目的:研究大鼠胃癌前病变形成过程中胃黏膜Sonic Hedgehog(Shh)信号通路的变化。方法:72只乳鼠随机分为正常组36只,造模组36只,雌雄各半。造模组灌服800 mg/L的1-甲基-3-硝基-1-亚硝基胍(MNNG)0.1 m L/d,正常组灌服生理盐水0.1 m L/d,共...目的:研究大鼠胃癌前病变形成过程中胃黏膜Sonic Hedgehog(Shh)信号通路的变化。方法:72只乳鼠随机分为正常组36只,造模组36只,雌雄各半。造模组灌服800 mg/L的1-甲基-3-硝基-1-亚硝基胍(MNNG)0.1 m L/d,正常组灌服生理盐水0.1 m L/d,共10 d。随后在实验观察第10周、22周、34周末每组分别雌雄各处死6只。HE染色检测胃黏膜组织病理学变化,q RTPCR法检测胃黏膜组织Shh、Ptch1、Smo、Gli1、Gli2、Gli3、Su Fu、Cyclin D1、Cyclin E1、c-Myc、β-actin m RNA的表达。Western blot检测胃黏膜组织Shh、Ptch1、Smo、Gli1、Su Fu、Cyclin D1、Cyclin E1、cMyc、p-c-Myc蛋白表达。结果:随造模时间的延长,模型组大鼠胃黏膜萎缩及异型增生逐渐加重,其胃黏膜内Shh、Smo、Gli1、Cyclin D1、Cyclin E1及c-Myc m RNA表达较正常组不同程度升高,而Ptch1和Su Fu m RNA不同程度降低。模型组胃黏膜内Shh、Smo、Gli1、Cyclin D1、Cyclin E1、p-c-Myc蛋白水平较正常组增加,Ptch1和Su Fu则降低,但差异无统计学意义。结论:大鼠胃癌前病变的形成过程中存在Shh信号通路的激活,提示Shh信号通路可能参与胃癌前病变的发生与发展。展开更多
目的观察大黄素对重症急性胰腺炎(SAP)肺损伤大鼠肺组织FGL2凝血酶原酶的影响。方法采用逆行胰胆管注射牛磺胆酸建立SAP肺损伤大鼠模型,分别以大黄素高(40 mg/kg)、中(20 mg/kg)、低剂量(10 mg/kg)进行干预,在造模3、6、12 h 3个时相点...目的观察大黄素对重症急性胰腺炎(SAP)肺损伤大鼠肺组织FGL2凝血酶原酶的影响。方法采用逆行胰胆管注射牛磺胆酸建立SAP肺损伤大鼠模型,分别以大黄素高(40 mg/kg)、中(20 mg/kg)、低剂量(10 mg/kg)进行干预,在造模3、6、12 h 3个时相点分批处死大鼠,采用qRT-PCR检测大鼠肺组织FGL2、TNF-αmRNA表达,免疫组化技术检测肺组织中FGL2蛋白表达,ELISA法检测肺组织TNF-α及TXB2、6-Keto-PGF1α水平。结果模型组大鼠3、6、12 h 3个时相点肺组织FGL2、TNF-αmRNA和蛋白表达,TXB2水平及TXB2/6-Keto-PGF1α比值较假手术组同一时相点明显增高(P<0.05或P<0.01),应用大黄素高、中、低剂量干预后,肺组织FGL2、TNF-αmRNA和蛋白表达,TXB2水平及TXB2/6-Keto-PGF1α比值较模型组同一时相点显著下降(P<0.05或P<0.01)。结论重症急性胰腺炎肺损伤时大黄素可以通过下调FGL2凝血酶原酶减轻胰腺炎肺损伤程度,这可能是大黄素抗SAP肺损伤的重要作用机制。展开更多
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
文摘目的:研究大鼠胃癌前病变形成过程中胃黏膜Sonic Hedgehog(Shh)信号通路的变化。方法:72只乳鼠随机分为正常组36只,造模组36只,雌雄各半。造模组灌服800 mg/L的1-甲基-3-硝基-1-亚硝基胍(MNNG)0.1 m L/d,正常组灌服生理盐水0.1 m L/d,共10 d。随后在实验观察第10周、22周、34周末每组分别雌雄各处死6只。HE染色检测胃黏膜组织病理学变化,q RTPCR法检测胃黏膜组织Shh、Ptch1、Smo、Gli1、Gli2、Gli3、Su Fu、Cyclin D1、Cyclin E1、c-Myc、β-actin m RNA的表达。Western blot检测胃黏膜组织Shh、Ptch1、Smo、Gli1、Su Fu、Cyclin D1、Cyclin E1、cMyc、p-c-Myc蛋白表达。结果:随造模时间的延长,模型组大鼠胃黏膜萎缩及异型增生逐渐加重,其胃黏膜内Shh、Smo、Gli1、Cyclin D1、Cyclin E1及c-Myc m RNA表达较正常组不同程度升高,而Ptch1和Su Fu m RNA不同程度降低。模型组胃黏膜内Shh、Smo、Gli1、Cyclin D1、Cyclin E1、p-c-Myc蛋白水平较正常组增加,Ptch1和Su Fu则降低,但差异无统计学意义。结论:大鼠胃癌前病变的形成过程中存在Shh信号通路的激活,提示Shh信号通路可能参与胃癌前病变的发生与发展。
文摘目的观察大黄素对重症急性胰腺炎(SAP)肺损伤大鼠肺组织FGL2凝血酶原酶的影响。方法采用逆行胰胆管注射牛磺胆酸建立SAP肺损伤大鼠模型,分别以大黄素高(40 mg/kg)、中(20 mg/kg)、低剂量(10 mg/kg)进行干预,在造模3、6、12 h 3个时相点分批处死大鼠,采用qRT-PCR检测大鼠肺组织FGL2、TNF-αmRNA表达,免疫组化技术检测肺组织中FGL2蛋白表达,ELISA法检测肺组织TNF-α及TXB2、6-Keto-PGF1α水平。结果模型组大鼠3、6、12 h 3个时相点肺组织FGL2、TNF-αmRNA和蛋白表达,TXB2水平及TXB2/6-Keto-PGF1α比值较假手术组同一时相点明显增高(P<0.05或P<0.01),应用大黄素高、中、低剂量干预后,肺组织FGL2、TNF-αmRNA和蛋白表达,TXB2水平及TXB2/6-Keto-PGF1α比值较模型组同一时相点显著下降(P<0.05或P<0.01)。结论重症急性胰腺炎肺损伤时大黄素可以通过下调FGL2凝血酶原酶减轻胰腺炎肺损伤程度,这可能是大黄素抗SAP肺损伤的重要作用机制。
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.
