Abstract: OBJECTIVE: To evaluate the protective efficacy of Sanqi(Radix Notoginseng) on cerebral hemorrhage in a rat model of traumatic brain injury(TBI) by investigating plasminogen activator inhibitor-1(PAI-1), tissue-type plasminogen activator(t-PA),nuclear factor-κB(NF-κB, p-p65), nitric oxide(NO),endothelin(ET), cluster differentiation(CD61 CD62),and coagulation.METHODS: The free-fall method was used to create a rat model of TBI. Forty-eight rats were randomly divided into six groups: the blank group,sham group, model group, low-dose Sanqi(Radix Notoginseng) group, middle-dose Sanqi(Radix Notoginseng) group, and high-dose Sanqi(Radix Notoginseng) group. At 24 h after the model was created, we investigated brain MRI, brain tissue morphology using HE staining, flow cytometry, and immunohistochemical changes.RESULTS: Cerebral hemorrhage was aggravated in TBI rats(observed in brain specimens, brain MRI,and brain tissue HE). Cerebral immunohistochemistry results demonstrated that the expression of t-PA, PAI-1 and p-p65 increased significantly in TBI rats, while t-PA/PAI-1 had a significant decrease. In addition, CD61 CD62, D2D, and ET were significantly increased in TBI rats, and PT and APTT were significantly prolonged; in contrast, NO was significantly decreased. Sanqi(Radix Notoginseng) decreased cerebral hemorrhage in TBI rats(observed in brain MRI and brain tissue HE), and increased t-PA/PAI-1, CD61 CD62 significantly. It also significantly decreased the expression of t-PA, PAI-1, and p-p65 in brain immunohistochemistry and significantly decreased PT, APTT, D2 D, and ET. However,there were no differences in NO between the model group and the Sanqi(Radix Notoginseng) group.CONCLUSION: Sanqi(Radix Notoginseng) can decrease the expression of p-p65, increase t-PA/PAI-1,and stem traumatic intracranial hemorrhage in a TBI rat model.

Key words: Sanqi(Radix Notoginseng);;Brain injuries,traumatic;;Plasminogen activator inhibitor-1;;Tissue-type plasminogen activator;;p-p65