Project title brain cell apoptosis after intracerebral hemorrhage

2000 ◽  
Vol 7 (8) ◽  
pp. 675-676
2014 ◽  
Vol 93 (1) ◽  
pp. 178-188 ◽  
Author(s):  
I-Neng Lee ◽  
Wan-Chun Cheng ◽  
Chiu-Yen Chung ◽  
Ming-Hsueh Lee ◽  
Martin Hsiu-Chu Lin ◽  
...  

2010 ◽  
Vol 4 ◽  
Author(s):  
Shakevia Johnson ◽  
Shawna Tazik ◽  
Deyin Lu ◽  
Chandra Johnson ◽  
Moussa B. H. Youdim ◽  
...  

2017 ◽  
Vol 13 (6) ◽  
pp. 2771-2774 ◽  
Author(s):  
Fu-Xia Song ◽  
Li Wang ◽  
Hong Liu ◽  
Ying-Li Wang ◽  
Yong Zou

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Haidong Wu ◽  
Peng Wang ◽  
Yi Li ◽  
Manhui Wu ◽  
Jiali Lin ◽  
...  

Objective. We investigated whether and how diazoxide can attenuate brain injury after cardiopulmonary resuscitation (CPR) by selective opening of mitochondrial ATP-sensitive potassium (mitoKATP) channels.Methods. Adult male Sprague-Dawley rats with induced cerebral ischemia (n=10per group) received an intraperitoneal injection of 0.1% dimethyl sulfoxide (1 mL; vehicle group), diazoxide (10 mg/kg; DZ group), or diazoxide (10 mg/kg) plus 5-hydroxydecanoate (5 mg/kg; DZ + 5-HD group) 30 min after CPR. The control group (sham group,n=5) underwent sham operation, without cardiac arrest. Mitochondrial respiratory control rate (RCR) was determined. Brain cell apoptosis was assessed using TUNEL staining. Expression of Bcl-2, Bax, and protein kinase C epsilon (PKCε) in the cerebral cortex was determined by Western blotting and immunohistochemistry.Results. The neurological deficit scores (NDS) in the vehicle group decreased significantly at 24 h and 48 h after CPR. Diazoxide significantly improved NDS and mitochondrial RCR after CPR at both time points; 5-HD cotreatment abolished these effects. Diazoxide decreased TUNEL-positive cells following CPR, upregulated Bcl-2 and PKCε, downregulated Bax, and increased the Bcl-2/Bax ratio; 5-HD cotreatment reversed these effects.Conclusions. Diazoxide attenuates postresuscitation brain injury, protects mitochondrial function, inhibits brain cell apoptosis, and activates the PKC pathway by opening mitoKATP channels.


2014 ◽  
Vol 9 (2) ◽  
pp. 164 ◽  
Author(s):  
Xiaoge Song ◽  
Xiaorong Hou ◽  
Rongjun Zhang ◽  
Hang Lv ◽  
Xinghui Cai ◽  
...  
Keyword(s):  

2019 ◽  
Vol 17 (2) ◽  
pp. 103-112
Author(s):  
Sri ANDARINI ◽  
Asmika MADJRI ◽  
Hidayat SUJUTI ◽  
Romi ROMI ◽  
Adi Surya PRATAMA ◽  
...  

Endosulfan is a persistent organic pollutant commonly used as an insecticide in Indonesia. It has been reported to cause teratogenic effects, i.e., to decrease humoral activity, produce inflammation, and induce apoptosis in various type of cells. This study investigated the effect of endosulfan on the expression of IL-1β, IL-6, IL-17, and TNF-α in rats (Rattus norvegicus), as well as the incidence of fetal brain cell apoptosis. This experiment was carried out on pregnant rats divided into 4 groups: negative control (I), endosulfan: 1 mg/kg (II), 10 mg/kg (III), and 50 mg/kg (IV). The solution of endosulfan was given daily during the 20-day test period. Rat serum was collected for the measurement of IL-1β, IL-6, IL-17, and TNF-α using the ELISA kit. Fetal rat brains were taken and stained with Annexin V for apoptosis detection. The proinflammatory cytokine levels in Groups II, III, and IV were higher than in Group I, with significant increases of IL-1β (p = 0.016), IL-6 (p = 0.009), IL-17 (p < 0.001), and TNF-α (p < 0.001). The intensity of Annexin V in 4 groups of rats showed that the incidence of apoptosis increased with increasing endosulfan doses. In conclusion, the administration of endosulfan in pregnant rats increased the expression of IL-1β, IL-6, IL-17, and TNF-α and triggered apoptosis in fetal brain cells.


2017 ◽  
Vol 30 (4) ◽  
pp. 413-419 ◽  
Author(s):  
Jianping Niu ◽  
Rui Hu

This study aimed to explore the role and mechanism(s) of flunarizine hydrochloride in the intracerebral hemorrhage (ICH) rats. The 32 adult male Sprague Dawley (SD) rats were randomly assigned into four groups: control group, sham group, ICH group, and FLU + ICH group. The effects of flunarizine hydrochloride were assessed on the basis of hematoma volume, blood–brain barrier (BBB) integrity, and brain water content in the ICH rat models. The role of flunarizine hydrochloride in cell recovery was assessed by behavioral scores, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot assay. Involvement of PI3K/AKT pathway in exerting the effect of flunarizine hydrochloride was also determined. Results showed that the hematoma volume, BBB integrity, and brain water content were significantly decreased in the FLU + ICH group. Cell apoptosis significantly increased in the ICH model group, while flunarizine hydrochloride decreased this increase. The expressions of glial cell line-derived neurotrophic factor (GDNF), neuroglobin (NGB), and p-AKT were increased after flunarizine hydrochloride treatment in ICH rats. In conclusion, flunarizine hydrochloride has protective effects against ICH by reducing brain injury, cell apoptosis, and the activation of P13K/AKT pathway. These findings provide a theoretical basis for the treatment of flunarizine hydrochloride in ICH.


2014 ◽  
Vol 44 ◽  
pp. 920-927 ◽  
Author(s):  
Ling ZHOU ◽  
Li DENG ◽  
Neng Bin CHANG ◽  
Ling DOU ◽  
Chao Xian YANG

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