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.

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.

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.