arcopenia is a systemic skeletal muscle disorder characterized by a decrease in skeletal muscle mass and progressive decline in function， with multiple signaling pathways involved in its occurrence and development. Among them， the AMP-activated protein kinase （AMPK） signaling pathway， as a key pathway regulating cellular energy homeostasis， plays an important role in the regulation of skeletal muscle metabolism and functional maintenance by improving abnormalities in glucose and lipid metabolism， balancing skeletal muscle protein synthesis and degradation， improving mitochondrial function， promoting autophagy， and inhibiting inflammatory responses and oxidative stress. This article reviews the research progress on how various traditional Chinese medicine （TCM） monomers， including polyphenols， flavonoids， and terpenoids； various traditional Chinese medicine extracts， such as those from Lycium barbarum ， Asini Corii Colla， and Panax quinquefolium ， and TCM compounds， such as Guiqi zhuangjin decoction， Jianpi qiangji granules， and Qigu capsules， intervene in sarcopenia by regulating the AMPK signaling pathway to promote muscle protein synthesis， inhibit protein degradation， improve mitochondrial function， and alleviate inflammation and oxidative stress. Additionally， their molecular mechanisms are explored. The aim is to deeply elucidate the basis of TCM in the prevention and treatment of sarcopenia and to provide theoretical support for the development of related innovative drugs.

This paper summarizes the experience of professor LIU Shangyi in differentiating and treating rectal carcinoma from the perspective of "treating ulcers as tumors". It is believed that the manifestations of rectal cancer， such as anal itching， cauliflower-like or ulcerative tumors， and bloody stools， are similar to external skin itching， skin ulceration， swelling， and skin bleeding. Therefore， the treatment principles of sores and ulcers department can be applied to treat tumors. Following the diagnostic and treatment approach of dermatology regarding the clinical typical symptoms， for anal itching， the main treatment is to dispel wind and remove dampness， clear heat to relieve itching， using "skin medicinals" such as Difuzi （Fructus Kochiae） and Baixianpi （Cortex Dictamni）， as well as wind medicinals such as Shengma （Rhizoma Cimicifugae） and Fangfeng （Radix Saposhnikoviae）. For constipation， the method of clearing heat and resolving toxins， unblocking the bowels and discharging heat can be used， commonly using Baitouweng （Radix Pulsatillae）， Donglingcao （Herba Rabdosiae Rubescentis） and Dahuang （Radix et Rhizoma Rhei）. In terms of mucosal ulcers， it is critical to differentiate between yin and yang； the treatment of yang ulcers should focus on clearing heat and resolving toxins， commonly using modified Xianfang Huoming Beverage （仙方活命饮）； for yin ulcers， emphasis should be placed on removing dampness and resolving phlegm， commonly with modified Yiyi Fuzi Baijiang Powder （薏苡附子败酱散）. For bloody stool， differentiation is made between deficiency and excess， with the use of Diyu （Radix Sanguisorbae） and Huaihua （Flos Sophorae） for excess syndrome to cool and stop blee-ding， and both herbs dry-fried until charred combined with liver-tonifying medicinals for deficiency syndrome

Cardiotoxicity induced by antineoplastic agents is an important factor affecting the prognosis of cancer patients. This article systematically summarizes the clinical manifestations of cardiotoxicity caused by chemotherapeutic drugs, molecular targeted cancer therapies, and immunotherapeutic drugs, and identifies the core injury mechanisms, including cardiomyocyte apoptosis, oxidative stress, and mitochondrial dysfunction. In Traditional Chinese Medicine (TCM) theory, anticancer drug-induced cardiotoxicity falls under the category of “heat toxins” characterized by dual deficiency of qi and blood, upward flaming of heart heat, stagnation of the heart vessels, and meridian obstruction induced by phlegm-dampness. Therefore, by reviewing the preventive and therapeutic effects and the underlying mechanisms of tonic medicines, interior heat-clearing medicines, blood-circulating and stasis-resolving medicines, phlegm-transforming, cough-suppressing and panting-relieving medicines, and interior-warming medicines, this paper concludes that TCM prevention and treatment of this condition adheres to the formulation principle of “reinforcing healthy qi, removing toxins, and resolving blood stasis”. Its mechanisms of action—including antioxidation effects, regulation of autophagic balance, antagonism of inflammatory responses, and improvement of microcirculation—are highly consistent with modern medical treatment strategies (e.g., dexrazoxane for inhibiting iron-dependent oxidative stress, statins for anti-inflammatory effects). This study provides theoretical support and practical guidance for the collaborative and precise prevention and treatment of anticancer drug-induced cardiotoxicity through the integration of traditional Chinese and Western medicine.

Objective To investigate the protective effect and potential mechanism of kinsenoside （KD）-the main ingredient of Anoectochilus roxburghii （AR） on alcoholic liver injury in mouse models of chronic and acute alcoholic liver injury, and provide a theoretical basis for the development of drugs for alcoholic liver injury. Methods Chronic and acute alcoholic liver injury mouse models were induced by feeding liquid diet containing 30% alcohol and gavage of high doses of alcohol （6 g/kg）, respectively. The KD （50 mg/kg） and AR （250 mg/kg） were administrated by intragastric administration. Body weight, liver index, serum alanine aminotransferase （ALT）, aspartate aminotransferase （AST） levels, serum total triglyceride （TG） and cholesterol （TC） levels were measured; hematoxylin-eosin and oil red O staining was performed on liver tissues; lipid metabolic related genes （PPARα and SREBP1） expression levels were detected by QPCR. Results Both models of alcoholic liver injury resulted in increased hepatic transaminase activity and elevated lipids, accompanied by massive vacuolar structure and lipid droplet formation in pathological liver sections. In the chronic alcoholic liver injury model, ALT and AST were significantly reduced after KD or AR treatment （P<0.05, P<0.001）; the transcriptional activity of SREBP1 was significantly reduced after KD or AR treatment （P<0.01, P<0.05）. In the acute alcoholic liver injury model, AST was significantly reduced after KD or AR treatment （P<0.01, P<0.01）, and TG level was significantly decreased （P<0.01, P<0.01）. Conclusion KD, as the main active ingredient of AR, played a major role in hepatoprotection in mice. KD treatment significantly alleviated chronic and acute alcoholic liver injury and reduced the lipid deposition in liver; KD promoted lipolysis by increasing PPARα and inhibiting the expression of SREBP1 to reduce the synthesis and accumulation of lipids, thus exerting its role in regulating lipid metabolism, which suggested that KD, as the active ingredient of AR, could be a potential drug for the treatment of ALD.

Background Studies have shown that benzo(a)pyrene (BaP) exhibits neurotoxicity and can induce cognitive dysfunction. Olfactory dysfunction is an early marker of mild cognitive impairment; however, the mechanism by which BaP exposure causes this impairment is still unclear. Objective To investigate the effects of BaP exposure on olfactory function in mice. Methods Thirty 5-month-old male C57BL/6 mice were randomly assigned to five groups (n=6 per group): blank control, solvent control (olive oil), and low, medium and high doses (0.72, 1.44, and 2.89 mg·kg⁻¹, respectively). Following one week of acclimatization, BaP was administered intranasally every other day. Behavioral changes were assessed using the buried food test and Morris water maze (MWM). Olfactory bulb tissues were subsequently harvested for analysis. Hematoxylin-eosin (HE) staining was used to evaluate pathological changes, while immunofluorescence and quantitative polymerase chain reaction (qPCR) were employed to examine the expression and distribution of protein and mRNA expressions and distributions of olfactory marker protein (OMP), membrane-spanning 4-pass A1 (MS4A1), trace amine-associated receptor1 (TAAR1). Results The buried food test revealed that BaP exposure significantly prolonged the time taken to find food in a dose-dependent manner (F=56.753, P< 0.01). MWM results showed significant main effects for both time (F=128.5, P<0.01) and dose (F=3.889, P<0.05), with a significant interaction effect between them (F=2.128, P<0.05). HE staining showed that in the 2.89 mg·kg⁻¹ group, although granule remained abundant, mitral cell layer neurons exhibited structural atrophy and deep staining. Immunofluorescence demonstrated a decreased distribution of OMP, MS4A1, and TAAR1 in the olfactory nerve layer and glomerular layers in the 2.89 mg·kg⁻¹ group compared with the blank control group (F=11.590, P<0.01; F=12.807, P<0.01; F=7.436, P<0.01). Furthermore, mRNA expression levels of OMP, MS4A1, and TAAR1 in the 2.89 mg·kg⁻¹ group were also significantly downregulated compared to the control group (F=6.720, P<0.01; F=16.931, P<0.01; F=48.060, P<0.01). Conclusion BaP exposure leads to olfactory dysfunction in mice by inducing pathological damage to mitral cells and reducing the expression of key olfactory receptors and markers in the olfactory bulb.

Background Studies have shown that benzo(a)pyrene (BaP) exhibits neurotoxicity and can induce cognitive dysfunction. Olfactory dysfunction is an early marker of mild cognitive impairment; however, the mechanism by which BaP exposure causes this impairment is still unclear. Objective To investigate the effects of BaP exposure on olfactory function in mice. Methods Thirty 5-month-old male C57BL/6 mice were randomly assigned to five groups (n=6 per group): blank control, solvent control (olive oil), and low, medium and high doses (0.72, 1.44, and 2.89 mg·kg⁻¹, respectively). Following one week of acclimatization, BaP was administered intranasally every other day. Behavioral changes were assessed using the buried food test and Morris water maze (MWM). Olfactory bulb tissues were subsequently harvested for analysis. Hematoxylin-eosin (HE) staining was used to evaluate pathological changes, while immunofluorescence and quantitative polymerase chain reaction (qPCR) were employed to examine the expression and distribution of protein and mRNA expressions and distributions of olfactory marker protein (OMP), membrane-spanning 4-pass A1 (MS4A1), trace amine-associated receptor1 (TAAR1). Results The buried food test revealed that BaP exposure significantly prolonged the time taken to find food in a dose-dependent manner (F=56.753, P< 0.01). MWM results showed significant main effects for both time (F=128.5, P<0.01) and dose (F=3.889, P<0.05), with a significant interaction effect between them (F=2.128, P<0.05). HE staining showed that in the 2.89 mg·kg⁻¹ group, although granule remained abundant, mitral cell layer neurons exhibited structural atrophy and deep staining. Immunofluorescence demonstrated a decreased distribution of OMP, MS4A1, and TAAR1 in the olfactory nerve layer and glomerular layers in the 2.89 mg·kg⁻¹ group compared with the blank control group (F=11.590, P<0.01; F=12.807, P<0.01; F=7.436, P<0.01). Furthermore, mRNA expression levels of OMP, MS4A1, and TAAR1 in the 2.89 mg·kg⁻¹ group were also significantly downregulated compared to the control group (F=6.720, P<0.01; F=16.931, P<0.01; F=48.060, P<0.01). Conclusion BaP exposure leads to olfactory dysfunction in mice by inducing pathological damage to mitral cells and reducing the expression of key olfactory receptors and markers in the olfactory bulb.

Xenotransplantation is confronted with multiple ethical risks currently， such as the insurmountable physiological barrier of incompatibility between different species， the failure to implement the right to informed consent， the erosion of the integrity and independence of patients’ identity， and the unfair distribution of transplantation opportunities. Nevertheless， China’s governance of the ethical risks of xenotransplantation encounters issues including the absence of special laws and regulations， the lack of targeted rule supply， and the lag of regulatory schemes. Therefore， it is necessary to take disease treatment promotion as the functional orientation， adopt the classification， connection， and complementarity of regulatory schemes as the structural orientation， and follow the whole life cycle of technological research and development， application， evaluation， and supervision as the process orientation. This aims to build a trinity risk regulation system integrating function， structure， and process， therefore ensuring the benign and sustainable development of xenotransplantation.

ObjectiveTo investigate the protective effect of Astragaloside Ⅳ （AS-Ⅳ） on D-galactose （D-gal）-induced cardiomyocytes senescence and its potential mechanisms. MethodsUsing H9C2 cardiomyocytes as a model， D-gal was used to induce cardiomyocyte senescence. Cell viability was assessed using the CCK-8 assay， senescenceextent was evaluated via β-galactosidase （SA-β-Gal） staining， reactive oxygen species （ROS） levels were measured to assess intracellular oxidative stress， apoptosis extent was determined using the TUNEL assay， and qRT-PCR and Western blot analyses were conducted to examine the expression levels of senescence-related genes and proteins （p21、p53） and key genes （STING， CXCL10， and MX-1） and proteins （STING， cGAS， p-IRF3/IRF3） of the stimulator of interferon genes （STING） pathway. ResultsThe 50 g/L D-gal significantly reduced myocardial cell viability， increased SA-β-Gal positivity， apoptosis rate， and intracellular reactive oxygen species levels， and upregulated the expression of p16， p21， and STING， cGAS， p-IRF3/IRF3 pathway proteins （P< 0.05）； After intervention with 200 μmol/L of AS-Ⅳ， cell viability was significantly enhanced， the SA-β-Gal-positive rate decreased， intracellular reactive oxygen species levels decreased， oxidative stress damage was alleviated， myocardial cell apoptosis was inhibited， and the mRNA and protein levels of aging-related p21 and p53 were downregulated （P＜0.05）. Further detection of STING pathway-related molecules showed that 200 μmol/L of AS-IV inhibited D-galactose-induced STING mRNA and protein expression and reduced p-IRF3/IRF3 protein expression levels， as demonstrated by qRT-PCR and Western blot results. However， the SA-β-Gal positivity rate， intracellular reactive oxygen species （ROS） levels， DNA damage results， and Western blot findings suggested that the STING agonist （STING agonist-7） could reverse the ameliorative effects of AS-Ⅳ on D-galactose-induced cardiomyocytes senescence. ConclusionAS-Ⅳ may mitigate D-gal-induced cardiomyocytes senescence by inhibiting STING pathway activation， providinga new strategy for the prevention and treatment of cardiovascular senescence-related diseases.

BACKGROUND:Parkinson's disease has the main pathological changes in the midbrain,especially in the dense substantia nigra,leading to impaired motor and non-motor function in patients.At present,research is limited by cellular heterogeneity,and its pathogenesis still needs to be further elucidated.In recent years,single-cell RNA sequencing(scRNA-seq)has gradually been applied in neurodegenerative diseases,which is of great significance for understanding intercellular heterogeneity,disease development mechanisms,and treatment strategies. OBJECTIVE:To review the research progress of scRNA-seq technology applied to Parkinson's disease in recent years,providing a theoretical basis for the application of scRNA-seq in the treatment and diagnosis of Parkinson's disease. METHODS:The first author used a computer system to search for relevant literature in the CNKI,WanFang,PubMed,and Web of Science databases,with the Chinese search terms"single-cell RNA sequencing,Parkinson's disease,cell heterogeneity,cell subtypes,dopaminergic neurons,glial cells"and English search terms"single-cell RNA seq,Parkinson disease,heterogenicity,subtypes,dopaminergic neurons,glial cells."71 articles were ultimately included for review and analysis. RESULTS AND CONCLUSION:(1)scRNA-seq is a high-throughput experimental technique that utilizes RNA sequencing at the single-cell level to quantify gene expression profiles in specific cell populations,revealing cellular mysteries at the molecular level.Compared with traditional sequencing techniques,scRNA-seq technology is used to reveal the diversity of cell types and changes in specific gene expression in complex tissues under various physiological and pathological conditions through automatic clustering analysis of cell transcriptome.(2)By using scRNA-seq,the development process of dopaminergic neurons and the unique functional characteristics of various cell subtypes are elucidated,in order to better understand potential therapeutic molecular targets.(3)The use of scRNA-seq analysis has improved our understanding of the response of Parkinson's disease glial cells,enabling us to comprehensively map and characterize different cell type populations,identify specific glial cell subpopulations related to neurodegeneration,and draw valuable single cell maps as reference data for future research.(4)The application of scRNA-seq to detect embryonic mice and stem cells will help improve the in vitro differentiation protocol and quality control of cell therapy,as well as evaluate the overall cell quality and developmental stage of dopaminergic neurons derived from stem cells.

Objective To evaluate the efficiency of health resource allocation in 22 types of hospital institutions in Guangdong Province from 2018 to 2022,identify their strengths and shortcomings in resource utilization,and offer evidence-based recommendations for optimizing medical resource allocation and policymaking.Methods The efficiency of health resource allocation was assessed using the DEA-BCC model and the DEA-Malmquist index model across the 22 hospital categories.Results In 2022,the overall resource allocation efficiency of the 22 types of hospital institutions in Guangdong Province was suboptimal,with an average score of 0.657.From 2018 to 2022,the mean total factor productivity(TFP)change index for these hospitals was 0.968,with only 6 categories exhibiting a TFP index exceeding 1.Conclusion The efficiency of health resource allocation in Guangdong's hospitals remains inadequate.Government authorities should enhance macro-level planning for regional resource distribution,accelerate advancements in medical technology,and establish a real-time monitoring framework.Concurrently,policy interventions and incentive mechanisms should be reinforced to ensure both scientifically sound allocation and effective utilization of medical resources.