A preliminary miRNA screening showed that expression levels of rno-miRNA-27a-3p were significantly increased in the serum and brain tissues of rats undergoing cerebral ischemia.In recent years,there is evidence of the...A preliminary miRNA screening showed that expression levels of rno-miRNA-27a-3p were significantly increased in the serum and brain tissues of rats undergoing cerebral ischemia.In recent years,there is evidence of the protective capacity of the saponins extracted from panax ginseng and its primary active ingredient ginsenosideRg1oncerebral ischemic injury.Methods:Fetal rat neurons(FRNs)were cultured in glucose-and-serumfree medium and exposed to hypoxia to establish a cerebral ischemia model in vitro(oxygen and glucose deprivation model,OGD).Antioxidant indexes(CAT,SOD),inflammatory markers(MPO,TNF-αand IL-6),and the expression of apoptosis and proliferation associated proteins(NF kB-p65,Caspase 3-cleaved,BCL-2)were examined.Results:Pre-treatment of Rg1(30–100μg/mL)could effectively inhibit the decline of antioxidant indexes(CAT,SOD)and increase in inflammatory markers(MPO,TNF-αand IL-6),and effectively inhibited the apoptosis in FRNs induced by OGD in a gradient-dependent manner.The mechanism analysis showed that the role of Rg1 in protecting against ischemia-induced neuron damage depends on its indirect up-regulation of PPAR protein via suppression of rnomiRNA-27a-3p.Moreover,these effects of Rg1 could be reversed by exogenous rno-miRNA-27a-3p and PPAR gene silencing in FRNs exposed to OGD.Conclusion:To summarize,our study demonstrates that Rg1 could effectively attenuate neuronal damage caused by cerebral ischemia via the rno-miRNA-27a-3p/PPARγpathway.Further,clarification of the novel mechanism will certainly improve our previous understanding of the role of Rg1 and enhancing its level in treatments for alleviating ischemic brain injury.展开更多
Arterioportal fistulas(APFs)are defined as vascular communications between the systemic arteries and portal circulation.APFs are classified as congenital or acquired,large or small,intrahepatic or extrahepatic,and tra...Arterioportal fistulas(APFs)are defined as vascular communications between the systemic arteries and portal circulation.APFs are classified as congenital or acquired,large or small,intrahepatic or extrahepatic,and traumatic or spontaneous.The consistent abnormal connection may result in severe presinusoidal portal hypertension,leading to gastrointestinal bleeding(GIB),ascites,elevated liver function enzymes,heart failure,diarrhea,and even pancreatitis or hematobilia in some unusual cases.Indeed,less than half reported cases have GIB,predominately caused by variceal rupture.Peptic ulcer bleeding has rarely been reported in the setting of APFs.Herein,we describe a case in which intrahepatic APF manifested as gastric ulcer bleeding,progressive portal thrombosis,and massive ascites,with these symptoms successfully relieved by endovascular treatment.展开更多
基金supported by the National Natural Science Foundation of China,Nos.81973317,81374007,81870977the Natural Science Foundation of Heilongjiang Province,HL2019H062+1 种基金the Projects of Basic Scientific Research Business Expenses in Higher Education Institutions of Heilongjiang Province,No.2018-KYYWF-MY-005the Students Innovative and the Entrepreneurship Training Scientific Research Foundation of Heilongjiang Province,No.102292017001.
文摘A preliminary miRNA screening showed that expression levels of rno-miRNA-27a-3p were significantly increased in the serum and brain tissues of rats undergoing cerebral ischemia.In recent years,there is evidence of the protective capacity of the saponins extracted from panax ginseng and its primary active ingredient ginsenosideRg1oncerebral ischemic injury.Methods:Fetal rat neurons(FRNs)were cultured in glucose-and-serumfree medium and exposed to hypoxia to establish a cerebral ischemia model in vitro(oxygen and glucose deprivation model,OGD).Antioxidant indexes(CAT,SOD),inflammatory markers(MPO,TNF-αand IL-6),and the expression of apoptosis and proliferation associated proteins(NF kB-p65,Caspase 3-cleaved,BCL-2)were examined.Results:Pre-treatment of Rg1(30–100μg/mL)could effectively inhibit the decline of antioxidant indexes(CAT,SOD)and increase in inflammatory markers(MPO,TNF-αand IL-6),and effectively inhibited the apoptosis in FRNs induced by OGD in a gradient-dependent manner.The mechanism analysis showed that the role of Rg1 in protecting against ischemia-induced neuron damage depends on its indirect up-regulation of PPAR protein via suppression of rnomiRNA-27a-3p.Moreover,these effects of Rg1 could be reversed by exogenous rno-miRNA-27a-3p and PPAR gene silencing in FRNs exposed to OGD.Conclusion:To summarize,our study demonstrates that Rg1 could effectively attenuate neuronal damage caused by cerebral ischemia via the rno-miRNA-27a-3p/PPARγpathway.Further,clarification of the novel mechanism will certainly improve our previous understanding of the role of Rg1 and enhancing its level in treatments for alleviating ischemic brain injury.
文摘Arterioportal fistulas(APFs)are defined as vascular communications between the systemic arteries and portal circulation.APFs are classified as congenital or acquired,large or small,intrahepatic or extrahepatic,and traumatic or spontaneous.The consistent abnormal connection may result in severe presinusoidal portal hypertension,leading to gastrointestinal bleeding(GIB),ascites,elevated liver function enzymes,heart failure,diarrhea,and even pancreatitis or hematobilia in some unusual cases.Indeed,less than half reported cases have GIB,predominately caused by variceal rupture.Peptic ulcer bleeding has rarely been reported in the setting of APFs.Herein,we describe a case in which intrahepatic APF manifested as gastric ulcer bleeding,progressive portal thrombosis,and massive ascites,with these symptoms successfully relieved by endovascular treatment.
