The pathophysiological process of ischemic stroke (IS) is highly complex. Current clinical treatments are limited by a narrow therapeutic time window and are inadequate for improving residual neurological dysfunction. Therefore, animal models have become essential tools for exploring the pathological mechanisms of this disease from both traditional Chinese medicine (TCM) and Western medicine perspectives,as well as for evaluating innovative therapeutic strategies. This review systematically outlines existing IS modeling methods and cutting-edge advances. It comparatively integrates the multi-layered pathogeneses in Western medicine, including excitotoxicity, oxidative stress, inflammatory responses, blood-brain barrier injury, ferroptosis, and PANoptosis, with the core TCM pathogenesis characterized by disorders of Qi and blood and functional imbalance caused by "wind, fire/heat, phlegm, blood stasis, and deficiency." Furthermore, this paper categorizes and compares the specific modeling techniques, evaluation indicators, and respective advantages and limitations of focal cerebral ischemia models, global cerebral ischemia models, and TCM disease-syndrome combined models, such as the Qi deficiency and blood stasis syndrome. Literature review suggests that, by exploring emerging cell death mechanisms like PANoptosis and introducing environmental stress or dietary interventions on the basis of ischemic modeling, specific TCM syndromes associated with IS can be preliminarily screened out and replicated. It provides a feasible approach for objectively elucidating the biological basis of TCM interventions involving multiple targets and pathways. Given that traditional single-disease models fail to fully capture the complexity and individual heterogeneity of the cerebral network microenvironment in clinical patients, future research on IS animal models should focus on the deep integration of TCM and Western medicine in pathogenesis. By leveraging multidisciplinary technologies, such as gene editing, high-resolution in vivo imaging, artificial intelligence-driven multi-omics analysis, and brain organoids, researchers can construct high-biomimetic, multi-dimensional models that closely mirror clinical scenarios, thereby effectively improving the success rate of translating innovative IS therapies from basic research to clinical application.

Objective:To explore whether LBP3 exerts anti-tumor effects by promoting production of short-chain fatty acids(SCFAs)by intestinal microbiota and regulating function of polymorphonuclear myeloid-derived suppressor cells(PMN-MDSC).Methods:A subcutaneous H22 liver cancer model was employed to assess anti-tumor activity of LBP3 and its regulatory effects on PMN-MDSC.Pseudo-sterile tumor-bearing mouse model was used to investigate role of intestinal microbiota in tumor suppression of LBP3.Fecal microbiota transplantation(FMT)was conducted to explore immune regulatory role of LBP3-modulated flora.Serum SCFAs levels in tumor-bearing mice were quantified using liquid chromatography-mass spectrometry,and effect of SCFAs butyrate on arginase 1(Arg-1)expression was evaluated in vitro.Results:Both low-dose(125 mg/kg)and high-dose(250 mg/kg)LBP3 signifi-cantly inhibited tumor growth in H22 tumor-bearing mice,also led to a marked reduction in proportion of PMN-MDSC in both spleen and tumor,a reduced proportion of Treg in lymphoid tissues,a decrease in Arg-1 level within tumor,infiltration of CD8+T cells into tumor was significantly enhanced.However,these effects of LBP3 were did not observed in pseudo-sterile mice,while the above changes could be reproduced after fecal supernatant transplantation in high-dose LBP3 treatment group,suggesting a crucial role for gut microbiota.Furthermore,co-expression of Ly6G and SCFA receptor GPR43 in tumor was also observed.LBP3 treatment resulted in increased levels of SCFAs,particularly butyrate,in both blood and tumor tissues.In vitro,butyrate was shown to inhibit Arg-1 expression in MSC-2 cells,further supporting hypothesis that SCFAs mediate immune-modulatory effects of LBP3.Conclusion:LBP3 exerts its anti-tumor effects by promoting SCFA production,which subsequently inhibits function of PMN-MDSC.This highlights LBP3's potential as an immunomodulatory agent in cancer therapy.

Objective:To explore whether LBP3 exerts anti-tumor effects by promoting production of short-chain fatty acids(SCFAs)by intestinal microbiota and regulating function of polymorphonuclear myeloid-derived suppressor cells(PMN-MDSC).Methods:A subcutaneous H22 liver cancer model was employed to assess anti-tumor activity of LBP3 and its regulatory effects on PMN-MDSC.Pseudo-sterile tumor-bearing mouse model was used to investigate role of intestinal microbiota in tumor suppression of LBP3.Fecal microbiota transplantation(FMT)was conducted to explore immune regulatory role of LBP3-modulated flora.Serum SCFAs levels in tumor-bearing mice were quantified using liquid chromatography-mass spectrometry,and effect of SCFAs butyrate on arginase 1(Arg-1)expression was evaluated in vitro.Results:Both low-dose(125 mg/kg)and high-dose(250 mg/kg)LBP3 signifi-cantly inhibited tumor growth in H22 tumor-bearing mice,also led to a marked reduction in proportion of PMN-MDSC in both spleen and tumor,a reduced proportion of Treg in lymphoid tissues,a decrease in Arg-1 level within tumor,infiltration of CD8+T cells into tumor was significantly enhanced.However,these effects of LBP3 were did not observed in pseudo-sterile mice,while the above changes could be reproduced after fecal supernatant transplantation in high-dose LBP3 treatment group,suggesting a crucial role for gut microbiota.Furthermore,co-expression of Ly6G and SCFA receptor GPR43 in tumor was also observed.LBP3 treatment resulted in increased levels of SCFAs,particularly butyrate,in both blood and tumor tissues.In vitro,butyrate was shown to inhibit Arg-1 expression in MSC-2 cells,further supporting hypothesis that SCFAs mediate immune-modulatory effects of LBP3.Conclusion:LBP3 exerts its anti-tumor effects by promoting SCFA production,which subsequently inhibits function of PMN-MDSC.This highlights LBP3's potential as an immunomodulatory agent in cancer therapy.

Objective To investigate the effect of emodin on immune suppression function of regulatory T cells in a mouse model of CT26 colon cancer. Methods Twenty-four mice were divided into the negative control group, the emodin group and the tumor group. The populations of CD8+CD3+T cells, the T cells producing IFN-γand the CD4+CD25+Tregs secreting IL-10 in different mouse tissues were detected by flow cytometry. Levels of IFN-γ, TNF- β1 and IL-10 in serum were determined by ELISA. Results Emodin could significantly increase the percent of CD8+CD3+T cells in tumor (P < 0.05) and improve the ability of IFN-γ secretion in T cells from peripheral blood and lymph nodes (P < 0.05). Emodin could reduce the levels of IFN-γ, TNF-β1 and IL-10 in the serum (P < 0.01) and inhibit IL-10 secretion in CD4+CD25+ Tregs (P < 0.01). Conclusion Emodin possesses the antitumor effect by affecting the immunosuppressive function of Tregs cells.

Purpose　The aim is to sulfonize Hunai polysaccharide fr om p leurotus tuber-rigium(Fr.)Sing. and to evaluate the antioxidative activities of the sulfated po lysaccharide (S-HNP).Methods　S-HNP was prepared by the reacti on of Hunai polysaccharide with chlorosulfonic acid-Pyridine. The antioxidative activities o f S-HNP were evaluated as follows: (1) the inhibition effects on Fe2+- Vc inducing the injury of rat liver mitochondria in vitro, (2) the protectiv e ef fect on CuSO4 -Phen-Vc-H2O2 inducing the damage of DNA, (3) the scaven ging effect on O*-2. Results　 S-HNP could protect mitochondria from lipid peroxidation induced by Fe2+-Vc, i ncluding the inhibitions of the increase of TBARS content, the swelling of mitoc hondria and the decrease of membrane fluidity, and protect DNA from the damage induced by CuSO4-Phen-Vc-H2O2， and scavenge O*-2 generated in the sel f-oxidation of pyrogallic acid. Conclusion　S-HNP exhibi ted marked antioxidative activities.