scholarly journals Xuesaitong injection (lyophilized) combined with aspirin and clopidogrel protect against focal cerebral ischemic/reperfusion injury in rats by suppressing oxidative stress and inflammation and regulating the NOX2/IL-6/STAT3 pathway

2020 ◽  
Vol 9 (6) ◽  
pp. 62-62
Author(s):  
Ting Zhu ◽  
Xiang-Bao Meng ◽  
Dong-Xia Dong ◽  
Li-Yu Zhao ◽  
Mu-Wen Qu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Ischemic Reperfusion Injury ◽  
Stat3 Pathway ◽  
Ischemic Reperfusion ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion

Knockdown lncRNA Neat1 regulates the activation of microglia and alleviate neuronal apoptosis through AKT/STAT3 pathway after cerebral ischemic reperfusion.

2020 ◽  
Author(s):  
Xunran Ni ◽  
Qian Su ◽  
Wenbo Xia ◽  
Yanli Zhang ◽  
Kejuan Jia ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Molecular Mechanisms ◽  
Ischemic Reperfusion Injury ◽  
Phenotypic Marker ◽  
Stat3 Pathway ◽  
Ischemic Reperfusion ◽  
Acute Cerebral Ischemia ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
Lncrna Neat1

Abstract Background Acute cerebral ischemia may cause serious consequences, one of them is brain injury caused by the uncontrolled reperfusion which occurs once the circulation is re-established. Neat1 is one of long non-coding RNA presents important roles in the immune system. However, the potential roles and underlying molecular mechanisms of it in cerebral ischemic reperfusion injury is still unclear.The aim of the present study was to investigate the function of LncRNA Neat1 in cerebral ischemic reperfusion injury and its possible advantage for neure.MethodsIn our study, oxygen glucose deprivation was used in vitro to mimic cerebral I/R injury. CCK8 was used to mesure cell viability and flow cytometry measured cell apoptosis. qRT-pcr was used to measure the phenotypic marker of M1 and M2 microglia, western blot was used to detect the protein expression of AKT/STAT3 pathway.ResultsKnockdown the LncRNA Neat1 alleviated the apoptosis induced by OGD/R and increased the cell viability.We further provided that Neat1 may inhibite microglia polarize to M1 phenotype to reduce the damage of immunoreaction caused after cerebral I/R injury through AKT/STAT3 pathway. ConclusionsWe evaluated the function and mechanism of lncRNA Neat1 in cerebral I/R injury, And LncRNA Neat1 may be a potential target for new therapeutic intervention.

scholarly journals Protective Effect of Pharmacological Preconditioning of Total Flavones of Abelmoschl Manihot on Cerebral Ischemic Reperfusion Injury in Rats

2007 ◽  
Vol 35 (04) ◽  
pp. 653-661 ◽  
Author(s):  
Ji-Yue Wen ◽  
Zhi-Wu Chen
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inos Mrna ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Infarction Volume ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
Pharmacological Preconditioning

The present study was to investigate the effect of pharmacological preconditioning of total flavones of Abelmoschl Manihot (TFA) on cerebral ischemic reperfusion injury in rats. Rat cerebral ischemia/reperfusion injury was induced by occluding the right middle cerebral artery (MCA). The infarct size was determined by staining with 2,3,5-triphenyl tetrazalium chloride (TTC). The serum malonaldehyde (MDA), nitric oxide (NO) and lactate dehydrogenase (LDH) levels were measured by using spectrophotometry; Inducible NO synthase (iNOS) mRNA expression was detected by RT-PCR method. The percentage of cerebral infarction volume was 28.1 ± 0.8 in the model group, while TFA or nimodipine (Nim) pretreatment 36 hours prior to the ischemic insult significantly decreased the infarction volume. Increases of serum LDH activity and MDA level were observed after ischemia/reperfusion, but these changes were inhibited in rats pretreated with either TFA (20, 40, 80, 160 mg/kg) or Nim, indicating a delayed protective effect of TFA preconditioning on cerebral ischemic reperfusion injury. In addition, the serum NO level and the cerebral iNOS mRNA were up-regulated, suggesting a possible mechanism for the protective effect of TFA pretreatment on cerebral ischemic reperfusion injury.

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