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.

Subarachnoid hemorrhage (SAH) is a serious intracranial hemorrhage characterized by acute bleeding into the subarachnoid space. The effects of shikonin, a natural compound from the roots of Lithospermum erythrorhizon, on oxidative stress and blood–brain barrier (BBB) injury in SAH was evaluated in this study. A rat model of SAH was established by endovascular perforation to mimic the rupture of intracranial aneurysms. Rats were then administered 25 mg/kg of shikonin or dimethylsulfoxide after surgery. Brain edema, SAH grade, and neurobehavioral scores were measured after 24 h of SAH to evaluate neurological impairment. Concentrations of the oxidative stress markers superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) in the brain cortex were determined using the corresponding commercially available assay kits. Evans blue staining was used to determine BBB permeability. Western blotting was used to quantify protein levels of tight junction proteins zonula occludens-1, Occludin, and Claudin-5. After modeling, the brain water content increased significantly whereas the neurobehavioral scores of rats with SAH decreased prominently. MDA levels increased and the levels of the antioxidant enzymes GSH and SOD decreased after SAH. These changes were reversed after shikonin administration. Shikonin treatment also inhibited Evans blue extravasation after SAH. Furthermore, reduction in the levels of tight junction proteins after SAH modeling was rescued after shikonin treatment. In conclusion, shikonin exerts a neuroprotective effect after SAH by mitigating BBB injury and inhibiting oxidative stress in the cerebral cortex.

Animal experiments are widely used in biomedical research for safety assessment, toxicological analysis, efficacy evaluation, and mechanism exploration. In recent years, the ethical review system has become more stringent, and awareness of animal welfare has continuously increased. To promote more efficient and cost-effective drug research and development, the United States passed the Food and Drug Administration (FDA) Modernization Act 2.0 in September 2022, which removed the federal mandate requiring animal testing in preclinical drug research. In April 2025, the FDA further proposed to adopt a series of "new alternative methods" in the research and development of drugs such as monoclonal antibodies, which included artificial intelligence computing models, organoid toxicity tests, and 3D micro-physiological systems, thereby gradually phasing out traditional animal experiment models. Among these cutting-edge technologies, 3D bioprinting models are a significant alternative and complement to animal models, owing to their high biomimetic properties, reproducibility, and scalability. This review provides a comprehensive overview of advancements and applications of 3D bioprinting technology in the fields of biomedical and pharmaceutical research. It starts by detailing the essential elements of 3D bioprinting, including the selection and functional design of biomaterials, along with an explanation of the principles and characteristics of various printing strategies, highlighting the advantages in constructing complex multicellular spatial structures, regulating microenvironments, and guiding cell fate. It then discusses the typical applications of 3D bioprinting in drug research and development,including high-throughput screening of drug efficacy by constructing disease models such as tumors, infectious diseases, and rare diseases, as well as conducting drug toxicology research by building organ-specific models such as those of liver and heart. Additionally,the review examines the role of 3D bioprinting in tissue engineering, discussing its contributions to the construction of functional tissues such as bone, cartilage, skin, and blood vessels, as well as the latest progress in regeneration and replacement. Furthermore, this review analyzes the complementary advantages of 3D bioprinting models and animal models in the research of disease progression, drug mechanisms, precision medicine, drug development, and tissue regeneration, and discusses the potential and challenges of their integration in improving model accuracy and physiological relevance. In conclusion, as a cutting-edge in vitro modeling and manufacturing technology, 3D bioprinting is gradually establishing a comprehensive application system covering disease modeling, drug screening, toxicity prediction, and tissue regeneration.

Animal experiments are widely used in biomedical research for safety assessment, toxicological analysis, efficacy evaluation, and mechanism exploration. In recent years, the ethical review system has become more stringent, and awareness of animal welfare has continuously increased. To promote more efficient and cost-effective drug research and development, the United States passed the Food and Drug Administration (FDA) Modernization Act 2.0 in September 2022, which removed the federal mandate requiring animal testing in preclinical drug research. In April 2025, the FDA further proposed to adopt a series of "new alternative methods" in the research and development of drugs such as monoclonal antibodies, which included artificial intelligence computing models, organoid toxicity tests, and 3D micro-physiological systems, thereby gradually phasing out traditional animal experiment models. Among these cutting-edge technologies, 3D bioprinting models are a significant alternative and complement to animal models, owing to their high biomimetic properties, reproducibility, and scalability. This review provides a comprehensive overview of advancements and applications of 3D bioprinting technology in the fields of biomedical and pharmaceutical research. It starts by detailing the essential elements of 3D bioprinting, including the selection and functional design of biomaterials, along with an explanation of the principles and characteristics of various printing strategies, highlighting the advantages in constructing complex multicellular spatial structures, regulating microenvironments, and guiding cell fate. It then discusses the typical applications of 3D bioprinting in drug research and development,including high-throughput screening of drug efficacy by constructing disease models such as tumors, infectious diseases, and rare diseases, as well as conducting drug toxicology research by building organ-specific models such as those of liver and heart. Additionally,the review examines the role of 3D bioprinting in tissue engineering, discussing its contributions to the construction of functional tissues such as bone, cartilage, skin, and blood vessels, as well as the latest progress in regeneration and replacement. Furthermore, this review analyzes the complementary advantages of 3D bioprinting models and animal models in the research of disease progression, drug mechanisms, precision medicine, drug development, and tissue regeneration, and discusses the potential and challenges of their integration in improving model accuracy and physiological relevance. In conclusion, as a cutting-edge in vitro modeling and manufacturing technology, 3D bioprinting is gradually establishing a comprehensive application system covering disease modeling, drug screening, toxicity prediction, and tissue regeneration.

Neuronal reprogramming is an innovative technique for converting non-neuronal somatic cells into neurons that can be used to replace lost or damaged neurons, providing a potential effective therapeutic strategy for central nervous system (CNS) injuries or diseases. Transcription factors have been used to induce neuronal reprogramming, while their reprogramming efficiency is relatively low, and the introduction of exogenous genes may result in host gene instability or induce gene mutation. Therefore, their future clinical application may be hindered by these safety concerns. Compared with transcription factors, small-molecule compounds have unique advantages in the field of neuronal reprogramming, which can overcome many limitations of traditional transcription factor-induced neuronal reprogramming. Here, we review the recent progress in the research of small-molecule compound-mediated neuronal reprogramming and its application in CNS regeneration and repair.
Humans ; Cellular Reprogramming/drug effects* ; Neurons/cytology* ; Animals ; Transcription Factors ; Small Molecule Libraries/pharmacology* ; Nerve Regeneration

Nuclear receptor co-activator 4 (NCOA4) acts as a selective cargo receptor that binds to ferritin, a cytoplasmic iron storage complex. By mediating ferritinophagy, NCOA4 regulates iron metabolism and releases free iron in the body, thus playing a crucial role in a variety of biological processes, including growth, development, and metabolism. Recent studies have shown that NCOA4-mediated ferritinophagy is closely associated with the occurrence and development of iron metabolism-related diseases, such as liver fibrosis, renal cell carcinoma, and neurodegenerative diseases. In addition, a number of clinical drugs have been identified to modulate NCOA4-mediated ferritinophagy, significantly affecting disease progression and treatment efficacy. This paper aims to review the current research progress on the role of NCOA4-mediated ferritinophagy in related diseases, in order to provide new ideas for targeted clinical therapy.
Humans ; Nuclear Receptor Coactivators/physiology* ; Ferritins/metabolism* ; Animals ; Neurodegenerative Diseases/metabolism* ; Iron/metabolism* ; Autophagy/physiology* ; Liver Cirrhosis/metabolism* ; Carcinoma, Renal Cell/metabolism* ; Kidney Neoplasms/physiopathology*

Skeletal muscle atrophy is characterized by a reduction in both the size and quantity of skeletal muscle fibers, resulting in impaired muscle strength and function. It mainly includes disuse muscle atrophy, aging muscle atrophy, denervated muscle atrophy and muscle atrophy caused by disease etc. As a cost-effective way, exercise has been widely used in the prevention and treatment of skeletal muscle atrophy, but its mechanism for improving skeletal muscle atrophy remains unclear. Recent studies have indicated that insulin-like growth factor 1 (IGF-1) plays an important role in improving muscle atrophy through exercise, in addition to promoting the survival of neurons, lowering blood sugar, and anti-inflammation. This article reviews recent findings on the mechanisms by which IGF-1 mediates exercise-induced improvement in skeletal muscle atrophy, providing a theoretical basis for the prevention and treatment of this disease.
Insulin-Like Growth Factor I/physiology* ; Muscular Atrophy/therapy* ; Humans ; Exercise/physiology* ; Muscle, Skeletal ; Animals ; Insulin-Like Peptides

ObjectiveTo explore the effects of compatibility of Ephedrae Herba，Asari Radix et Rhizoma， and Aconiti Lateralis Radix Praeparata on the expression of type 2 innate lymphoid cells（ILC2s）-related factors in the lung of allergic rhinitis（AR）mice. MethodsAccording to the random number table method，fifty-four C57BL/6J mice were randomly divided into the following groups： Blank group，model group，Mahuang Fuzi Xixintang group，Asari Radix et Rhizoma and Aconiti Lateralis Radix Praeparata group，Ephedrae Herba and Asari Radix et Rhizoma group，Ephedrae Herba and Aconiti Lateralis Radix Praeparata group，Ephedrae Herba group，Aconiti Lateralis Radix Praeparata group， and Asari Radix et Rhizoma group （6 mice in each group）. Except the blank group，the other groups were subjected to intraperitoneal injection of ovalbumin（OVA）and intranasal challenge to induce AR. After the AR model was established，the mice in the blank group and the model group were given 0.2 mL·d^-1 normal saline by gavage，while those in the Mahuang Fuzi Xixintang group（2.31 g·kg^-1），Asari Radix et Rhizoma and Aconiti Lateralis Radix Praeparata group（1.54 g·kg^-1）， Ephedrae Herba and Asari Radix et Rhizoma group（1.16 g·kg^-1）， Ephedrae Herba and Aconiti Lateralis Radix Praeparata group（1.93 g·kg^-1），Ephedrae Herba group（0.77 g·kg^-1），Aconiti Lateralis Radix Praeparata group（1.16 g·kg^-1），and Asari Radix et Rhizoma group（0.39 g·kg^-1）were given corresponding medicine by gavage，with the treatment lasting for 14 consecutive days. The survival state of mice in each group was observed， and the levels of serum immunoglobulins E（IgE）after intranasal challenge were measured by enzyme-linked immunosorbent assay（ELISA）. The pathological changes of nasal and lung tissues were observed by hematoxylin-eosin（HE）staining. The expression of ILC2s in lung tissue of mice was detected by immunofluorescence（IF）. The mRNA expression of GATA binding protein 3（GATA3），retinoic acid receptor-related orphan receptor-α（RORα）， and inhibitor of DNA binding 2（ID2）in the lung tissue of mice was detected by quantitative real-time polymerase chain reaction（real-time PCR）. The levels of IgE，interleukin（IL）-4，IL-5， and IL-13 in serum were detected by ELISA. ResultsCompared with the blank group，the model group had poor survival state of mice and significantly increased serum IgE level after intranasal challenge（p<0.01）. Additionally，the mice in the model group showed a large amount of neutrophil infiltration in the mucosa of the posterior turbinate， obvious nasal mucosal bleeding and purulent secretion，shed epithelium， thickened bronchial wall，obvious intravascular hyperemia and edema，diffusion and infiltration of a large number of inflammatory cells，seriously damaged alveolar structure，and local lung consolidation. The model group also exhibited significantly increased expression of ILC2s in the lung tissue（P<0.01），increased mRNA expression of GATA3 and RORα，decreased mRNA expression of ID2（P<0.05，P<0.01），and increased levels of serum IgE， IL-4，IL-5，and IL-13（P<0.05，P<0.01）. Compared with the model group，the Mahuang Fuzi Xixintang group and the other medicine treatment groups showed improved survival state of mice， significantly reduced inflammatory cell infiltration in the nasal and lung tissues，a small amount of nasal mucosal bleeding，trachea wall thinning，and no hyperemia，edema， and nasal secretions. Furthermore， the expression of ILC2s in lung tissue was significantly decreased（P<0.01）. The mRNA expression level of GATA3 was decreased（P<0.05），especially in the Aconiti Lateralis Radix Praeparata group（P<0.01）. The expression mRNA levels of RORα were decreased only in the Ephedrae Herba and Aconiti Lateralis Radix Praeparata group and the Ephedrae Herba group（P<0.05）. The levels of serum IgE were decreased（P<0.05）， and IL-5 levels were significantly decreased（P<0.01）. IL-4 levels were significantly decreased in the groups except the Aconiti Lateralis Radix Praeparata group（P<0.01），and the level of IL-13 in the Mahuang Fuzi Xixintang group was decreased（P<0.05）. The levels of IL-13 in were significantly decreased in the Ephedrae Herba and Aconiti Lateralis Radix Praeparata group， Ephedrae Herba group， Aconiti Lateralis Radix Praeparata group， and Asari Radix et Rhizoma group（P<0.01）. ConclusionDifferent compatibility of Ephedrae Herba，Asari Radix et Rhizoma， and Aconiti Lateralis Radix Praeparata can reduce the inflammation of OVA-induced AR mice and has more advantages in reducing the secretion of IgE and IL-5. The compatibility of Ephedrae Herba and Aconiti Lateralis Radix Praeparata has the most advantage in reducing the mRNA expression of GATA3 and RORα to inhibit the expression of ILC2s and thus exert the anti-allergic effect，while the other compatibility has the extensive advantage in inhibiting the mRNA expression of GATA3.

ObjectiveTo explore the effects of compatibility of Ephedrae Herba，Asari Radix et Rhizoma， and Aconiti Lateralis Radix Praeparata on the expression of type 2 innate lymphoid cells（ILC2s）-related factors in the lung of allergic rhinitis（AR）mice. MethodsAccording to the random number table method，fifty-four C57BL/6J mice were randomly divided into the following groups： Blank group，model group，Mahuang Fuzi Xixintang group，Asari Radix et Rhizoma and Aconiti Lateralis Radix Praeparata group，Ephedrae Herba and Asari Radix et Rhizoma group，Ephedrae Herba and Aconiti Lateralis Radix Praeparata group，Ephedrae Herba group，Aconiti Lateralis Radix Praeparata group， and Asari Radix et Rhizoma group （6 mice in each group）. Except the blank group，the other groups were subjected to intraperitoneal injection of ovalbumin（OVA）and intranasal challenge to induce AR. After the AR model was established，the mice in the blank group and the model group were given 0.2 mL·d^-1 normal saline by gavage，while those in the Mahuang Fuzi Xixintang group（2.31 g·kg^-1），Asari Radix et Rhizoma and Aconiti Lateralis Radix Praeparata group（1.54 g·kg^-1）， Ephedrae Herba and Asari Radix et Rhizoma group（1.16 g·kg^-1）， Ephedrae Herba and Aconiti Lateralis Radix Praeparata group（1.93 g·kg^-1），Ephedrae Herba group（0.77 g·kg^-1），Aconiti Lateralis Radix Praeparata group（1.16 g·kg^-1），and Asari Radix et Rhizoma group（0.39 g·kg^-1）were given corresponding medicine by gavage，with the treatment lasting for 14 consecutive days. The survival state of mice in each group was observed， and the levels of serum immunoglobulins E（IgE）after intranasal challenge were measured by enzyme-linked immunosorbent assay（ELISA）. The pathological changes of nasal and lung tissues were observed by hematoxylin-eosin（HE）staining. The expression of ILC2s in lung tissue of mice was detected by immunofluorescence（IF）. The mRNA expression of GATA binding protein 3（GATA3），retinoic acid receptor-related orphan receptor-α（RORα）， and inhibitor of DNA binding 2（ID2）in the lung tissue of mice was detected by quantitative real-time polymerase chain reaction（real-time PCR）. The levels of IgE，interleukin（IL）-4，IL-5， and IL-13 in serum were detected by ELISA. ResultsCompared with the blank group，the model group had poor survival state of mice and significantly increased serum IgE level after intranasal challenge（p<0.01）. Additionally，the mice in the model group showed a large amount of neutrophil infiltration in the mucosa of the posterior turbinate， obvious nasal mucosal bleeding and purulent secretion，shed epithelium， thickened bronchial wall，obvious intravascular hyperemia and edema，diffusion and infiltration of a large number of inflammatory cells，seriously damaged alveolar structure，and local lung consolidation. The model group also exhibited significantly increased expression of ILC2s in the lung tissue（P<0.01），increased mRNA expression of GATA3 and RORα，decreased mRNA expression of ID2（P<0.05，P<0.01），and increased levels of serum IgE， IL-4，IL-5，and IL-13（P<0.05，P<0.01）. Compared with the model group，the Mahuang Fuzi Xixintang group and the other medicine treatment groups showed improved survival state of mice， significantly reduced inflammatory cell infiltration in the nasal and lung tissues，a small amount of nasal mucosal bleeding，trachea wall thinning，and no hyperemia，edema， and nasal secretions. Furthermore， the expression of ILC2s in lung tissue was significantly decreased（P<0.01）. The mRNA expression level of GATA3 was decreased（P<0.05），especially in the Aconiti Lateralis Radix Praeparata group（P<0.01）. The expression mRNA levels of RORα were decreased only in the Ephedrae Herba and Aconiti Lateralis Radix Praeparata group and the Ephedrae Herba group（P<0.05）. The levels of serum IgE were decreased（P<0.05）， and IL-5 levels were significantly decreased（P<0.01）. IL-4 levels were significantly decreased in the groups except the Aconiti Lateralis Radix Praeparata group（P<0.01），and the level of IL-13 in the Mahuang Fuzi Xixintang group was decreased（P<0.05）. The levels of IL-13 in were significantly decreased in the Ephedrae Herba and Aconiti Lateralis Radix Praeparata group， Ephedrae Herba group， Aconiti Lateralis Radix Praeparata group， and Asari Radix et Rhizoma group（P<0.01）. ConclusionDifferent compatibility of Ephedrae Herba，Asari Radix et Rhizoma， and Aconiti Lateralis Radix Praeparata can reduce the inflammation of OVA-induced AR mice and has more advantages in reducing the secretion of IgE and IL-5. The compatibility of Ephedrae Herba and Aconiti Lateralis Radix Praeparata has the most advantage in reducing the mRNA expression of GATA3 and RORα to inhibit the expression of ILC2s and thus exert the anti-allergic effect，while the other compatibility has the extensive advantage in inhibiting the mRNA expression of GATA3.

Subarachnoid hemorrhage (SAH) is a serious intracranial hemorrhage characterized by acute bleeding into the subarachnoid space. The effects of shikonin, a natural compound from the roots of Lithospermum erythrorhizon, on oxidative stress and blood–brain barrier (BBB) injury in SAH was evaluated in this study. A rat model of SAH was established by endovascular perforation to mimic the rupture of intracranial aneurysms. Rats were then administered 25 mg/kg of shikonin or dimethylsulfoxide after surgery. Brain edema, SAH grade, and neurobehavioral scores were measured after 24 h of SAH to evaluate neurological impairment. Concentrations of the oxidative stress markers superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) in the brain cortex were determined using the corresponding commercially available assay kits. Evans blue staining was used to determine BBB permeability. Western blotting was used to quantify protein levels of tight junction proteins zonula occludens-1, Occludin, and Claudin-5. After modeling, the brain water content increased significantly whereas the neurobehavioral scores of rats with SAH decreased prominently. MDA levels increased and the levels of the antioxidant enzymes GSH and SOD decreased after SAH. These changes were reversed after shikonin administration. Shikonin treatment also inhibited Evans blue extravasation after SAH. Furthermore, reduction in the levels of tight junction proteins after SAH modeling was rescued after shikonin treatment. In conclusion, shikonin exerts a neuroprotective effect after SAH by mitigating BBB injury and inhibiting oxidative stress in the cerebral cortex.