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    26 June 2025, Volume 15 Issue 3 Previous Issue   

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    Effects of Puerarin on the Regulation of the Canonical Wnt Signaling Pathway in Osteoporotic Rats
    WEN Le, WANG Ling-wei, WANG Ting, ZHANG Wen-long
    2025, 15 (3):  1.  DOI: 10.3969/j.issn.2095-1396.2025.03.001
    Abstract ( 3 )   PDF (2630KB) ( 3 )  
    Objective: To investigate the effects of puerarin on the pathohistochemistry of the femoral head, bone mineral density (BMD), serum calcium and phosphorus levels in osteoporotic rats, and to analyze its regulatory role in the canonical Wnt signaling pathway. Methods: Thirty-six SPF-grade female Wistar rats were used, and 30 of them successfully established the model of osteoporosis rats were randomly divided into sham operation group, model group and puerarin group. The bone mineral density of the femoral head, the levels of calcium and phosphorus in serum, the gray value of Wnt3a, Wnt5a and β-catenin signaling pathway related proteins and the relative expression levels of mRNA in the femoral head were compared among the three groups. Results: Compared with the sham operation group, In the model group, the trabecular bone number and thickness significantly decreased, while the trabecular separation markedly increased (P<0.01). The relative expression levels of Wnt3a, Wnt5a and β-catenin signaling pathway related proteins and mRNA in Wnt signaling pathway were significantly decreased (P<0.05). Compared with the model group, In the puerarin group, trabecular bone number and thickness significantly increased, while trabecular separation decreased (P<0.01). The protein gray value and mRNA relative expression levels of Wnt3a, Wnt5a and β-catenin in femoral head tissue were significantly increased (P<0.05). Conclusion: Puerarin has a therapeutic effect on osteoporotic rats, and it exerts its effect by regulating Wnt3a, Wnt5a, and β-catenin in the classical Wnt signaling pathway.
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    Literature Analysis of 46 Cases of Allergic Shock Caused by Ceftriaxone Sodium
    ZHANG Ben-chang, WANG Ze-yu, QIAO Ting-ting, WANG Yu, YAN Juan
    2025, 15 (3):  7.  DOI: 10.3969/j.issn.2095-1396.2025.03.002
    Abstract ( 5 )   PDF (1251KB) ( 2 )  
    Objective: To analyze the clinical characteristics and patterns of allergic shock induced by ceftriaxone sodium, and provide a basis for ensuring the safety of clinical medication. Methods: A search was conducted on the literature on ceftriaxone sodium induced anaphylactic shock published domestically and internationally from 2011 to 2024. Case reports of ceftriaxone sodium induced anaphylactic shock were selected and retrospectively analyzed. Results: A total of 46 cases of allergic shock caused by ceftriaxone sodium were retrieved. Among these cases, 73.9% experienced allergic shock during the first use of the drug, 26.1% experienced allergic shock after continuous use, and 4 cases experienced allergic shock during skin testing; The overall mortality rate reached 10.8%. Conclusion: The clinical application of ceftriaxone sodium requires strict adherence to diagnostic and treatment standards, individualized medication plans tailored to individual patient differences, monitoring of individual vital signs, and establishment of emergency response plans for acute allergic reactions to ensure patient medication safety.
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    Radiation-Induced Cognitive Impairment: Advances in Pathogenesis and Therapeutic Agents
    JIANG Qin, WANG Yu-tong, HUANG Yu-qi, XU Zi-xuan, LU Ying-mei
    2025, 15 (3):  13.  DOI: 10.3969/j.issn.2095-1396.2025.03.003
    Abstract ( 4 )   PDF (2055KB) ( 2 )  
    Radiotherapy remains the cornerstone treatment for primary brain tumors and brain metastases, largely due to the limited ability of chemotherapeutic agents to achieve therapeutic concentrations in the brain parenchyma. However, clinical studies consistently report that patients frequently develop severe neurotoxic sequelae during the late phases postradiotherapy, with cognitive impairment emerging as the most debilitating complication. This decline in neurocognitive function profoundly impacts patients’ quality of life and long-term prognosis. Despite decades of research into radiation-induced cognitive impairment, the precise molecular and cellular mechanisms driving this pathology remain poorly understood, posing a major barrier to effective prevention and treatment strategies. Historically, investigations into radiation-induced cognitive impairment have focused on late-stage, irreversible neurodegenerative changes. Recent advances in neuroimaging and functional assessment techniques, however, have uncovered subtle yet significant structural and functional disturbances in the central nervous system (CNS) during the acute and subacute post-irradiation phases. These early alterations— including microvascular injury, neuroinflammation, and synaptic dysfunction—may initiate cascades of chronic pathological processes that culminate in irreversible late-stage cognitive deficits. This paradigm shift underscores the critical need to elucidate the interplay between acute radiation injury and chronic neurodegeneration. In this review, we synthesize current knowledge on: 1) Acute CNS injury responses to radiation, including oxidative stress, blood-brain barrier disruption, and glial activation. 2) Structural and functional remodeling of neural circuits, such as hippocampal neurogenesis suppression and white matter tract degeneration. 3) Mechanistic links between early cellular damage and late cognitive decline, focusing on neuroimmune crosstalk and epigenetic dysregulation. Furthermore, we highlight recent breakthroughs in therapeutic development, including small-molecule inhibitors targeting neuroinflammatory pathways (e.g., TGF-β, NLRP3 inflammasome), antioxidants to mitigate oxidative stress, and neurotrophic factors to promote neural repair. By bridging preclinical mechanistic insights with translational opportunities, this analysis aims to advance both the biological understanding and clinical management of radiation-induced cognitive impairment.
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    Multidimensional Advances in Epilepsy Treatment: From Molecular Mechanisms to Clinical Strategies and Future Directions
    ZHAO Jiao-jiao, YANG Lei, ZHANG Wei
    2025, 15 (3):  24.  DOI: 10.3969/j.issn.2095-1396.2025.03.004
    Abstract ( 4 )   PDF (1110KB) ( 2 )  
    Epilepsy, a globally pervasive chronic central nervous system disorder, is characterized by an imbalance between neuronal excitation and inhibition, primarily involving the interplay of glutamate and GABA systems. This comprehensive review delineates the cuttingedge research developments in the field of epilepsy treatment, spanning an extensive spectrum from molecular pathophysiological mechanisms to clinical therapeutic strategies, with a foresight into future research trajectories. The review meticulously examines the pivotal roles of AMPA and NMDA receptors in the genesis of epileptic seizures, as well as the implications of GABA receptor dysfunction on disease progression. Regarding therapeutic strategies, the article juxtaposes the mechanisms of action of conventional and newer antiepileptic drugs, placing special emphasis on the significance of non-pharmacological interventions, such as the ketogenic diet and lifestyle modifications, in the comprehensive management of epilepsy. Furthermore, the review explores the potential of personalized medicine and the integration of Western and traditional Chinese medicine, aiming to offer more precise and effective treatment options for patients with epilepsy. By providing an in-depth analysis of existing treatment modalities and prognosticating future research directions, this review furnishes a scientific foundation and innovative perspectives for advancements in epilepsy treatment.
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    Exploring the Thinking of Differentiation and Treatment of Spinal Cord Injury Based on the Collateral Disease Theory and the Mechanism of the Blood-Spinal Cord Barrier
    ZHANG Xing-xing, LIANG Jia-yu, SUN Yue, WEN Meng-xin, ZHONG Hui, LI Qiang, LI Liang
    2025, 15 (3):  30.  DOI: 10.3969/j.issn.2095-1396.2025.03.005
    Abstract ( 2 )   PDF (1431KB) ( 2 )  
    Spinal cord injury (SCI) is the damage to the structure or function of the spinal cord caused by factors such as traffic accidents, falls from heights, and sports traumas. Clinically, the core symptoms include motor function impairment, sensory loss, and disorders of defecation and urination. Its pathological essence involves the cascade injury triggered by neuronal necrosis, axonal rupture, and the disruption of the blood-spinal cord barrier (BSCB). When the spinal cord is injured, it will lead to serious consequences such as sensory loss and difficulties in defecation and urination, which greatly affect the quality of life of patients. The collateral disease theory is a crucial component of the traditional Chinese medicine system. Its core lies in exploring the normal physiological operation and abnormal pathological manifestations of the collateral vessel system, as well as its correlations with various diseases. This article starts from the collateral disease theory and combines the BSCB mechanism to analyze the pathogenesis and treatment approaches of spinal cord injury.
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    Research on the Animal Model of Type 2 Diabetes Mellitus with Damp-Heat Syndrome in Combination with Disease Evidence: A Review
    LI Jia-jie, LIU Jin-xing, ZHOU Ze, WANG Ya-ping, LIAO Jia-bao, LUO Cheng, YAN He-guo, LI Hong-mei, LI Qin, WEN Wei-bo
    2025, 15 (3):  38.  DOI: 10.3969/j.issn.2095-1396.2025.03.006
    Abstract ( 4 )   PDF (1674KB) ( 1 )  
    Epilepsy, a globally pervasive chronic central nervous system disorder, is characterized by an imbalance between neuronal excitation and inhibition, primarily involving the interplay of glutamate and GABA systems. This comprehensive review delineates the cutting-edge research developments in the field of epilepsy treatment, spanning an extensive spectrum from molecular pathophysiological mechanisms to clinical therapeutic strategies, with a foresight into future research trajectories. The review meticulously examines the pivotal roles of AMPA and NMDA receptors in the genesis of epileptic seizures, as well as the implications of GABA receptor dysfunction on disease progression. Regarding therapeutic strategies, the article juxtaposes the mechanisms of action of conventional and newer antiepileptic drugs, placing special emphasis on the significance of non-pharmacological interventions, such as the ketogenic diet and lifestyle modifications, in the comprehensive management of epilepsy. Furthermore, the review explores the potential of personalized medicine and the integration of Western and traditional Chinese medicine, aiming to offer more precise and effective treatment options for patients with epilepsy. By providing an in-depth analysis of existing treatment modalities and prognosticating future.
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