Pluchea lanceolata protects hippocampal neurons from endothelin-1 induced ischemic injury to ameliorate cognitive deficits

2018 ◽  
Vol 94 ◽  
pp. 75-85 ◽  
Author(s):  
Ravi Mundugaru ◽  
Senthilkumar Sivanesan ◽  
Aurel Popa-Wagner ◽  
Padmaja Udaykumar ◽  
Ramalingam Kirubagaran ◽  
...  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xin-Ming Luo ◽  
Jing Zhao ◽  
Wen-Yue Wu ◽  
Jie Fu ◽  
Zheng-Yu Li ◽  
...  

Abstract Background Status epilepticus (SE) is a life-threatening neurological disorder. The hippocampus, as an important area of the brain that regulates cognitive function, is usually damaged after SE, and cognitive deficits often result from hippocampal neurons lost after SE. Fyn, a non-receptor Src family of tyrosine kinases, is potentially associated with the onset of seizure. Saracatinib, a Fyn inhibitor, suppresses epileptogenesis and reduces epileptiform spikes. However, whether saracatinib inhibits cognitive deficits after SE is still unknown. Methods In the present study, a pilocarpine-induced SE mouse model was used to answer this question by using the Morris water maze and normal object recognition behavioral tests. Results We found that saracatinib inhibited the loss in cognitive function following SE. Furthermore, we found that the number of hippocampal neurons in the saracatinib treatment group was increased, when compared to the SE group. Conclusions These results showed that saracatinib can improve cognitive functions by reducing the loss of hippocampal neurons after SE, suggesting that Fyn dysfunction is involved in cognitive deficits after SE, and that the inhibition of Fyn is a possible treatment to improve cognitive function in SE patients.


2020 ◽  
Vol 36 (8) ◽  
pp. 875-894
Author(s):  
Cheng Chen ◽  
Li Liu ◽  
Ya-Qiao Shu ◽  
Ping Jing ◽  
Yun Lu ◽  
...  

2020 ◽  
Vol 39 (6) ◽  
pp. 816-827
Author(s):  
M Zhang ◽  
DJ Ge ◽  
Z Su ◽  
B Qi

The repairing effect and potential mechanism of miR-137 on cerebral ischemic injury in rats was investigated. The volume of cerebral infarction and calculated brain water content was detected by triphenyltetrazolium chloride staining. The expression of inflammatory factors was detected by enzyme-linked immunosorbent assay. The pathological damage of brain tissue was analyzed by hematoxylin and eosin and Nissl staining. The apoptosis in ischemic brain tissue was detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling. The levels of STAT1 and JAK1 proteins were analyzed by Western blot. The expression of miR-137 in primary hippocampal neurons was detected by reverse transcription polymerase chain reaction. miR-137 overexpression significantly improved brain damage in rats. miR-137 overexpression can reduce the expression of TNF-α, IL-1β, and IL-6. miR-137 overexpression can reduce the degree of brain tissue damage and inhibit the expression of JAK1 and STAT1 proteins. miR-137 overexpression can reduce oxygen-glucose deprivation (OGD)/R-induced cell damage, improve cell proliferation, and reduce apoptotic rate. JAK1 and STAT1 protein expression was inhibited in hippocampal neurons after OGD/R treatment after transfection with miR-137 mimic. After the addition of the Filgotinib inhibitor, the levels of JAK1 and STAT1 proteins were significantly reduced. The results suggested that miR-137 overexpression can effectively improve ischemic injury after focal cerebral ischemia and protect against by inhibiting JAK1/STAT1 pathway.


1993 ◽  
Vol 96 (1) ◽  
pp. 89-99 ◽  
Author(s):  
A. Ueki ◽  
L. Rosén ◽  
B. Andbjer ◽  
L. F. Agnati ◽  
Å. Hallström ◽  
...  

Author(s):  
Damon J. DiSabato ◽  
Daniel P. Nemeth ◽  
Xiaoyu Liu ◽  
Kristina G. Witcher ◽  
Shane M. O’Neil ◽  
...  

2015 ◽  
Vol 20 (5) ◽  
pp. 273-283 ◽  
Author(s):  
Dorota L. Stankowska ◽  
Vignesh R. Krishnamoorthy ◽  
Dorette Z. Ellis ◽  
Raghu R. Krishnamoorthy

2016 ◽  
Vol 113 (42) ◽  
pp. E6526-E6534 ◽  
Author(s):  
Niels R. Reinders ◽  
Yvonne Pao ◽  
Maria C. Renner ◽  
Carla M. da Silva-Matos ◽  
Tessa R. Lodder ◽  
...  

Amyloid-β (Aβ) is a prime suspect for causing cognitive deficits during the early phases of Alzheimer’s disease (AD). Experiments in AD mouse models have shown that soluble oligomeric clusters of Aβ degrade synapses and impair memory formation. We show that all Aβ-driven effects measured in these mice depend on AMPA receptor (AMPAR) subunit GluA3. Hippocampal neurons that lack GluA3 were resistant against Aβ-mediated synaptic depression and spine loss. In addition, Aβ oligomers blocked long-term synaptic potentiation only in neurons that expressed GluA3. Furthermore, although Aβ-overproducing mice showed significant memory impairment, memories in GluA3-deficient congenics remained unaffected. These experiments indicate that the presence of GluA3-containing AMPARs is critical for Aβ-mediated synaptic and cognitive deficits.


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