1.Treatment Principles and Paradigm of Diabetic Microvascular Complications Responding Specifically to Traditional Chinese Medicine
Anzhu WANG ; Xing HANG ; Lili ZHANG ; Xiaorong ZHU ; Dantao PENG ; Ying FAN ; Min ZHANG ; Wenliang LYU ; Guoliang ZHANG ; Xiai WU ; Jia MI ; Jiaxing TIAN ; Wei ZHANG ; Han WANG ; Yuan XU ; .LI PINGPING ; Zhenyu WANG ; Ying ZHANG ; Dongmei SUN ; Yi HE ; Mei MO ; Xiaoxiao ZHANG ; Linhua ZHAO
Chinese Journal of Experimental Traditional Medical Formulae 2026;32(5):272-279
To explore the advantages of traditional Chinese medicine (TCM) and integrative TCM-Western medicine approaches in the treatment of diabetic microvascular complications (DMC), refine key pathophysiological insights and treatment principles, and promote academic innovation and strategic research planning in the prevention and treatment of DMC. The 38th session of the Expert Salon on Diseases Responding Specifically to Traditional Chinese Medicine, hosted by the China Association of Chinese Medicine, was held in Beijing, 2024. Experts in TCM, Western medicine, and interdisciplinary fields convened to conduct a systematic discussion on the pathogenesis, diagnostic and treatment challenges, and mechanism research related to DMC, ultimately forming a consensus on key directions. Four major research recommendations were proposed. The first is addressing clinical bottlenecks in the prevention and control of DMC by optimizing TCM-based evidence evaluation systems. The second is refining TCM core pathogenesis across DMC stages and establishing corresponding "disease-pattern-time" framework. The third is innovating mechanism research strategies to facilitate a shift from holistic regulation to targeted intervention in TCM. The fourth is advancing interdisciplinary collaboration to enhance the role of TCM in new drug development, research prioritization, and guideline formulation. TCM and integrative approaches offer distinct advantages in managing DMC. With a focus on the diseases responding specifically to TCM, strengthening evidence-based support and mechanism interpretation and promoting the integration of clinical care and research innovation will provide strong momentum for the modernization of TCM and the advancement of national health strategies.
2.Advances in Diabetic Peripheral Neuropathy Treatment by Traditional Chinese Medicine Based on Cellular Senescence: A Review
Qixian MA ; Shiyu HAN ; Hui HUANG ; Jing TIAN ; Xu HAN ; Qingguang CHEN ; Hao LU
Chinese Journal of Experimental Traditional Medical Formulae 2026;32(5):322-330
Diabetic Peripheral Neuropathy (DPN) is one of the most common and harmful complications of type 2 diabetes. DPN's pathogenesis include high blood sugar-induced oxidative stress, inflammation, and mitochondrial dysfunction. These factors are combined to damage nerve fibers, leading to sensory issues, pain, and numbness. Through a coordinated effect, these factors trigger nerve fiber damage and lead to sensory abnormalities, pain and numbness in limbs, and other symptoms, seriously restricting patients' activities of daily living and mobility. Recent research highlights that cellular senescence plays a critical role in DPN. Cellular senescence is manifested by the loss of cell proliferation ability, and further aggravates nerve damage via oxidative stress, mitochondrial dysfunction, autophagy impairment, inflammatory reaction, and other mechanisms, accelerating DPN occurrence and progression. In terms of medical treatment, current methods focus on blood sugar control, pain relief medicine, and microcirculation improvement, while no therapy has been developed based on cellular senescence. In contrast, traditional Chinese medicine (TCM) shows a unique advantage in DPN prevention and treatment via cellular senescence modulation. TCM emphasizes a holistic approach, as well as syndrome differentiation and treatment, effective in anti-aging and nerve damage repair. Recent studies show that TCM active ingredients, including puerarin, ginsenosides, and berberine, can reduce inflammation, oxidative stress, and apoptosis via signaling pathway regulation, thereby slowing cellular senescence to alleviate nerve damage. Furthermore, TCM compounds such as Buyang Huanwutang, Taohong Siwutang, and Huangqi Guizhi Wuwutang exert synergistic effects on cellular senescence-related pathways to improve nerve health and reduce DPN clinical symptoms. Therefore, this paper reviews the literature related to the interaction between cellular senescence and DPN from the perspective of cellular senescence, summarizing the mechanism of DPN and TCM intervention strategies.
3.Hygiene status of public items in typical public places in Shanghai from 2010 to 2024
Fengchan HAN ; Shaofeng SUI ; Yewen SHI ; Ling TONG ; Mingjing XU ; Xianliang WANG ; Tian CHEN
Journal of Environmental and Occupational Medicine 2026;43(3):311-316
Background Public places are important areas for daily human activities. Frequent contact with public items promotes their role as vehicles for microbial spread, creating a substantial risk for the transmission of pathogenic microorganisms. Objective To understand the hygiene status and influencing factors of public items in typical public places in Shanghai from 2010 to 2024, and to provide a scientific basis for optimizing the hygiene management of public items. Methods Based on the monitoring data of public items in public places in Shanghai from 2010 to 2024, the hygiene status was evaluated in three stages: 2010–2019, 2020–2022, and 2023–2024. Chi-square test and logistic regression were used to analyze the impact of factors such as monitoring stages, public place types, and public item categories on the hygiene status. Results The public items in
4.Concentrations characteristics of common air pollutants and health risk assessment of practitioners in hair and beauty salons in Shanghai, 2016–2024
Jiao CHEN ; Tian CHEN ; Xiaoyu WANG ; Yewen SHI ; Fengchan HAN ; Yi HE ; Xiaodong SUN ; Xianliang WANG
Journal of Environmental and Occupational Medicine 2026;43(3):326-332
Background As common public facilities essential to daily life, hair and beauty salons frequently contain various airborne toxic and hazardous pollutants potentially leading to adverse health effects for salon practitioners. Objective To characterize the indoor air pollution profiles of common contaminants in hair and beauty salons in Shanghai and to evaluate the associated health risks for practitioners, in order to provide a scientific basis for strengthening the public health management in Shanghai and protecting the health of practitioners. Methods The air quality monitoring data of hair and beauty salons in Shanghai from 2016 to 2024 were obtained from the “Health Hazard Factors Monitoring Program for Public Places” of the National Institute of Environmental Health, Chinese Center for Disease Control and Prevention. Monitoring indicators included particulate matter ≤10 μm in aerodynamic diameter (PM10), particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5), formaldehyde, ammonia, benzene, toluene, and xylene. Indicator compliance rates were calculated across various years in accordance with GB 9666-1996 Hygienic standard for barber shop and beauty shop and GB 37488-2019 Hygiene indicators and limit for public places; specifically, PM2.5 was assessed against the limits stipulated in GB/T 18883-2022 Standards for indoor air quality. A questionnaire survey was conducted among salon practitioners to collect weekly working days and daily working hours. The non-carcinogenic risks associated with inhalation exposure to formaldehyde, ammonia, benzene, toluene, and xylene as well as the carcinogenic risks posed by formaldehyde and benzene were evaluated following WS/T 777-2021 Technical guide for environmental health risk assessment of chemical exposure and the U.S. Environmental Protection Agency inhalation risk model. Results The overall compliance rates of PM10, formaldehyde, ammonia, benzene, and toluene in the air of hair and beauty salons in Shanghai from 2016 to 2024 were 92.13%, 96.59%, 96.15%, 94.93%, and 94.97%, respectively; the overall compliance rate of xylene was a little lower (85.92%), and the overall compliance rate of PM2.5 was 57.18%. The P50 concentrations of PM10, PM2.5, formaldehyde, ammonia, benzene, toluene, and xylene did not exceed the corresponding limits. The P50 of non-carcinogenic risk indicator (hazard quotient, HQ) for formaldehyde, ammonia, benzene, toluene, and xylene were <1. The probabilities of non-carcinogenic risk HQ >1 for formaldehyde and xylene were 41.4% and 10.9%, respectively, which were higher than that of other pollutants. The P50 of carcinogenic risk (CR) for formaldehyde and benzene were between 1.0×10−6 and 1.0×10−4, while the probabilities of CR >1.0×10−4 were 16.9% and 14.0%, respectively. Conclusion The overall compliance rate of common pollutant concentrations in the air of hair and beauty salons in Shanghai is high, and the hygienic condition meets the requirements of national standards. The non-carcinogenic health risks posed by formaldehyde and xylene to employees (with formaldehyde being more prominent), as well as the carcinogenic risks associated with formaldehyde and benzene, deserve heightened attention in future health supervision.
5.Genetic disease diagnosis and treatment in Shanghai: Survey and countermeasures for clinical genetics specialist training.
Xiaoju HUANG ; Lin HAN ; Li CAO ; Taosheng HUANG ; Duan MA ; Jian WANG ; Wenjuan QIU ; Fanyi ZENG ; Luming SUN ; Chenming XU ; Songchang CHEN ; Xinyu KUANG ; Hong TIAN
Chinese Journal of Medical Genetics 2026;43(4):241-247
OBJECTIVE:
To investigate the current status of clinical genetics specialization development and the diagnostic and therapeutic capabilities for hereditary diseases across medical institutions in Shanghai, and to assess the necessity and feasibility of establishing training bases for clinical genetics specialists.
METHODS:
By employing a cross-sectional survey design, the Clinical Genetics Committee of Shanghai Medical Association has conducted questionnaire surveys from March to April 2025 across 54 healthcare institutions in Shanghai (including 33 tertiary hospitals and 21 secondary hospitals). The survey involved administrative departments and medical personnel from 15 clinical specialties. The survey has covered current genetic disease diagnosis and treatment practices, relevant and specialised disease types, genetic department establishment, testing capabilities, personnel teams, and training requirements.
RESULTS:
The results revealed that 78.0% of clinical departments surveyed had treated patients with hereditary disorders. Shanghai possesses diagnostic and therapeutic expertise for over 95% of hereditary diseases listed in its rare disease catalogue, reflecting both the practical clinical demand for such conditions and the city's overall diagnostic and therapeutic strengths in this field. Nevertheless, significant disparities exist in the development of genetics departments across different tiers of healthcare institutions. Resources for genetic testing capabilities (including molecular, cellular, and biochemical testing) are also unevenly distributed across different tiers of hospitals. The survey further revealed that only 26.0% of departments believe that their current physician structure fully meets the diagnostic and treatment demands. Over 90% of departments consider standard training for clinical genetic specialists necessary, with 74.0% expressing willingness to participate in establishing training bases. Based on above findings and thorough deliberation, the Clinical Genetics Committee of the Shanghai Medical Association proposes advancing specialist training and discipline development through establishing a standard training system. The committee has drafted a three-year training protocol featuring a "joint training"-centered model, recommending a pilot-first, dynamically optimized strategy for steadily advancing training base development.
CONCLUSION
Shanghai faces substantial demand for genetic disease diagnosis and treatment, yet exhibits shortcomings in clinical genetics specialization development, resource allocation, and talent pipeline cultivation. To establish a standard training system holds significant practical importance and is underpinned by a broad demand.
Humans
;
China
;
Surveys and Questionnaires
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Genetic Diseases, Inborn/genetics*
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Cross-Sectional Studies
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Genetics, Medical/education*
;
Genetic Testing
6.Fibroblast Growth Factors in Parkinson’s Disease: Multi-target Neuroprotective Mechanisms Involving Neuroinflammation, Cellular Stress, and Ferroptosis
Hui WANG ; Zi-Gui ZHOU ; Teng-Teng HAN ; Chang-Zhi YANG ; Xue-Wen TIAN
Progress in Biochemistry and Biophysics 2026;53(4):855-874
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of dopaminergic neurons in the substantia nigra pars compacta and the pathological accumulation ofα‑synuclein. Although extensive progress has been made in elucidating its pathogenesis, current therapeutic approaches remain largely symptomatic, and effective disease-modifying treatments are still unavailable. Increasing evidence indicates that PD is driven by the interaction of multiple pathological processes, including neuroinflammation, iron homeostasis dysregulation and ferroptosis, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, oxidative stress, and impaired protein homeostasis, which together contribute to neuronal vulnerability and degeneration. Fibroblast growth factors (FGFs) comprise a family of 22 ligands that play important roles in neural development, stress responses, metabolic regulation, and the maintenance of nervous system homeostasis. Recent studies have shown that several FGF family members, such as FGF1, FGF2, FGF9, and FGF21, exert neuroprotective effects in cellular and animal models of PD. These effects include the regulation of inflammatory responses, oxidative stress, iron homeostasis, cellular stress adaptation, and neuronal survival. Compared with therapeutic strategies targeting a single pathogenic pathway, FGFs appear to influence multiple disease-related processes, suggesting their potential relevance to the complex pathophysiology of PD. Experimental evidence indicates that altered FGF signaling may contribute to dopaminergic neuron dysfunction through the coordinated regulation of several interconnected mechanisms. FGFs have been reported to modulate neuroinflammation by affecting the activation of microglia and astrocytes, thereby influencing the inflammatory environment in the central nervous system. In addition, FGFs are involved in the regulation of iron homeostasis and ferroptosis, partly through antioxidant signaling pathways associated with NRF2, SLC7A11, and GPX4. Moreover, FGFs can alleviate ER stress and mitochondrial dysfunction by activating intracellular signaling pathways such as PI3K/AKT, AMPK-PGC-1α, as well as SIRT1-dependent programs, which support cellular energy metabolism and redox balance. Recent advances in single-cell and spatial transcriptomic studies further suggest that FGF signaling is not limited to neuron-intrinsic mechanisms but also involves interactions among different glial cell types. Altered FGF ligand-receptor communication between astrocytes and oligodendrocytes has been observed in PD models and is associated with increased susceptibility of dopaminergic neurons to oxidative stress and ferroptosis. These findings indicate that the biological effects of FGFs are influenced by cell type and disease stage and may vary under different pathological conditions. In this review, we summarize recent progress in understanding the roles of FGF family members in PD, with a focus on their involvement in iron homeostasis dysregulation and ferroptosis, neuroinflammation, cellular stress responses, and neuronal protection and regeneration. By integrating current evidence, this review aims to provide a clearer understanding of how FGFs participate in PD pathogenesis and to offer a theoretical basis for future studies exploring their potential value in disease-modifying therapeutic strategies.
7.Compact Fundus Imaging System Using Shack-Hartmann Wavefront Sensing for High-speed Auto-focus
Zhe-Kai LIN ; Long CHEN ; Geng-Yong ZHENG ; Jin-Tian HUANG ; Jia-Xin DONG ; Shang-Pan YANG ; Wen-Zheng DING ; Ding-An HAN ; Xue-Hua WANG ; Ya-Guang ZENG
Progress in Biochemistry and Biophysics 2026;53(4):1076-1086
ObjectiveThe widespread adoption of portable fundus cameras for primary care and community screening is hindered by limitations in current autofocus(AF) technologies. Image-based methods relying on sharpness evaluation require iterative searches, resulting in slow convergence, while projection-based techniques are susceptible to optical artifacts and calibration errors. To address these challenges, this study introduces a novel AF system based on direct wavefront sensing, designed to deliver simultaneous high speed, high precision, and operational robustness within the compact form factor essential for portable ophthalmic devices. MethodsOur approach fundamentally reimagines the AF process by directly measuring the ocular wavefront aberration. We developed a custom portable fundus camera integrating a miniaturized Shack-Hartmann wavefront sensor (SHWS) into the optical path. An 850 nm laser diode projects a point source onto the retina via oblique illumination to minimize corneal reflections. Light scattered from this spot carries the eye’s refractive error through the imaging optics and is directed to the SHWS, positioned at a plane optically conjugate to the primary color CMOS imaging sensor. A microlens array within the SHWS samples the incident wavefront, generating a pattern of focal spots on a CCD. Real-time centroid analysis of these spots provides a map of local wavefront slopes. These measurements are processed through a singular value decomposition (SVD) algorithm to fit a Zernike polynomial basis set, enabling real-time reconstruction of the wavefront phase. The defocus component (S) is extracted from the second-order Zernike coefficients, providing a direct, quantitative measure of the refractive error in diopters. This value serves as a precise error signal in a closed-loop control system, which commands a voice-coil actuated focusing lens to its null position in a single, deterministic step, eliminating the need for iterative search algorithms. ResultsComprehensive evaluation demonstrated the system’s high performance. Testing on a calibrated model eye (OEMI-7) established a highly linear relationship between the computed defocus S and the focusing lens position across a ±20 Diopter (D) compensation range, achievable within a 5 mm mechanical travel. The system achieved a focusing precision of 0.08 D, corresponding to an 18-fold improvement over a conventional projection spot-size method tested under identical conditions. The total focus acquisition time, encompassing wavefront measurement, computation, and lens actuation, averaged under 0.5 s. Clinical validation with 25 human volunteers (50 eyes, refractive range -15 D to +10 D) confirmed practical efficacy. The wavefront-sensing AF succeeded in 92% of attempts with a mean time of 0.5 s, substantially outperforming a projection-based benchmark which achieved only a 32% success rate with an average time of 4.25 s. The system provided instantaneous directional guidance and maintained stability during minor ocular movements. Objective assessment of image quality, via amplitude contrast of retinal vasculature, showed consistent and significant enhancement following AF correction across the entire tested diopter range. ConclusionThis work successfully implements and validates a direct wavefront-sensing autofocus paradigm for portable fundus cameras. By directly quantifying and compensating for the optical defocus aberration, this method bypasses the fundamental limitations of image-processing and projection-based techniques, enabling rapid, precise, and deterministic diopter compensation. The developed system delivers an exceptional combination of a wide operational range (±20 D), high accuracy (0.08 D), fast convergence (0.5 s), and a compact physical footprint. This technology provides a practical and high-performance focusing solution capable of enhancing the reliability, throughput, and diagnostic utility of portable retinal imaging in large-scale screening applications. Future efforts will be directed towards system cost optimization and performance adaptation for diverse ocular conditions.
8.Effect of laminin subunit α3 on epithelial-mesenchymal transition, invasion, and metastasis abilities of pancreatic cancer
Nenghong YANG ; Likun REN ; She TIAN ; Min HAN ; Zhu LI ; Yuxiang ZHAO ; Peng LIU
Journal of Clinical Hepatology 2025;41(2):322-332
ObjectiveTo investigate the effect of laminin subunit α3 (LAMA3) on the epithelial-mesenchymal transition (EMT), invasion, and metastasis abilities of pancreatic cancer (PC). MethodsA comprehensive analysis was performed for tumor- and EMT-related databases to identify the EMT genes associated with PC, especially LAMA3. The methods of qRT-PCR and Western blot were used to measure the expression level of LAMA3 in PC tissue and cell lines; immunofluorescence assay was used to determine the localization of LAMA3 in PANC-1 cells; Transwell assay was used to investigate the effect of LAMA3 on the invasion and migration abilities of PC cells. The t-test was used for comparison of continuous data between groups. ResultsThe analysis of the TCGA database identified 3 EMT-related oncogenes for PC, i.e., LAMA3, AREG, and SDC1. The LASSO-Cox regression model showed that LAMA3 had the most significant impact on the prognosis of PC (risk score=0.256 1×LAMA3+0.043 1×SDC1+0.071 4×AREG). The Cox model and nomogram showed that the high expression of LAMA3 was an independent risk factor for the poor prognosis of PC (hazard ratio=1.32, 95% confidence interval: 1.07 — 1.62, P<0.01). Experimental results showed that there was a significant increase in the expression of LAMA3 in pancreatic cancer tissue compared with the normal pancreatic tissue. Compared with the HPDE cell line, there were varying degrees of increase in the expression of LAMA3 in pancreatic cancer AsPC-1, BxPC-3, PANC-1, MIA PaCa-2, and SW1990 cell lines, with the highest expression level in PANC-1 cells. The enrichment analysis showed that LAMA3 was associated with the biological processes and signaling pathways such as EMT, collagen metabolism, extracellular matrix degradation, the TGF-β pathway, and the PI3K pathway. After the knockdown of LAMA3, there were significant reductions in the expression levels of N-Cadherin, Vimentin, and Snail, while there was a significant increase in the expression level of E-Cadherin. Transwell assay showed that there were significant reductions in the invasion and migration abilities of PANC-1 cells after the knockdown of LAMA3. ConclusionLAMA3 is highly expressed in PC and can promote the EMT, invasion, and migration of PC cells, and therefore, LAMA3 may be used as a novel diagnostic marker and a new therapeutic target for PC.
9.A three-party evolutionary game analysis of patient privacy protection in live surgery
Han TIAN ; Jinping WU ; Yan ZHANG ; Jianyu ZHOU
Chinese Medical Ethics 2025;38(1):123-130
With the rapid development of network technology, live surgery has become the new way of surgery teaching. However, the issue of patient privacy protection caused by live surgery has received widespread attention. Based on the evolutionary game theory, this paper constructed an evolutionary game model from the three-party perspectives of doctors, patients, and government and analyzed the game behaviors of the three parties in the process of live surgery. Matlab software was utilized to conduct dynamic simulation and numerical simulation analysis. It was found that the factors affecting the choice of doctors’ strategies included protection costs, the cost of privacy leakage, the benefits of protection, high-traffic benefits, and other aspects; the factors affecting the choice of patient strategies encompassed surgical costs, the risk of privacy leakage, additional benefits, and other aspects; the factors affecting the choice of government strategies embodied regulatory costs and the improvement of credibility. To realize a win-win situation among doctors, patients, and the government, the three parties need to work together to ensure that patient privacy is not violated and find a balance between expanding the influence of medical education and protecting patient privacy.
10.Morin inhibits ubiquitination degradation of BCL-2 associated agonist of cell death and synergizes with BCL-2 inhibitor in gastric cancer cells.
Yi WANG ; Xiao-Yu SUN ; Fang-Qi MA ; Ming-Ming REN ; Ruo-Han ZHAO ; Meng-Meng QIN ; Xiao-Hong ZHU ; Yan XU ; Ni-da CAO ; Yuan-Yuan CHEN ; Tian-Geng DONG ; Yong-Fu PAN ; Ai-Guang ZHAO
Journal of Integrative Medicine 2025;23(3):320-332
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
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Flavonoids/therapeutic use*
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Stomach Neoplasms/pathology*
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Animals
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Proto-Oncogene Proteins c-bcl-2/metabolism*
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Cell Line, Tumor
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Apoptosis/drug effects*
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Cell Proliferation/drug effects*
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Ubiquitination/drug effects*
;
Mice
;
Drug Synergism
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Mice, Inbred BALB C
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Mice, Nude
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Xenograft Model Antitumor Assays
;
Flavones

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