Therapeutic Neuroprotective Effects of XQ-1H in a Rat Model of Permanent Focal Cerebral Ischemia

Pharmacology ◽  
2012 ◽  
Vol 89 (1-2) ◽  
pp. 1-6 ◽  
Author(s):  
Qichuan Yang ◽  
Weirong Fang ◽  
Peng Lv ◽  
Xiaohan Geng ◽  
Yunman Li ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Rat Model ◽  
Focal Cerebral Ischemia ◽  
Neuroprotective Effects

scholarly journals Neuroprotective Effects of a Novel Inhibitor of c-Jun N-Terminal Kinase in the Rat Model of Transient Focal Cerebral Ischemia

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1860 ◽  
Author(s):  
Mark B. Plotnikov ◽  
Galina A. Chernysheva ◽  
Vera I. Smolyakova ◽  
Oleg I. Aliev ◽  
Eugene S. Trofimova ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Rat Model ◽  
Focal Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Specific Inhibitor ◽  
Fold Increase ◽  
Neuroprotective Activity ◽  
Prophylactic Regimen ◽  
Neuroprotective Effects

A novel specific inhibitor of c-Jun N-terminal kinase, 11H-indeno[1,2-b]quinoxalin-11-one oxime sodium salt (IQ-1S), has a high affinity to JNK3 compared to JNK1/JNK2. The aim of this work was to study the mechanisms of neuroprotective activity of IQ-1S in the models of reversible focal cerebral ischemia (FCI) in Wistar rats. The animals were administered with an intraperitoneal injection of IQ-1S (5 and 25 mg/kg) or citicoline (500 mg/kg). Administration of IQ-1S exerted a pronounced dose-dependent neuroprotective effect, not inferior to the effects of citicoline. Administration of IQ-1S at doses of 5 and 25 mg/kg reduced the infarct size by 20% and 50%, respectively, 48 h after FCI, whereas administration of citicoline reduced the infarct size by 34%. The administration of IQ-1S was associated with a faster amelioration of neurological status. Control rats showed a 2.0-fold increase in phospho-c-Jun levels in the hippocampus compared to the corresponding values in sham-operated rats 4 h after FCI. Administration of IQ-1S at a dose of 25 mg/kg reduced JNK-dependent phosphorylation of c-Jun by 20%. Our findings suggest that IQ-1S inhibits JNK enzymatic activity in the hippocampus and protects against stroke injury when administered in the therapeutic and prophylactic regimen in the rat model of FCI.

scholarly journals Functional Recovery after Scutellarin Treatment in Transient Cerebral Ischemic Rats: A Pilot Study with18F-Fluorodeoxyglucose MicroPET

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Jin-hui Li ◽  
Jing Lu ◽  
Hong Zhang
Keyword(s):  
Cerebral Ischemia ◽  
Rat Model ◽  
Neurological Deficit ◽  
Neuronal Maturation ◽  
Vascular Density ◽  
Sham Operation ◽  
Therapeutic Effects ◽  
Neuroprotective Effects ◽  
Neuronal Marker ◽  
Cerebral Ischemic

Objective. To investigate neuroprotective effects of scutellarin (Scu) in a rat model of cerebral ischemia with use of18F-fluorodeoxyglucose (18F-FDG) micro positron emission tomography (microPET).Method. Middle cerebral artery occlusion was used to establish cerebral ischemia. Rats were divided into 5 groups: sham operation, cerebral ischemia-reperfusion untreated (CIRU) group, Scu-25 group (Scu 25 mg/kg/d), Scu-50 group (Scu 50 mg/kg/d), and nimodipine (10 mg/Kg/d). The treatment groups were given for 2 weeks. The therapeutic effects in terms of cerebral infarct volume, neurological deficit scores, and cerebral glucose metabolism were evaluated. Levels of vascular density factor (vWF), glial marker (GFAP), and mature neuronal marker (NeuN) were assessed by immunohistochemistry.Results. The neurological deficit scores were significantly decreased in the Scu-50 group compared to the CIRU group (P<0.001).18F-FDG accumulation in the ipsilateral cerebral infarction increased steadily over time in Scu-50 group compared with CIRU group (P<0.01) and Scu-25 group (P<0.01). Immunohistochemical analysis demonstrated Scu-50 enhanced neuronal maturation.Conclusion.18F-FDG microPET imaging demonstrated metabolic recovery after Scu-50 treatment in the rat model of cerebral ischemia. The neuroprotective effects of Scu on cerebral ischemic injury might be associated with increased regional glucose activity and neuronal maturation.

Sign in / Sign up

Export Citation Format

Share Document