 90 (all P < .05). VEGF and BDNF levels on day 0 were associated with prognosis of patients with AIS; therefore, they have a predictive value for the prognosis of acute cerebral infarction. Conclusions XSECC therapy can improve clinical outcomes in patients with acute and recurrent cerebral infarctions. Its mechanism of action may be associated with the secretion of VEGF and BDNF.

Objective:To study the biological role and related mechanism of autophagy in acute lung injury (ALI) of hemorrhagic shock mice.Methods:According to random number table method, wild-type male C57BL/6 mice were divided into control group, ALI group, rapamycin group and 3-methyladenine (3-MA) group, with 8 mice in each group. Light chain 3 (LC3) gene knockout mice with C57BL/6 background were divided into LC3 knockout group and LC3 knockout+ALI group, with 8 mice in each group. Control group, ALI group, LC3 knockout group, LC3 knockout+ALI group were intraperitoneally injected with 2 mL/kg normal saline, rapamycin group was intraperitoneally injected with 3 mg/kg autophagy activator rapamycin, 3-MA group was intraperitoneally injected with 15 mg/kg autophagy inhibitor 3-MA, all of which were given for 3 consecutive days. 2 hours after the last administration, the hemorrhagic shock induced ALI model was established. 24 hours after modeling, the lung index was calculated. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of lung tissue and lung injury score was performed. The expressions of autophagy genes LC3-Ⅱ/LC3-Ⅰ and Beclin-1 in lung tissue were detected by Western blotting. The contents of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and malondialdehyde (MDA) in lung tissue were detected according to the steps of the kit.Results:Compared with the control group, the lung tissue structure was destroyed and exudation increased, lung index, lung injury score, the expressions of LC3-Ⅱ/LC3-Ⅰ, Beclin-1, and the contents of TNF-α, IL-6 and MDA in lung tissue significantly increased in the ALI group. Compared with the ALI group, the structural damage and exudation of lung tissue were reduced in the rapamycin group, lung index, lung injury score and the contents of TNF-α, IL-6 and MDA in lung tissue decreased, while the expressions of LC3-Ⅱ/LC3-Ⅰ and Beclin-1 in lung tissue increased [lung index: (7.56±0.39)% vs. (9.12±0.59)%, lung injury score: 3.04±0.58 vs. 9.32±2.14, TNF-α (ng/mg): 1.85±0.32 vs. 3.51±0.62, IL-6 (ng/mg): 1.61±0.32 vs. 2.52±0.44, MDA (nmol/mg): 1.03±0.16 vs. 1.88±0.24, LC3-Ⅱ/LC3-Ⅰ: 1.21±0.12 vs. 0.39±0.05, Beclin-1/β-actin: 1.10±0.12 vs. 0.58±0.06, all P < 0.05], while lung tissue structure damage was aggravated and exudation was further increased in the 3-MA group, lung index, lung injury score and the contents of TNF-α, IL-6 and MDA in lung tissue increased, the expressions of LC3-Ⅱ/LC3-Ⅰ and Beclin-1 in lung tissue decreased [lung index: (10.44±0.62)% vs. (9.12±0.59)%, lung injury score: 11.59±2.28 vs. 9.32±2.14, TNF-α (ng/mg): 4.77±0.71 vs. 3.51±0.62, IL-6 (ng/mg): 3.44±0.52 vs. 2.52±0.44, MDA (nmol/mg): 2.71±0.42 vs. 1.88±0.24, LC3-Ⅱ/LC3-Ⅰ: 0.25±0.04 vs. 0.39±0.05, Beclin-1/β-actin: 0.21±0.03 vs. 0.58±0.06, all P < 0.05]. Lung index, lung injury score and the contents of TNF-α, IL-6 and MDA in lung tissue of LC3 knockout ALI mice were higher than those of wild-type ALI mice [lung index: (10.44±0.75)% vs. (9.12±0.59)%, lung injury score: 12.41±2.86 vs. 9.32±2.14, TNF-α (ng/mg): 4.85±0.72 vs. 3.51±0.62, IL-6 (ng/mg): 3.28±0.51 vs. 2.52±0.44, MDA (nmol/mg): 2.75±0.41 vs. 1.88±0.24, all P < 0.05]. Conclusion:Autophagy plays a protective role in ALI of hemorrhagic shock mice, and the related molecular mechanism is the inhibition of inflammatory response and oxidative stress response.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.

AIM:To investigate the inhibitory effect of the"decoction for soothing liver and removing stasis and toxicity(SGQYJDF)"on hepatocellular carcinoma(HCC)proliferation in nude mice by inducing ferroptosis via the tumor protein 53(p53)/solute carrier family 7 member 11(SLC7A11/xCT)/glutathione peroxidase 4(GPX4)pathway.METHODS:An ectopic subcutaneous tumor model was established by injecting SK-Hep-1 cells subcutaneously into the right axilla of nude mice.Upon formation of tumor,the mice were randomly divided into five groups(i.e.,control group,low-,medium-and high-dose SGQYJDF groups and medium-dose SGQYJDF plus Sorafenib group).Each group of mice was orally administered with the corresponding therapy for 14 consecutive days,during which the tumor size was observed regularly.At the end of treatment,the tumor growth inhibition rate was calculated based on tumor mass,and histopatho-logical changes were observed by HE staining.Then,the levels of malondialdehyde(MDA),glutathione(GSH)and fer-rous ions(Fe2+)were detected by colorimetric assays.The expression of the proliferation markers Ki-67 and GPX4 was de-tected by immunohistochemistry(IHC).The expression of p53 and xCT was detected by Immunofluorescence(IF).And the expression of p53,xCT and GPX4 was determined by Western blot.RESULTS:(1)SGQYJDF was found to dose-de-pendently decrease tumor volume(P＜0.01)and inhibit tumor mass growth(P＜0.01),and meanwhile,reduce the per-centage of Ki-67-positive cells(P＜0.01)and their proliferation ability in tumor tissues,as compared to the control group.(2)In terms of Ferroptosis-related indicators,SGQYJDF was found to dose-dependently increase the levels of Fe2+ and MDA but decrease the level of GSH in tumor tissues(P＜0.01),as compared to the control group.(3)In terms of protein expression,SGQYJDF was found to dose-dependently upregulate the expression of p53(P＜0.05)but inhibit the expres-sion of xCT(P＜0.05)and GPX4(P＜0.01).Notably,medium-dose SGQYJDF plus sorafenib showed a stronger effect than high-dose SGQYJDF.CONCLUSION:Our findings suggest that SGQYJDF can induce Ferroptosis to inhibit the proliferation of subcutaneously transplanted tumor tissues in nude mice by upregulating the expression of p53,and inhibit-ing the expression of xCT and GPX4.

Objective:To evaluate the effect of dexmedetomidine-based anesthesia on cerebral oxygen saturation in the patients undergoing total laparoscopic hysterectomy.Methods:Fifty American Society of Anesthesiologists Physical Status classificationⅠorⅡpatients, aged 20-64 yr, undergoing elective total laparoscopic hysterectomy, were divided into 2 groups ( n=25 each) using a random number table method: conventional group (C group) and dexmedetomidine group (D group). Bilateral regoinal oxygen saturation (rSO 2) was monitored using a cerebral oxygen saturation monitor. In D group, dexmedetomidine was intravenously infused as a bolus of 0.5 μg/kg before anesthesia induction, and 10 min later dexmedetomidine was then given by an infusion of 0.5 μg·kg -1·h -1 until 30 min before the end of operation. The equal volume of normal saline was given instead in C group. The remaining anesthesia regimen was the same in two groups. The maximum (LrSO 2max, RrSO 2max) and minimum (LrSO 2min, RrSO 2min) of bilateral rSO 2 were recorded from entry to 2 min after induction (D 1), from >2 min after induction to completion of tracheal intubation (D 2), from completion of tracheal intubation to the end of skin incision (D 3), from skin incision to completion of pneumoperitoneum (D 4), from pneumoperitoneum to completion of Trendelenburg position (D 5), within 20 min of Trendelenburg position (D 6), >20-40 min of Trendelenburg position (D 7), >40-60 min of Trendelenburg position (D 8), and from >60 min of Trendelenburg position to 10 min after return to supine position (D 9). The occurrence of 60% baseline value 0.05). Compared with C group, the LrSO 2min, LrSO 2max, RrSO 2min, and RrSO 2max were significantly increased in D 4-D 8 periods in D group ( P<0.05). No bilateral rSO 2 <75% baseline value was found in group D. Conclusions:Dexmetomidine-based anesthesia can elevate intraoperative rSO 2 in the patients undergoing total laparoscopic hysterectomy.

Objective:To detect the expression of long non-coding RNA (LncRNA) ARAP1-AS1 in pancreatic cancer, and to preliminarily explore its effects on the biological behaviors of proliferation, apoptosis, migration and invasion of pancreatic cancer cell.Methods:The pancreatic cancer tissue specimens and corresponding paracancerous tissue specimens of 25 patients were collected, and the expression of ARAP1-AS1 was detected by qPCR. Human pancreatic cancer cell line PANC-1 was cultured in vitro and divided into control group, siRNA-control group (transfected with siRNA control sequence), knockout group (transfected with ARAP1-AS1 siRNA), pcDNA3.1-control group (transfected with pcDNA3.1) and overexpression group (transfected with pcDNA3.1-ARAP1-AS1), qPCR method was used to detect the transfection efficiency, CCK-8 method was used to detect the cell proliferation ability, flow cytometry was used to detect the cell apoptosis, scratch test was used to detect the cell migration ability, Transwell method was used to detect the cell invasion ability, Western blot (WB) method was used to detect the expression of proliferating cell nuclear antigen (PCNA), B lymphoma-2 protein (Bcl-2), Bcl-2 related X protein (Bax), matrix metalloproteinase-9 (MMP-9) proteins.Results:The expression level of ARAP1-AS1 in pancreatic cancer tissues was significantly higher than that in adjacent tissues (2.26±0.13 vs 1.00±0.00) ( P<0.05). Compared with the siRNA-control group, the ARAP1-AS1 level (1.01±0.02 vs 0.29±0.03), PCNA, Bcl-2, MMP-9 protein levels, cell OD value (0.57±0.05 vs 0.23±0.03), scratch healing rate (78.53±7.02 vs 48.60±5.26), and number of invasions (229.63±22.59 vs 104.25±15.04) in PANC-1 cells of the knockout group were significantly reduced ( P<0.05), the Bax protein level and the apoptosis rate (4.52±0.42 vs 32.40±1.84) were significantly increased ( P<0.05). Compared with the pcDNA3.1-control group, the ARAP1-AS1 level (1.02±0.03 vs 2.06±0.08), PCNA, Bcl-2, MMP-9 protein levels, cell OD value (0.57±0.05 vs 0.90±0.08), scratch healing rate (77.65±6.67 vs 91.22±7.34), and number of invasions (225.34±19.65 vs 327.50±25.40) in PANC-1 cells of the overexpression group were significantly increased ( P<0.05), the Bax protein level and the apoptosis rate (4.58±0.48 vs 2.29±0.24) were significantly reduced ( P<0.05) . Conclusion:LncRNA ARAP1-AS1 is highly expressed in pancreatic cancer, which can promote the proliferation, migration and invasion of pancreatic cancer cells PANC-1, and reduce cell apoptosis.