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 plasmi...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(CD61CD62),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,CD61CD62,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,CD61CD62 significantly.It also significantly decreased the expression of t-PA,PAI-1,and p-p65 in brain immunohistochemistry and significantly decreased PT,APTT,D2D,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.展开更多
基金Supported by the Zhejiang Provincial Natural Science Foundation of China under Grant No.LQY19H080001,LS20C110001,LY17H290006)the Zhejiang Provincial Program for the Cultivation of High-Level Innovative Health Talents(No.2014-108)+1 种基金the Zhejiang Science and Technology Program of Traditional Chinese Medicine(No.2019ZA053)the Wenling City Key Discipline Group of Oncology(No.2016-127)。
文摘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(CD61CD62),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,CD61CD62,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,CD61CD62 significantly.It also significantly decreased the expression of t-PA,PAI-1,and p-p65 in brain immunohistochemistry and significantly decreased PT,APTT,D2D,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.
