Objective: To systematically evaluate the clinical efficacy of topical preparations of Mongolian medicine Manggari hot compress therapy (hereafter referred to as Manggari hot compress therapy) in treating cervical spondylotic radiculopathy (CSR) and explore the possible pharmacological material basis in the formula, providing evidence for the clinical application of Mongolian medicine in the treatment of CSR. Methods: The clinical trial employed a randomized, controlled, open-label, and outcome-assessor-blinded design. The CSR patients who were treated at the Department of Traditional Therapeutics Outpatient Clinic, Xilinguole Meng Mongolian General Hospital between July 1, 2024 and August 31, 2025, were enrolled. They were randomly assigned to three groups: an oral control group (administration of oral administration of mecobalamin tablets combined with cervical electric traction), an experimental group (Manggari external hot compress), and a patch control group (flurbiprofen gel plaster). The intervention lasted two weeks. Before and after treatment, the following subjective indicators were recorded: Mongolian Medicine Syndrome (MMS) score, Visual Analog Scale (VAS) score, Northwick Park Neck Pain Questionnaire (NPQ) score, and tongue morphology. Serum levels of inflammatory markers [tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β)] and oxidative stress markers [malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, and glutathione peroxidase (GSH-Px) activity] were measured using enzyme-linked immunosorbent assay (ELISA). Overall therapeutic efficacy was evaluated. One month after treatment completion, a follow-up assessment was conducted, and the MMS, VAS, and NPQ scores were recorded again for all patients. For the pharmacological substance exploration, ultra-high-performance liquid chromatography-Q-exactive orbitrap-mass (UHPLC-QE-MS) was employed to analyze blood-absorbed prototype components of Manggari, under both positive and negative ion modes. The targeting relationship between the core active compounds and the target protein was validated using molecular docking. Results: This study ultimately included 90 patients with CSR for analysis. Baseline characteristics showed no statistically significant differences among the three groups (P > 0.05). (i) Symptom scores. After treatment, the MMS, VAS, and NPQ scores decreased significantly from baseline in all three groups (P < 0.001). At follow-up, there was no significant difference in MMS, VAS, and NPQ scores of the experimental group compared with those at the end of the treatment (P > 0.05). After treatment, the experimental group showed significantly greater reductions in MMS, VAS, and NPQ scores than oral control and patch control groups (P < 0.001). At follow-up, these differences remained significant (P < 0.001). (ii) Inflammatory and oxidative stress markers. After treatment, serum levels of TNF-α, IL-6, and IL-1β, and MDA activity decreased significantly from baseline in all three groups (P < 0.001), and SOD content and GSH-Px activity increased significantly from baseline (P < 0.05). After treatment, the experimental group had significantly lower serum levels of TNF-α, IL-6, and IL-1β than oral and patch control groups. Additionally, it exhibited lower MDA activity and higher SOD content and GSH-Px activity compared with the two control groups. (P < 0.05). (iii) Overall efficacy. The total effective rate was 93.33% in the experimental group, 86.66% in the oral control group, and 83.33% in the patch control group. (iv) Pharmacological substance analysis. A total of 152 compounds were identified in the blood-absorbed components of Manggari. Among them, the core compounds—4-hydroxycoumarin, N-methylanthranilic acid, genistein, and ginsenoside-Rk1—showed binding energies to the key target proteins TNF-α and IL-1β range from − 4.7 to − 7.1 kcal/mol, with the majority of the binding energies being below − 5.0 kcal/mol, suggesting that it generally has a good binding affinity. Conclusion Mongolian medicine hot compress therapy effectively modulates inflammatory and oxidative stress responses through the combined action of its thermal effects and active pharmaceutical ingredients Manggari. It inhibits cervical nerve root inflammation and alleviates radicular pain, improving clinical symptoms, reducing pain severity, and alleviating neck functional disability.

Background/Aims: Acetyl coenzyme A (acetyl-CoA) is one of the most essential metabolites in cell metabolism but its function and concentration in hepatocellular carcinoma (HCC) remain elusive and controversial. Methods: A comprehensive analysis of acetyl-CoA levels and acetyl-CoA synthetase 2 (ACSS2) expression across a range of samples, including patient specimens from both hepatitis B virus (HBV) positive and HBV negative HCC individuals, HBV-transgenic mouse HCC models, and multiple cell lines. Furthermore, to evaluate the functional significance of ACSS2 in HBV-related HCC, we implemented both genetic and pharmacological inhibition strategies targeting ACSS2. Molecular mechanism and mitophagy assessment were revealed by cleavage under target and tagmentation sequencing, RNA sequencing, bioinformatic analyses, transmission electron microscopy and JC-1 staining. Results: Our study revealed a distinct metabolic signature of HBV-related HCC, marked by elevated acetyl-CoA, which was driven by ACSS2. ACSS2 was upregulated by the carbohydrate response element-binding protein in HBV-related HCC. Furthermore, ACSS2 improved tumor cell proliferation, an effect that was dependent on its enzymatic activity. Mechanistically, ACSS2-induced acetyl-CoA accumulation activated voltage-dependent anion channels 1 transcription through increased H3K27ac occupancy, which subsequently promoted mitophagy and HBV-related HCC tumorigenesis. Notably, targeting ACSS2 by depletion or inhibition with a catalytic inhibitor significantly suppressed tumor growth. Conclusions These findings not only illustrate the interplay between metabolic reprogramming, epigenetic modification, and tumorigenesis in the context of HBV infection, but also highlight ACSS2 as a novel metabolic vulnerability in HBV-related HCC. Therefore, targeting ACSS2 could be a novel strategy against HBV-related HCC.

Objective To evaluate the feasibility and efficacy of the three-guidewire technique for retrograde stent placement in the treatment of ureteral mucosal sleeve avulsion (UMSA). Methods A retrospective analysis was conducted on the clinical data of 12 patients with UMSA secondary to ureteroscopic lithotripsy for ureteral calculi in our hospital during Jul. 2010 and Oct. 2023. The three-guidewire technique was employed for retrograde stent placement during the procedure. A secondary ureteroscopic lithotripsy was performed one month postoperatively.Results Double-J stent was successfully placed in all 12 patients, with a mean stent insertion time of 23.3(16-30)minutes. No intraoperative exacerbation of mucosal avulsion occurred. One patient was lost to follow-up. At the one-month postoperative ureteroscopic examination and lithotripsy, 81.8% (9/11) cases exhibited unobstructed ureters, while 18.2%(2/11) developed annular membranous strictures, which were resolved following dilation. During subsequent follow-up, the postoperative creatinine level after double-J stent removal showed a mild decrease compared to the preoperative level [87.9(72-100)μmol/L vs. 90.1(69-108)μmol/L]. Up to 90.9%(10/11) patients remained free of hydronephrosis, with only 1 case (9.1%) requiring laparoscopic ureterovesical reimplantation for hydronephrosis 4 months postoperatively. Conclusion The three-guidewire technique for retrograde stent placement in the treatment of UMSA demonstrates strong operability, high success rates, favorable outcomes, and a low incidence of ureteral stricture, which warrant wide clinical promotion.

ObjectiveTo evaluate the comparative clinical outcomes of zero-profile interbody fusion （Zero-P） and traditional anterior cervical discectomy and fusion with titanium plate （ACDF-plate） for three-level cervical spondylosis， providing a reference to optimize surgical strategies for three-level cervical spondylosis. MethodsIn this retrospective comparative study， 113 patients were included and assigned to either the Zero-P group （n=51） or the ACDF-plate group （n=62） according to their surgical approaches. Clinical outcomes were evaluated and compared between the two groups using operative time， intraoperative blood loss， length of hospital stay， visual analog scale （VAS） scores， cervical range of motion （ROM）， neck disability index （NDI）， Cervical Disability Index （CDI）， Japanese orthopaedic association （JOA） scores， and postoperative complication rates. ResultsCompared with the ACDF-plate group， the Zero-P group had a shorter operative time and less intraoperative blood loss （P<0.05）； the neck pain VAS score was lower on the 1st day and 1st week after surgery （P<0.05）； the cervical flexion range of motion was higher at 1 month after surgery （P<0.05）； the JOA score was higher at 3 months after surgery， while the NDI and CDI scores were lower （P<0.05）； the total incidence of complications （11.76%） was significantly lower than that in the plate fixation group （35.48%）， and the incidence of neck foreign body sensation/stiffness was lower （P<0.05）. ConclusionZero-P not only demonstrates safety and efficacy comparable to the ACDF-plate， but also highlights the significant value of the minimally invasive concept in facilitating early recovery. Both procedures have their respective emphasis on biomechanical maintenance and minimally invasive benefits， providing a clear evidence-based reference for individualized and precise surgical decision-making in three-level cervical spondylosis.

Heart failure （HF） is the end-stage of various cardiovascular diseases， with high morbidity and mortality. The existing “new quadruple” standard treatment can hardly reverse the core pathological process of myocardial remodeling， and long-term medication may pose risks of drug resistance and adverse reactions. Therefore， new therapeutic targets and strategies are urgently needed. Metabolic reprogramming is the upstream core mechanism regulating phenotypic polarization and functional activation of macrophages， which drives the occurrence and development of HF through the core axis of metabolic reprogramming-immune imbalance-ventricular remodeling and has become a cutting-edge potential target for the prevention and treatment of HF. Traditional Chinese medicine （TCM） has a long history in the prevention and treatment of HF. A large number of studies in recent years have confirmed that different therapeutic methods of TCM can correct the polarization imbalance， restore the homeostasis of myocardial immune microenvironment， inhibit myocardial injury， and delay the pathological process of HF by targeting and regulating the metabolic reprogramming of glucose， lipids， mitochondria， and amino acids in macrophages. This paper systematically expounds the core pathological mechanism of metabolic reprogramming of macrophages in HF， sorts out the research progress of TCM in preventing and treating HF by intervening this target， analyzes the regulatory rules， summarizes the limitations of existing research， and puts forward future directions. This review aims to provide a systematic theoretical reference and new research ideas for TCM clinical diagnosis and treatment and new drug development of HF.

AIM To study the chemical constituents from the bark of Toona sinensis(A.Juss.)Roem and their anti-inflammatory activity.METHODS Silica gel,RP-18 reverse phase silica gel and HPLC were used for isolation and purification,then the structures of obtained compounds were identified by physicochemical properties and spectral data.Their anti-inflammatory activity were evaluated by RAW264.7 model.RESULTS Sixteen compounds were isolated and identified as(9Z)-18-hydroxyo-ctadec-9-en-4,6-diyn-3-one(1),toonapolyyne C(2),(9S,10E,16R)-octadec-10-ene-12,14-diyne-1,9,16-triol(3),(9S,10E,16R)-9,16-dihydroxyoctadec-10-ene-12,14-diy-n-1-yl acetate(4),toonapolyyne A(5),toonasindiyne B(6),scopoletin(7),sco-parone(8),3-O-acetyl(-)-epicatechin(9),p-ethoxyacetanilide(10),kulonic acid(11),β-sitosterol-3-O-β-D-glucopyranoside(12),vanillic acid(13),cleomiscosin A(14),(-)-isolariciresinol(15),resveratrol(16).The IC50 values of compounds 3-4,6,11-13 for NO were 6.90,10.49,20.03,9.49,18.34,24.36 μmol/L,respectively.CONCLUSION Compound 1 is a new polyacetylene,8-16 are isolated from T.sinensis for the first time.Compounds 3-4,6,11-13 have good anti-inflammatory activity.

Objective To identify the multidimensional needs of postoperative gastric cancer patients for home-based nutritional management based on patient journey maps,and to provide a reference for carrying out nutritional management interventions.Methods Using descriptive qualitative research methods,we facilitated semi-structured in-depth interviews with 9 pairs of postoperative gastric cancer homebound patients and their primary caregivers from a tertiary general hospital in Yichang City,China,from September 2024 to January 2025,and analysed the data and drew the patient journey maps by content analysis.Results Totally 24 sub-themes were summarised from 4 aspects,namely tasks,emotions,pain points and opportunity points,and journey maps involving the acute recovery period,the transitional adaptation period and the nutritional reconstruction period were formed.Conclusion The nutritional needs of homebound patients after gastric cancer surgery are complex and variable,and their needs for dietary guidance,eating-related symptom management,and real-time counselling are highlighted.In the future,appropriate intervention strategies can be developed based on the journey maps to meet the multidimensional nutritional needs of patients.

Theory and technology of Medical Immunology are widely used in scientific research.Our teaching and research group uses experimental teaching of Medical Immunology as a platform to carry out practice of scientific research project-based experi-mental system among"5+3"integration students.By completing a mini-project research including experimental design-experimental operation-research article writing,students cultivated scientific research thinking and exercised scientific research practice ability,and generally reported that the course is very difficult,but after completing it,it is very rewarding.

With the rapid development of artificial intelligence(AI),how to digitize the teaching of Medical Immunology is a new challenge posed by the times and education.This study is based on the advanced teaching model of Medical Immunology,which includes lectures-PAD class-flipped classrooms-expert lecture.By introducing knowledge mapping and AI teaching assistant into the entire learning process,the students not only deepen their understanding of the knowledge system of Medical Immunology,but also ex-ercise their ability to apply immunological knowledge to solve practical clinical problems,enhance their self-learning ability,expres-sion ability,communication ability,on-site performance ability,and cultivate a spirit of unity,cooperation,and exploration.The practice of empowering Medical Immunology teaching with digital intelligence achieves the integration of theory and application,the linkage between in class and out of class teaching,the connection between commonalities and individualities,and the union of abili-ties and qualities in Medical Immunology teaching.It also provides practical basis for exploring the implementation path of digital intel-ligence empowerment in Medical Immunology teaching.

OBJECTIVE: Gastric cancer (GC) is one of the most common malignancies seen in clinic and requires novel treatment options. Morin is a natural flavonoid extracted from the flower stalk of a highly valuable medicinal plant Prunella vulgaris L., which exhibits an anti-cancer effect in multiple types of tumors. However, the therapeutic effect and underlying mechanism of morin in treating GC remains elusive. The study aims to explore the therapeutic effect and underlying molecular mechanisms of morin in GC. METHODS: For in vitro experiments, the proliferation inhibition of morin was measured by cell counting kit-8 assay and colony formation assay in human GC cell line MKN45, human gastric adenocarcinoma cell line AGS, and human gastric epithelial cell line GES-1; for apoptosis analysis, microscopic photography, Western blotting, ubiquitination analysis, quantitative polymerase chain reaction analysis, flow cytometry, and RNA interference technology were employed. For in vivo studies, immunohistochemistry, biomedical analysis, and Western blotting were used to assess the efficacy and safety of morin in a xenograft mouse model of GC. RESULTS: Morin significantly inhibited the proliferation of GC cells MKN45 and AGS in a dose- and time-dependent manner, but did not inhibit human gastric epithelial cells GES-1. Only the caspase inhibitor Z-VAD-FMK was able to significantly reverse the inhibition of proliferation by morin in both GC cells, suggesting that apoptosis was the main type of cell death during the treatment. Morin induced intrinsic apoptosis in a dose-dependent manner in GC cells, which mainly relied on B cell leukemia/lymphoma 2 (BCL-2) associated agonist of cell death (BAD) but not phorbol-12-myristate-13-acetate-induced protein 1. The upregulation of BAD by morin was due to blocking the ubiquitination degradation of BAD, rather than the transcription regulation and the phosphorylation of BAD. Furthermore, the combination of morin and BCL-2 inhibitor navitoclax (also known as ABT-737) produced a synergistic inhibitory effect in GC cells through amplifying apoptotic signals. In addition, morin treatment significantly suppressed the growth of GC in vivo by upregulating BAD and the subsequent activation of its downstream apoptosis pathway. CONCLUSION Morin suppressed GC by inducing apoptosis, which was mainly due to blocking the ubiquitination-based degradation of the pro-apoptotic protein BAD. The combination of morin and the BCL-2 inhibitor ABT-737 synergistically amplified apoptotic signals in GC cells, which may overcome the drug resistance of the BCL-2 inhibitor. These findings indicated that morin was a potent and promising agent for GC treatment. Please cite this article as: Wang Y, Sun XY, Ma FQ, Ren MM, Zhao RH, Qin MM, Zhu XH, Xu Y, Cao ND, Chen YY, Dong TG, Pan YF, Zhao AG. Morin inhibits ubiquitination degradation of BCL-2 associated agonist of cell death and synergizes with BCL-2 inhibitor in gastric cancer cells. J Integr Med. 2025; 23(3): 320-332.
Humans ; Flavonoids/therapeutic use* ; Stomach Neoplasms/pathology* ; Animals ; Proto-Oncogene Proteins c-bcl-2/metabolism* ; Cell Line, Tumor ; Apoptosis/drug effects* ; Cell Proliferation/drug effects* ; Ubiquitination/drug effects* ; Mice ; Drug Synergism ; Mice, Inbred BALB C ; Mice, Nude ; Xenograft Model Antitumor Assays ; Flavones