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ZX
Verified CAS / Academic Author2 Decoded Studies

Prof. ZHANG Xiao-Yang

School of Chemistry and Chemical Engineering, Shihezi University

Co-Affiliations:Wuhan University

Research Publications & English Decoded Briefs

Showing 2 publications
Journal of Fuel Chemistry and Technology2026DOI: 10.1016/S1872-5813(26)60672-X

Mechanism of Ce/La/Zr doping on the structure and anti-coking performance of Ni/MgO-MgAl2O4 catalyst

Dry reforming of methane (DRM) converts CH4 and CO2 into syngas, offering a route to mitigate greenhouse gases. Ni-based catalysts suffer from sintering and carbon deposition at high temperatures. This work employs MgO-MgAl2O4 composite supports to regulate Ni loading and introduces Ce, La, and Zr as promoters to investigate their effects on DRM activity, structural stability, and surface oxygen species. Optimal Ni loading of 12.5% yields highest CH4 and CO2 conversions. Promoter introduction slightly suppresses low-temperature activity but substantially modifies support local structure and metal-support interface, improving NiO dispersion and increasing surface oxygen vacancies and active oxygen species (Oβ). These changes enhance CO2 adsorption-activation and suppress carbon deposition. After 20 h DRM, Ce-promoted catalyst shows smallest Ni particle growth (6.23→8.07 nm) and lowest carbon deposition, demonstrating superior stability and anti-coking capability. The study elucidates how Ce, La, and Zr enhance sintering and coking resistance via interfacial electronic modulation and improved oxygen storage/release, guiding rational design of stable Ni-based DRM catalysts.

SCIENCE CHINA Materials2025DOI: 10.1007/s40843-025-3348-1

Nanotherapeutic Platform-Mediated Cholesterol Metabolism Regulation for Boosting Antitumor Chemo-Immunotherapy

Chemotherapy induces immunogenic cell death (ICD) but is compromised by elevated cholesterol in the tumor microenvironment (TME), which activates myeloid-derived suppressor cells (MDSCs) and exhausts CD8+ T cells. A poly(lactide-co-glycolide) (PLGA)-based nanoplatform (COD/MTO@PLGA@FA) co-loading mitoxantrone (MTO) and cholesterol oxidase (COD) was engineered to respond to acidic TME, releasing MTO and COD. MTO kills tumor cells and triggers ICD; COD consumes cholesterol, downregulating PD-1 on tumor-infiltrating CD8+ T cells and inhibiting MDSC activation. In 4T1 tumor-bearing mice, COD/MTO@PLGA@FA plus αPD-L1 increased splenic CD4+ and CD8+ T cells from 63.4% to 72.3% and 25.7% to 32.5%, respectively. CD8+PD-1+ T cells decreased to 5.93% versus 35.9% (PBS), 31.4% (αPD-L1), 29.0% (MTO@PLGA), 23.0% (COD/MTO@PLGA), and 12.2% (COD/MTO@PLGA@FA). MDSC infiltration dropped from 16.3% to 2.25% (combination) and 6.14% (COD/MTO@PLGA@FA alone). DC maturation in tumor-draining lymph nodes reached 35.3% with the combination. The platform reverses CD8+ T cell exhaustion and remodels the immunosuppressive TME, significantly inhibiting tumor growth. This strategy offers a practical approach to enhance chemo-immunotherapy by targeting cholesterol metabolism.