The global incidence rate of cancer is increasing yearly,and chemotherapy-induced gastrointestinal mucosal injury has become a crucial factor affecting patients'therapeutic prognosis;however,there is currently a lack of effective therapeutic drugs to address this issue.There is thus an urgent need to establish more ideal animal models of chemotherapy-induced gastrointestinal mucosal injury,to support the exploration of its pathogenesis and the development of therapeutic drugs.This review considered relevant literature published during the period from 2019 to 2024,to provide a comprehensive summary and analysis from several perspectives,including the selection of experimental animals,chemotherapeutic drugs and modeling method,evaluation indicators,and practical applications.Furthermore,we highlight several existing issues with current models,including the lack of standardized modeling method,insufficient research on models with a tumor background,and inadequate exploration of novel cell death mechanisms.This collation of the literature also revealed the gradual emergence of traditional Chinese medicine as a research hotspot,with potential for the treatment of gastrointestinal mucosal injury.Further studies of effective medicines are warranted to identify interventional strategies for chemotherapy-induced gastrointestinal mucosal injury.

The global incidence rate of cancer is increasing yearly,and chemotherapy-induced gastrointestinal mucosal injury has become a crucial factor affecting patients'therapeutic prognosis;however,there is currently a lack of effective therapeutic drugs to address this issue.There is thus an urgent need to establish more ideal animal models of chemotherapy-induced gastrointestinal mucosal injury,to support the exploration of its pathogenesis and the development of therapeutic drugs.This review considered relevant literature published during the period from 2019 to 2024,to provide a comprehensive summary and analysis from several perspectives,including the selection of experimental animals,chemotherapeutic drugs and modeling method,evaluation indicators,and practical applications.Furthermore,we highlight several existing issues with current models,including the lack of standardized modeling method,insufficient research on models with a tumor background,and inadequate exploration of novel cell death mechanisms.This collation of the literature also revealed the gradual emergence of traditional Chinese medicine as a research hotspot,with potential for the treatment of gastrointestinal mucosal injury.Further studies of effective medicines are warranted to identify interventional strategies for chemotherapy-induced gastrointestinal mucosal injury.

OBJECTIVETo investigate the inhibitory effect of arsenic trioxide (As₂O₃) combined with tetradecanoylphorbol acetate (TPA) on the proliferation of Kasumi-1 cell line and its mechanism.

METHODSKasumi-1 cells were treated with 200 nmol/L TPA, different concentrations of As₂O₃ alone and combined with 200 nmol/L TPA. The proliferative inhibition rates were determined with CCK-8. Annexin V was adopted to detect apoptosis. Colony formation assay was used to determine the cloning efficiency. Flow cytometry was used to detect the cell differentiation and cell cycle changes. Western blot was employed to detect the expression of P38 and p-P38.

RESULTSThe proliferation inhibition rates of Kasumi-1 cells by TPA combined with different concentrations of As₂O₃ (0.2, 2.0 and 20.0 mmol/L)for 48 h were (25.56 ± 7.29)%, (60.63 ± 6.64)%, and (73.37 ± 2.15)%, the apoptosis rates were (61.65 ± 2.62)%, (75.39 ± 1.04)%, and (89.95 ± 1.46)%, and the colony formation rates were (76.17 ± 2.06)%, (38.50 ± 1.87)%, and (18.53 ± 2.20)%, respectively, compared with the different concentrations of As₂O₃ alone groups, the difference was statistically significant (P<0.05). Cells treated with both TPA and As₂O₃ expressed more CD11b antigens compared with the cells exposed to As₂O₃ alone. TPA treated Kasumi-1 cells were arrested at G1 phase compared with the control group, while As₂O₃ increased the percentage of Kasumi-1 cells in the G2 phase. Combination treatment increased the expression of p-P38 of Kasumi-1 cells compared with the cells exposed to As₂O₃ alone.

CONCLUSIONTPA can enhance the effect of As₂O₃ on inducing apoptosis and regulating cell cycle, thereby enhancing its anti-leukemia effect.

Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Cell Differentiation ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Oxides ; pharmacology ; Phorbol Esters ; pharmacology