BACKGROUND: We explored the dynamic expression of platelet-derived growth factor-D (PDGF-D) and phosphorylated platelet-derived growth factor receptor-β (p-PDGFR-β) after traumatic brain injury in rats to provide theoretical basis for selecting therapeutic target and intervention time after traumatic brain injury. METHODS: This study prepared the weight drop/impact acceleration-induced traumatic brain injury (TBI) model in rats, including sham group and TBI groups at different observation time points (6 hours, 12 hours, 24 hours, 3 days, and 7 days after TBI). The dynamic expression of PDGF-D and p-PDGFR-β after TBI were detected by western blot and immunofluorescence staining. RESULTS: The expression level of PDGF-D and p-PDGFR-β after TBI was detected by western blot. The PDGF-D level was increased (p < 0.05) 6 hours after TBI and remained at the high level until 3 days after TBI (p < 0.05). The p-PDGFR-β level was increased (p < 0.05) 12 hours after TBI and remained at the high level until 3 days after TBI (p < 0.05). PDGF-D and p-PDGFR-β in brain tissues were found by immunofluorescence in the perihematoma area 24 hours after TBI. CONCLUSIONS: This study revealed the expression phenomenon of PDGF-D and p-PDGFR-β after TBI in rats, suggesting that PDGF-D participates in the process of secondary brain injury after TBI through specific binding with PDGFR-β, which provides a theoretical basis for further research on selecting therapeutic targets and intervention times after TBI.
BACKGROUND: We explored the dynamic expression of platelet-derived growth factor-D (PDGF-D) and phosphorylated platelet-derived growth factor receptor-β (p-PDGFR-β) after traumatic brain injury in rats to provide theoretical basis for selecting therapeutic target and intervention time after traumatic brain injury. METHODS: This study prepared the weight drop/impact acceleration-induced traumatic brain injury (TBI) model in rats, including sham group and TBI groups at different observation time points (6 hours, 12 hours, 24 hours, 3 days, and 7 days after TBI). The dynamic expression of PDGF-D and p-PDGFR-β after TBI were detected by western blot and immunofluorescence staining. RESULTS: The expression level of PDGF-D and p-PDGFR-β after TBI was detected by western blot. The PDGF-D level was increased (p < 0.05) 6 hours after TBI and remained at the high level until 3 days after TBI (p < 0.05). The p-PDGFR-β level was increased (p < 0.05) 12 hours after TBI and remained at the high level until 3 days after TBI (p < 0.05). PDGF-D and p-PDGFR-β in brain tissues were found by immunofluorescence in the perihematoma area 24 hours after TBI. CONCLUSIONS: This study revealed the expression phenomenon of PDGF-D and p-PDGFR-β after TBI in rats, suggesting that PDGF-D participates in the process of secondary brain injury after TBI through specific binding with PDGFR-β, which provides a theoretical basis for further research on selecting therapeutic targets and intervention times after TBI.