Abstract: Objective To establish and characterize two chronic stress-related dry-eye models using chronic unpredictable mild restraint (CUMR) and chronic unpredictable rhythm disturbance (CURD), respectively, and to compare their phenotypic presentations, metabolomic profiles, and correlations with traditional Chinese medicine syndrome patterns. Methods Healthy male specific-pathogen-free rats were divided into control, CUMR, and CURD groups. Rats in the CUMR group underwent single-cage housing combined with behavioral restraint daily, while CURD rats received random daily rhythm interventions. After 6 weeks of modeling, dry-eye rats associated with Yu syndrome were assessed for general conditions, behavioral performance, and dry-eye parameters. Histopathological alterations in the conjunctiva, cornea, and lacrimal gland were examined by hematoxylin-eosin staining. Serum concentrations of 5-hydroxytryptamine (5-HT) and cortisol, and cornea levels of tumor necrosis factor-α ( TNF-α) and interleukin-1β ( IL-1β), were quantified by enzyme-linked immunosorbent assay. Serum metabolomic profiling was conducted using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry. Results (1) There were significant differences in appearance and behavior between the CUMR and CURD groups. (2)Compared with the control group, cornea fluorescein staining(CFS) was significantly increased in the CUMR and CURD groups, while tear flow and tear-film breakup time ( BUT) were significantly decreased,especially in the CUMR group. (3)There was no obvious inflammatory cell infiltration in the cornea in the CUMR or CURD group. Compared with the control group, there were significantly fewer conjunctival goblet cells in the CUMR and CURD groups, and the area of lacrimal gland vacuolation was significantly increased. ( 4) Serum 5-HT was significantly decreased and cortisol was significantly increased in the CUMR group compared with the CURD group,but there were no significant differences in cornea tissue TNF-α and IL-1β levels. (5) Serum metabolomic analysis revealed 235 differential metabolites in the CUMR and CURD groups, demonstrating a significant separation trend. Conclusions Distinct stress-modeling paradigms differentially impact host metabolism, culminating in divergent TCM syndrome manifestations and dry-eye phenotypes. The CUMR model exemplifies a dry-eye phenotype consistent with “Liver Depression and Spleen Deficiency,” potentially mediated by perturbations in tryptophan metabolism, while the CURD model aligns with “Stagnation Heat in the Liver Channel,” likely arising from disruptions in the tricarboxylic acid cycle.

Abstract: Objective To construct and evaluate a mouse model of pressure overload-induced heart failure with dampness syndrome. Methods C57BL / 6 mice were divided randomly into sham, thoracotomy and aortic restriction (TAC), and TAC-dampness ( TAC-D) groups ( n = 7 mice per group). Mice in the sham group underwent thoracotomy without aortic constriction, while mice in the TAC group underwent aortic arch constriction to induce pressure overload-induced heart failure. All mice were housed in a normal environment. In addition to TAC surgery, TAC-D mice were placed in a controlled temperature and humidity chamber for 8 h / d to induce dampness syndrome, with the remaining time spent in a normal environment. This protocol was maintained for 8 weeks. The macroscopic manifestations were assessed using the “ Evaluation Scale for Dampness Syndrome Animal Models in Traditional Chinese Medicine”. Modern medical techniques were employed to measure cardiac function, myocardial histopathology, immune homeostasis, serum N-terminal pro-B-type natriuretic peptide ( NT-proBNP ), and lipid levels. Fecal 16S rDNA sequencing and serum non-targeted metabolomics were conducted to develop novel evaluation indicators for the heart failure with dampness syndrome mouse model. Results Mice in the TAC-D group exhibited fatigue, lethargy, reduced responsiveness to external stimuli, and anal soiling. Mice in both heart failure groups demonstrated marked cardiac dysfunction, myocardial injury, immune homeostasis imbalance, elevated serum NTproBNP levels, and reduced lipid levels, especially in the TAC-D group. Fecal 16S rDNA sequencing and serum nontargeted metabolomics revealed significant alterations in the gut microbiota and metabolites following dampness syndrome induction. Linear discriminant analysis effect size analysis ( > 2) showed that the bacterial genera Enterorhabdus, Eubacterium, Corynebacterium, Christensenellaceae and Erysipelatoclostridium were significantly enriched in the TAC-D group. Metabolomics kyoto encyclopedia of genes and genomes(KEGG) enrichment analysis indicated that differential metabolites in the TAC-D group were primarily enriched in glycerophospholipid metabolism,arachidonic acid metabolism, and bile secretion pathways. Pearson’s correlation analysis revealed significant negative correlations between the bacterial genera Eubacterium and Erysipelatoclostridium and metabolites involved in arachidonic acid metabolism, including 16R-hydroxy-5,8,11,14-eicosatetraenoic acid (HETE), 6-keto PGE1, PENMe2(16 ∶ 1 ( 9Z) / 20 ∶ 3 ( 8Z,11Z,14Z)), Prostaglandin F2a, TXB2, Oxoglutaric acid, and 12 ( R)-HETE. Conclusions The combination of aortic arch constriction and a controlled temperature and humidity environment successfully established a mouse model of pressure overload-induced heart failure with dampness syndrome. The “Evaluation Scale for Dampness Syndrome Animal Models in Traditional Chinese Medicine”, cardiac function, serum NT-proBNP, myocardial histopathology, and immune homeostasis can serve as conventional evaluation indicators for this model. Additionally, the incorporation of disturbances in the gut bacterial genera Eubacterium and Erysipelatoclostridium and arachidonic acid metabolism further develops an innovative evaluation system for the heart failure with dampness syndrome mouse model.

Abstract: Objective To determine the absorption rate and anti-osteoporosis efficacy of calcium zinc vitamin D vitamin K oral solution ( YQJ) and its components in Caco-2 cells and zebrafish, and explore its potential mechanism based on transcriptome sequencing. Methods We compared the calcium-ion absorption rates of YQJ and its components in Caco-2 cells, to simulate gastrointestinal absorption. An osteoporosis model was induced using dexamethasone. Bone density was detected by Alizarin Red staining and dual validation of drug efficacy was analyzed using transgenic (ola. sp7: nlsGFP) osteoblast fluorescence. Zebrafish were divided into YQJ 250 μg / mL, MC, and NC groups (3 biological replicates each). Transcriptome sequencing was carried out and differentially expressed genes at the intersection of the three groups were screened using | log₂ fold-change | ≥ 2 and Q value ≤ 0. 001. Differential genes underwent functional annotation and enrichment analyses to screen out the expression pathway of YQJ antiosteoporosis genes, followed by quantitative polymerase chain reaction validation. Results The absolute calciumabsorption rate in YQJ-treated Caco-2 cells was 42. 6%, which was 1. 70 fold higher than that of the calcium citratealone group, 1. 59, 1. 58, and 1. 56 fold higher than the calcium citrate + vitamin (V) D₃ , calcium citrate + VK2 ,and calcium citrate + ( casein phosphopeptides) CPP groups, respectively, and 1. 33 fold higher than the calcium citrate + zinc gluconate + D₃ group, indicating a significant synergistic effect of YQJ on promoting calcium absorption. YQJ significantly restored zebrafish skull density and increased osteogenic fluorescence intensity, and 125 μg / mL YQJ increased the anti-osteoporosis effect by 24% ~ 25% compared with calcium citrate alone. Sequencing identified 335 and 231 differentially expressed genes in MC group / NC group and YQJ group / MC group, respectively, with 58 overlapping genes at the intersection of the three groups. Functional enrichment of overlapping genes revealed that YQJ’s anti-osteoporosis effect involved four pathways and 11 key genes. Using qPCR verification, YQJ significantly restored the mRNA expression levels of c3a. 1, cp, coro1a, cldni, and bmpr1aa. Conclusions The in vitro calciumabsorption rate and anti-osteoporosis efficacy of YQJ both demonstrated synergistic effects, with its anti-osteoporosis effect specifically increasing skull density and osteoblast signaling intensity. Transcriptome sequencing revealed that YQJ primarily functions by modulating the complement and coagulation cascade, ferroptosis, phagosome, oxidative stress response signaling pathways, and other functional proteins, involving the regulation of key genes such as c3a. 1,c3a. 2, c3a. 6, c9, c5, cfb, coro1a, cp, mpx, cldni, and bmpr1aa.

Abstract: Objective To explore the potential active components and underlying mechanisms of Buzhong Yiqi Decoction ( BZYQD) in ameliorating chemotherapy-induced sarcopenia ( CIS) using integrated strategies of network pharmacology and in vivo validation. Methods The active components of BZYQD and their targets were identified using the TCMSP platform. CIS-related targets were obtained from the GeneCards and OMIM databases. We constructed a protein-protein interaction network by taking the intersection targets of drugs and diseases and identifying the core targets. We carried out gene ontology ( GO) functional annotation and kyoto encyclopedia of genes and genomes pathway ( KEGG) enrichment. Molecular docking and visualization were performed using AutodockTools 1. 5. 7 and PyMOL 2. 7. 1. The therapeutic effects of BZYQD on CIS were validated in animal experiments. Results The core targets at the drugs/ diseases intersection included Akt1, TP53, tumor necrosis factor (TNF), interleukin (IL)-1β, and IL-6. Molecular docking analysis indicated that the core targets and main active components had favorable binding affinities. In the experiment on SD rats, body mass, grip strength, exhaustive swimming time, and myofiber cross-sectional area were significantly decreased in the model (M group) compared with the control group (C group). Serum levels of TNF-α, IL-1β, and IL-6 detected by enzyme-linked immunosorbent assay were significantly elevated. The phospho (p)-nuclear factor (NF)-κB p65/ NF-κB p65 ratio was significantly increased, while the p-Akt /Akt and p-phosphoinositide 3-kinase ( PI3K) / PI3K ratios were significantly decreased, as shown by Western Blot.Administration of BZYQD ameliorated these alterations in a dose-dependent manner, with the most pronounced effects in the HBYD group. Conclusions BZYQD may improve CIS by regulating the PI3K/ Akt / NF-κB signaling pathway.

Abstract: Objective To compare the composition and diversity of lung and gut microbiota between Chinese and golden hamsters using 16S rDNA sequencing, to provide a new perspective for understanding their applications in human disease research. Methods SPF-grade Chinese hamsters and golden hamsters (6 males and 6 females per group) aged 6 ~ 8 weeks were selected. Bronchoalveolar lavage fluid, small intestinal contents, and large intestinal contents were collected under sterile conditions. Species annotation and α-diversity and β-diversity analyses were performed using 16S rDNA sequencing. Linear discriminant analysis effect size ( LEfSe) analysis was employed to identify potential biomarkers. Results The α-diversity of the lung and small intestinal microbiota was significantly higher in golden hamsters (especially males) than in Chinese hamsters (P<0. 05), while the diversity of the large intestinal microbiota was significantly higher in Chinese hamsters ( P<0. 05 ). Regarding β-diversity, the composition of the lung, small intestinal, and large intestinal microbiota differed significantly between the two types of hamsters (P<0. 01). LEfSe analysis revealed differential occurrence of the phylum Firmicutes in the lung microbiota in golden hamsters, and differential occurrence of the phyla Bacteroidota ( females) and Proteobacteria (males) in Chinese hamsters. Regarding the small intestinal and large intestinal microbiota, Firmicutes and Bacteroidota were differential phyla in Chinese and golden hamsters, respectively. Conclusions The composition and diversity of the lung and gut microbiota differed significantly between Chinese and golden hamsters, which may be related to their distinct applications in human disease research. This study provides a new perspective for understanding the applications of these two types of hamsters in human disease research and lays a theoretical foundation for future efforts to improve their health status and their value as experimental models by modulating their microbiota.

Abstract: Objective To establish rapid-aging and cardiac-aging mouse models by intraperitoneal injection of doxorubicin (DOX) at different doses and frequencies, to optimize model-evaluation indices, and provide diseasemodel support for anti-aging drug evaluation. Methods ( 1) For the rapid-aging model, mice were divided into model 1 (5 mg / kg, once every 7 d), model 2 (8 mg / kg, once every 10 d), model 3 (8 mg / kg, once every 7 d), model 4 (10 mg / kg, once every 10 d), and model 5 (10 mg / kg, once every 7 d) groups. DOX was administered by three intraperitoneal injections and mice were observed continuously for 60 d to record survival rate. (2) For the cardiac-aging model, mice were divided into control, model-1 (2 mg / kg), model-2 (5 mg / kg), model-3 (8 mg /kg), and model-4 (10 mg / kg) groups. Injections were given twice, once every 10 d, for 30 d. After completion,ejection fraction (EF), fractional shortening (FS), and peak blood flow velocity were evaluated by small animal highfrequency ultrasound imaging. Serum levels of creatine kinase-MB ( CK-MB), lactate dehydrogenase ( LDH), interleukin ( IL)-6, and IL-1β, and myocardial-tissue levels of superoxide dismutase ( SOD), malondialdehyde (MDA), glutathione peroxidase ( GSH-Px), succinate dehydrogenase, and catalase were measured. Myocardial tissue pathology, fibronectin, β-galactosidase staining ( β-gal), and p16 protein, along with other cardiac agingrelated indicators, were assessed. Results (1) In the rapid-aging mouse model, body mass and survival rate showed significant downward trends in all modeling groups. Decreases in body mass and survival rate became more pronounced with increasing DOX dose and shortened modeling interval. (2) In the cardiac-aging model, compared with the control group, DOX 2, 5, 8, and 10 mg / kg significantly increased LDH levels (P<0. 01) and decreased GSH-Px activity (P<0. 05 or P<0. 01), and DOX 5, 8, and 10 mg / kg significantly decreased body mass (P<0. 01), EF, FS, and peak blood flow velocity ( P<0. 05 or P<0. 01). Serum IL-6 levels were significantly increased, SOD content was significantly decreased, and β-galactosidase and p16 protein expression levels were significantly elevated (P<0. 05 or P<0. 01). Myocardial tissue showed hydropic and vacuolar degeneration. DOX8 and 10 mg / kg also significantly increased CK-MB levels and cardiac fibrosis, and DOX 10 mg / kg increased IL-1β and MDA contents (P<0. 01). Conclusions Intraperitoneal injection of DOX 10 mg / kg once every 10 d for three injections successfully established a rapid-aging mouse model, while intraperitoneal injection of DOX 5 or 8 mg / kg once every 10 d for two injections successfully established a cardiac-aging mouse model, which induced changes in cardiac function, myocardial enzymes, inflammation, oxidative stress, aging markers, cardiac pathology, and fibrosis consistent with physiological and pathological characteristics of cardiac aging.

Abstract: Objective To investigate the differential therapeutic effects of XuanFei HuaZhuo pill (XFHZP) on rat pneumonia models with damp-heat pneumonia (DH) syndrome, and to elucidate the underlying mechanisms using proteomics, to provide experimental evidence for the use of traditional Chinese medicine ( TCM) in the treatment of pneumonia. Methods A DH group model was established. Therapeutic effects were evaluated via clinical signs and scores ( general information, tongue, ear, claw nail, urine, feces), lung index, histopathology (hematoxylin-eosin), enzyme-linked immunosorbent assay for pulmonary interleukin (IL)-6 and tumor necrosis factor (TNF)-α levels, hematology ( white blood cell count ( WBC), granulocytes ( Gran), monocytes ( Mon), mean platelet volume (MPV)), and pulmonary function ( respiratory frequency (F), minute ventilation (MV)). Astral data-independent acquisition quantitative proteomics was performed on the right inferior lung lobes from control (CON) group, DH group, and XFHZP + DH group to identify differentially expressed proteins (DEPs) between CON vs. DH and DH vs. XFHZP + DH groups. Key DEPs were verified by immunohistochemistry and Western Blot, including their downstream targets ( phospho-MLC2, phospho-eIF4E). Results Compared with CON group, DH group exhibited hyperactive behavior, red tongues, ear-vessel dilation, yellow urine, and sticky feces, and displayed elevated lung indices, alveolar wall thickening, inflammatory infiltration, and capillary congestion, plus increased IL-6 and TNF-α (P<0. 05), WBC, Gran, Mon, MPV, F (P<0. 05), and reduced MV ( P<0. 05). XFHZP treatment significanly ameliorated lung pathology, reduiced IL-6、TNF-α (P<0. 05), and nomalized WBC、 Gran、Mon、 MPV、 F (P<0. 05), MV (P<0. 05) in DH rats (XFHZP + DH). Proteomics identified 1348 DEPs in the CON vs. DH and 448 in the DH vs. XFHZP + DH group, including AAK1、CACNα2δ1、eIF4E、HSD11β1、ROCK1、TDP1. KEGG analysis highlighted cGMP-dependent protein kinase G and insulin-signaling pathways as potential mechanisms for XFHZP in DH pneumonia. ROCK1 / MKNK1 was upregulated in DH lungs, accompanied by increased MLC2 / eIF4E phosphorylation, which were suppressed by XFHZP. Conclusions XFHZP exerts significant therapeutic effects on DH syndrome pneumonia, likely by downregulating ROCK1 / MKNK1 expression, inhibiting MLC2 / eIF4E phosphorylation, relaxing airway smooth muscle, and attenuating inflammation. This study provides molecular-level evidence for XFHZP’s efficacy and offers novel insights into TCM-based pneumonia treatment.

Abstract: Objective To investigate the effects and underlying mechanisms of Lonicera japonica in delaying renal aging. Methods A mouse model of renal aging was established via intraperitoneal injection of D-galactose (Dgal), with concurrent administration of Lonicera japonica decoction by oral gavage. Following behavioral assessments,kidney tissues were collected from each group for enzyme-linked immunosorbent assay ( ELISA) and senescenceassociated β-galactosidase ( SA-β-gal) staining to evaluate model induction and the protective effects of Lonicera japonica. Integrated microRNA ( miRNA) transcriptomic and proteomic sequencing analyses were conducted to identify significantly differentially expressed miRNA ( DEMs) and protein ( DEPs). Functional annotation and pathway enrichment of these DEMs and DEPs were performed using gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) databases. Results Behavioral tests, including the Morris water maze and forced swimming test, revealed significant impairments in learning, memory, and exercise endurance in model mice compared with controls ( P<0. 05). Lonicera japonica markedly ameliorated these aging-related deficits ( P<0. 05). Renal interleukin (IL)-6 levels and the percentage of SA-β-gal-positive area were significantly elevated in the model group relative to the control group ( P<0. 001), and both were significantly reduced following Lonicera japonica intervention ( P<0. 01). Integrated omics analysis identified 11 significant DEMs and eight significant DEPs. Intersection analysis of target genes revealed miR-146b-3p / Tmprss13 as a key regulatory pair, while miR-150-3p / Brpf1 and miR-1934-5p / Cln8 were identified as miRNA-protein pairs concurrently downregulated by Lonicera japonica. GO and KEGG enrichment analyses indicated that Lonicera japonica may delay renal aging by activating Lonicera japonica-regulated Ecsit (LjREcsit), a differentially expressed gene involved in the mitogen-activated protein kinase (MAPK) signaling pathway. Conclusions Lonicera japonica attenuates D-gal-induced renal aging in mice,possibly via mechanisms involving inhibition of miR-146b-3p leading to activation of Tmprss13, or coordinated downregulation of miR-150-3p / Brpf1 and miR-1934-5p / Cln8. Modulation of the MAPK signaling pathway via LjREcsit also represents a critical mechanism through which Lonicera japonica exerts its renoprotective and anti-aging effects.

Abstract: Objective To investigate renal injury, functional impairment, histopathological characteristics,and molecular features accompanying HCC development in the context of non-alcoholic steatohepatitis, utilizing a novel MASH-HCC murine model ( HRAS-HCC). This research seeks to elucidate the underlying mechanisms of MASH-HCC-induced renal injury, thereby providing an essential model tool for clinical investigations into disease pathogenesis and the exploration of diagnostic and therapeutic strategies. Methods HRAS-HCC transgenic mice generated in-house were employed, with littermate negative controls and wild-type C57BL / 6 mice as comparators. At 5 weeks of age, tamoxifen was administered to induce hepatocyte-specific HRAS expression, thereby initiating and propagating MASH-HCC. Body mass, general condition, and behavioral parameters were monitored serially during disease progression ( weeks 1 ~ 4). Blood was collected at predetermined time points for biochemical analyses.Structural and fibrotic changes in renal tissue were evaluated by hematoxylin-eosin(HE) and Masson staining. Results Compared with the HRAS^NON-TAM group, Within 4 weeks, HRAS-HCC mice transitioned from MASH through hepatic fibrosis to established HCC, manifesting jaundice, tachypnea, kyphosis, hematochezia, hepatosplenomegaly, and other clinical signs. At week 4, serum alkaline phosphatase(ALP) was significantly decreased (P<0. 05), whereas blood urea nitrogen(UREA), uric acid(UC), and creatinine(CREA) were markedly elevated (P<0. 05). HE staining revealed temporally heterogeneous renal lesions, including tubular basophilia, hyaline glomerulopathy, and tubular epithelial cytoplasmic hyaline droplet formation. Masson staining demonstrated renal fibrosis whose onset (weeks 2 ~ 3) and severity paralleled those of hepatic fibrosis/ cirrhosis(weeks 2 ~ 3). Further analysis of kidney injury-related molecular expression revealed at week 3 showed up-regulation of keratin-18, SMAD3, fibronectin, and transforming growth factor-β mRNAs ( P<0. 05 ). Protein-protein interaction analyses further indicated direct interactions among human HRAS, fibronectin (FN1), and SMAD3. Conclusions These data establish a positive correlation between MASH HCC-induced renal injury and the degree of hepatic fibrosis, clarify the attendant histopathological and molecular signatures, and implicate the HRAS-SMAD3-FN1 axis as a putative mechanistic pathway. The HRAS-HCC mouse model uniquely recapitulates key clinicopathological features of human MASH-HCC complicated by CKD, thereby providing a robust pre-clinical platform for mechanistic dissection and therapeutic development.

Abstract:Sepsis is a life-threatening condition associated with high mortality rates in clinical settings. The subsequent immunosuppressive state is strongly correlated with adverse patient outcomes. Establishing robust animal models is therefore essential for elucidating the pathophysiological mechanisms of sepsis-induced immunosuppression and developing therapeutic interventions. Current models, however, are predominantly employed in sepsis hyperinflammation studies, while their utilization specifically for the immunosuppression phase remains limited. In addition, standardized assessment criteria for immunosuppression are lacking across different investigations.Commonly employed models include cecal ligation and puncture ( CLP ) and lipopolysaccharide ( LPS ) administration. Although cecal ligation and puncture effectively recapitulates the clinical pathology, it suffers from significant outcome variability. Conversely, although lipopolysaccharide administration is technically straightforward,its artificial nature fails to replicate the polymicrobial pathogenesis of natural infection. Quantitative analysis of immune cell populations, cytokine profiles, and immune organ status provides a reliable assessment of immunosuppression severity in animal models. By synthesizing recent literature, this review consolidates the method ologies and assessment parameters for establishing immunosuppressive sepsis models. By critically evaluating the strengths and limitations of each approach, the review aims to establish a standardized experimental framework for the future development of optimized sepsis models.

Abstract:Cancer-associated fibroblasts (CAFs) influence the progression and treatment of prostate cancer (PCa) by remodeling the tumor microenvironment (TME). Identifying the key molecular drivers of this remodeling is critical for advancing cancer research. The monoamine oxidase (MAO) family, comprising the subtypes MAOA and MAOB, is a group of mitochondrial outer membrane oxidases that regulate monoamine metabolism through oxidative deamination. Aberrant MAO expression is closely associated with PCa growth, invasion, metastasis, poor prognosis,and TME remodeling. This review, based on various animal models, systematically summarizes the biological roles of the distinct MAO subtypes in CAFs and their contributions to PCa pathogenesis. We further explore the potential of MAO inhibitors in combination therapies for PCa, focusing on their differential expression profiles and functional specificity. In addition, we propose precision diagnostic and therapeutic strategies targeting MAO subtypes, with the aim of identifying novel therapeutic targets for personalized PCa treatment.

Abstract:Chronic obstructive pulmonary disease ( COPD) and pulmonary interstitial fibrosis ( PIF) are chronic pulmonary diseases that severely impair lung function. COPD combined with PIF (COPD-PIF) exacerbates lung-tissue damage, accelerates disease progression, and significantly worsens patient prognosis. However, the exact pathogenesis of COPD-PIF remains unclear, and effective treatment options are still lacking. Animal models have recently played a crucial role in elucidating the pathological mechanisms of COPD-PIF and facilitating new drug development. Current COPD models are primarily established by single-factor induction ( such as cigarette smoke exposure or lipopolysaccharide injection) or multi-factor combination method, while PIF models mainly rely on bleomycin induction. The administration route ( e. g. , intratracheal instillation, aerosol inhalation, or intravenous injection) affects the stability and reproducibility of these models. Although various COPD-PIF animal models have been developed and utilized for research, challenges remain in establishing a standardized and reliable model that fully mimics human disease characteristics. Additionally, although the order in which COPD and PIF are induced may influence the pathological manifestations, there is no consensus in current studies. Further investigations into the pathogenesis of COPD-PIF and the identification of effective therapeutic strategies require more research focusing on optimizing modeling techniques, improving model stability and reproducibility, and developing animal models that better reflect the clinical characteristics of COPD-PIF. These efforts will contribute to advancing fundamental research and facilitating new drug development in this field.

Abstract:Anticipatory nausea and vomiting (ANV) is a learned form of nausea and vomiting that occurs when chemotherapy-induced nausea and vomiting are inadequately controlled. Patients often develop nausea and vomiting prior to subsequent chemotherapy sessions, a phenomenon termed ANV, with the severity correlating positively with the patient’s anxiety and depression levels. Although approximately 20% ~ 30% of patients develop ANV by the fourth chemotherapy cycle, current treatment options for ANV remain limited, highlighting the need to elucidate its pathogenesis, explore effective therapies, and develop novel pharmacological agents. The establishment of ANV animal models plays an indispensable role in this process; however, no ideal preclinical model has yet fully and accurately replicated all features of ANV onset and progression observed in chemotherapy patients. This article systematically reviews recent advances in method ologies for establishing ANV animal models, including the selection of experimental species, common emetic agents, and protocols for modeling ANV in rats using lithium chloride. The review aims to provide references to aid the design of more precise animal models and to offer a foundation for further investigations into ANV mechanisms and potential drug development.

Abstract:Skeletal muscle injury ( SMI) is relatively common in clinical practice, and there are different understandings and approaches to its pathogenesis and treatment strategies between Chinese and western medicine.The development of animal models of SMI that can reflect the clinical characteristics of Chinese and western medicine is of great significance to the in-depth study of its pathogenesis and the exploration of effective treatment method. In this paper, starting from the Chinese and western medical etiology and pathogenesis, diagnostic criteria, and identification and typing of SMI, we conducted a comprehensive evaluation of the construction method and characteristics of the existing animal models and their compatibility with Chinese and western medical conditions. The result showed that the heavy falling blow model had the highest degree of agreement with Chinese and western medical conditions, with 69. 6% of Chinese and Western medical agreement and 49. 4% of Chinese medical agreement;followed by the exercise-induced model, with 49. 8% of western medical agreement and 44. 1% of Chinese medical agreement; and chemical stimulation and ischemia / reperfusion models had the lowest degree of agreement. Overall,the animal models of SMI involved in this paper were better than the Chinese medical model in terms of western medical agreement, and the existing models were difficult to correspond accurately with the Chinese medical diagnosis and typing. Therefore, the construction of animal models that can accurately reflect the characteristics of Chinese and western medicine and Chinese medicine patterns is still an important direction for future research.