The expression and significance of PFKFB3 in brain tissue after stroke

Objective: To explore the expression and significance of 6-phosphofructose-2-kinase/fructose-2, 6-bisphosphatase 3 (PFKFB3) in brain tissue after stroke. Method: In this study, 64 male C57BL/6 mice with a body weight of 25±5g were selected. They were divided into the sham operation group (16 rats) and the ischemic model group (48 rats). The ischemic model group was further divided into the following groups according to the duration of ischemia: 2-hour ischemia group, 6-hour ischemia group, and 12-hour ischemia group (16 rats in each group). After MCAO modeling by the thread plug method, TTC staining, HE staining and immunohistochemical staining were performed. Result: The TTC staining results showed that after MCAO modeling, with the extension of time, the infarction area of brain tissue at different time points (2 hours, 6 hours, 12 hours) continuously expanded (P< 0.05), and the severity of infarction also continuously deepened. The results of HE staining showed that after MCAO modeling, when observing the coronal section infarction of the brain tissue of mice at different time points (2 hours, 6 hours, and 12 hours), it could be seen that the brain tissue of the 2-hour group had mild edema, and vacuoles of different sizes appeared in the intercellular Spaces. After 6 hours, the brain tissue edema worsened, the tissue became loose, and the intercellular and vascular Spaces widened. After 12 hours, the brain tissue was highly edematous, with inflammatory cell infiltration. Some neurons were significantly degenerated and necrotic, the nuclear structure was blurred, and the nucleoli disappeared. The immunohistochemical staining results showed that after MCAO modeling, the level of PFKFB3 in brain tissue gradually increased at different time points (2 hours, 6 hours, and 12 hours) with the increase of time (P< 0.05). Conclusion: After a stroke, the longer the infarction time, the larger the infarction area, the more severe the brain injury, and the higher the expression of PFKFB3. This discovery provides a new idea for the future use of PFKFB3 inhibitors in the treatment of stroke. Funding: Research Project Supported by Sanjin Talents - Leading Talent Project for Scientific and Technological Innovation, Key Research Project for High-level Science and Technology Talents in Lvliang City (2023RC08,2024RC19). National Key Clinical Specialty Construction Project Research Special Project. Shanxi Medical University Undergraduate Teaching Reform and Innovation Project (XJ2025019) This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.