Traditional molecular medicine experimental teaching often suffers from a disconnection between theory and practice, as well as fragmented experimental content, making it difficult for students to integrate multi-level knowledge to address complex scientific problems. To address this, we redesigned our Molecular Medicine Experimental Techniques course around the pathophysiology of cerebral ischemia-reperfusion injury (CIRI), with a focus on the mechanism of ferroptosis. Our integrated pedagogical model links an in vivo transient middle cerebral artery occlusion (tMCAO) mouse model with an in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model in HT22 neuronal cells. Within this framework, students first observe in vivo phenotypes in the tMCAO model, including increased brain iron content, downregulated GPX4 expression, and accumulation of the lipid peroxidation marker 4-HNE. They then use the OGD/R cell model to validate key ferroptosis features at the molecular and ultrastructural levels, such as enhanced lipid peroxidation, glutathione depletion, and mitochondrial damage. This “phenotype-to-mechanism” approach allows students to intuitively understand the role of ferroptosis in CIRI while systematically mastering the full research cycle, from establishing disease models and applying multi-technique assays to integrating and interpreting data. By translating a cutting-edge scientific topic into a coherent experimental teaching module, this reform effectively bridges the gap between theoretical knowledge and hands-on research practice. It fosters students’ integrative scientific thinking and enhances their ability to tackle complex biomedical questions, offering a transferable paradigm for advancing high-level experimental training in molecular medicine.