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Mitochondrial protection by low doses of insulin-like growth factor-Ⅰin experimental cirrhosis 被引量:11
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作者 Raquel Pérez María García-Fernández +5 位作者 Matías Díaz-Sánchez Juan E Puche Gloria Delgado Marian Conchillo Jordi Muntané Inma Castilla-Cortázar 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第17期2731-2739,共9页
AIM: To characterize the mitochondrial dysfunction in experimental cirrhosis and to study whether insulin-like growth factor-Ⅰ (IGF-Ⅰ ) therapy (4 wk) is able to induce beneficial effects on damaged mitochondri... AIM: To characterize the mitochondrial dysfunction in experimental cirrhosis and to study whether insulin-like growth factor-Ⅰ (IGF-Ⅰ ) therapy (4 wk) is able to induce beneficial effects on damaged mitochondria leading to cellular protection. METHODS: Wistar rats were divided into three groups: Control group, untreated cirrhotic rats and cirrhotic rats treated with IGF-Ⅰ treatment (2 μg/1O0 g bw/d). Mitochondrial function was analyzed by flow cytometry in isolated hepatic mitochondria, caspase 3 activation was assessed by Western blot and apoptosis by TUNEL in the three expedmental groups. RESULTS: Untreated cirrhotic rats showed a mitochondrial dysfunction characterized by a significant reduction of mitochondrial membrane potential (in status 4 and 3); an increase of intramitochondrial reactive oxigen species (ROS) generation and a significant reduction of ATPase activity. IGF-Ⅰ therapy normalized mitochondrial function by increasing the membrane potential and ATPase activity and reducing the intramitochondrial free radical production. Activity of the electron transport complexes Ⅰ and Ⅲ was increased in both cirrhotic groups. In addition, untreated cirrhotic rats showed an increase of caspase 3 activation and apoptosis. IGF- Ⅰ therapy reduced the expression of the active peptide of caspase 3 and resulted in reduced apoptosis. CONCLUSION: These results show that IGF- Ⅰ exerts a mitochondrial protection in experimental cirrhosis leading to reduced apoptosis and increased ATP production. 展开更多
关键词 Insulin-like growth factor- CIRRHOSIS mitochondrial protection CASPASES APOPTOSIS Oxidativedamage
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Pre-B-cell colony-enhancing factor as a target for protecting against apoptotic neuronal death and mitochondrial damage in ischemia 被引量:6
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作者 Xiaowan Wang Shinghua Ding 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第12期1914-1915,共2页
Focal ischemic stroke(FIS)results from the lack of blood flow in a particular region of the brain and accounts for about 80%of all human strokes.Although tremendous efforts have been made in translational research,t... Focal ischemic stroke(FIS)results from the lack of blood flow in a particular region of the brain and accounts for about 80%of all human strokes.Although tremendous efforts have been made in translational research,the treatment strategies are still limited.Tissue plasminogen activator is the only FDA-approved drug currently available for acute stroke treatment, 展开更多
关键词 PBEF Pre-B-cell colony-enhancing factor as a target for protecting against apoptotic neuronal death and mitochondrial damage in ischemia NAD cell AIF MCAO
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A shape shifting organelle: unusual mitochondrial phenotype determined with three-dimensional electron microscopy reconstruction
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作者 Eugenia Trushina 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第6期900-901,共2页
Mitochondria,the powerhouses of the cell,are dynamic organelles that constantly move and change their size and morphology to meet energetic demands of the cell(Wai and Langer,2016).Recent studies demonstrated that e... Mitochondria,the powerhouses of the cell,are dynamic organelles that constantly move and change their size and morphology to meet energetic demands of the cell(Wai and Langer,2016).Recent studies demonstrated that energy production is dependent on the ability of mitochondria to undergo cycles of fission and fusion collectively termed“mitochondrial dynamics”(Youle and van der Bliek,2012). 展开更多
关键词 mitochondrial phenotype Langer constantly fission hippocampal neuronal unusual protective deprivation
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