Luteolin attenuates neuronal apoptosis in the hippocampi of diabetic encephalopathy rats | |
Alternative Title | Luteolin attenuates neuronal apoptosis in the hippocampi of diabetic encephalopathy rats ☆ |
Ren Guiru; Kong Jingjing; Jia Ning; Shang Xiuli | |
2013 | |
Source Publication | NEURAL REGENERATION RESEARCH
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ISSN | 1673-5374 |
Volume | 8Issue:12Pages:1071-1080 |
Abstract | Luteolin (3',4',5,7-tetrahydroxyflavone) has powerful anti-apoptotic and antioxidant properties. This study aimed to investigate the effects of luteolin on hyperglycemia-mediated apoptosis in the hippocampi of rats with streptozotocin-induced diabetic encephalopathy after injection into the tail veins, and the molecular mechanisms involved. Biochemistry and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling detection results showed that luteolin treatment (given twice daily for 15 days) significantly inhibited hyperglycemia-mediated apoptosis, decreased malondialdehyde levels and increased glutathione levels in the hippocampi of streptozotocin-induced diabetic rats. Western blot analysis revealed that luteolin also inhibited the expression of apoptosis-related factors and cytochrome c release from mitochondria. Luteolin also improved the learning and memory abilities of rats with diabetic encephalopathy in a water maze test. Further western blot analysis revealed that luteolin treatment facilitated neuronal cell survival through activation of the phosphatidylinositol 3-kinase/Akt signaling pathway, an extracellular signal pathway involved in the suppression of cell apoptosis and promotion of cell survival. These experimental findings indicate that luteolin can inhibit apoptosis of hippocampal nerve cells in rats with diabetic encephalopathy, and that this effect is mediated by an indirect antioxidative effect, the inhibition of activation of apoptosis-related factors and the activation of phosphatidylinositol 3-kinase/Akt signal pathway. |
Other Abstract | Luteolin (3’,4’,5,7-tetrahydroxyflavone) has powerful anti-apoptotic and antioxidant properties. This study aimed to investigate the effects of luteolin on hyperglycemia-mediated apoptosis in the hippocampi of rats with streptozotocin-induced diabetic encephalopathy after injection into the tail veins, and the molecular mechanisms involved. Biochemistry and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling detection results showed that luteolin treatment (given twice daily for 15 days) significantly inhibited hyperglycemia-mediated apoptosis, decreased malondialdehyde levels and increased glutathione levels in the hippocampi of streptozotocin-induced diabetic rats. Western blot analysis revealed that luteolin also inhibited the expression of apoptosis-related factors and cytochrome c release from mitochondria. Luteolin also improved the learning and memory abilities of rats with diabetic encephalopathy in a water maze test. Further western blot analysis revealed that luteolin treatment facilitated neuronal cell survival through activation of the phosphatidylinositol 3-kinase |
Keyword | OXIDATIVE STRESS CELL-DEATH DYSFUNCTION DISEASE neural regeneration brain injury diabetic mellitus luteolin apoptosis learning and memory spatial recognition memory nerve cells hippocampus anti-oxidation neuroregeneration |
Indexed By | CSCD |
Language | 英语 |
CSCD ID | CSCD:4818406 |
Citation statistics | |
Document Type | 期刊论文 |
Identifier | http://ir.imr.ac.cn/handle/321006/156910 |
Collection | 中国科学院金属研究所 |
Affiliation | 中国科学院金属研究所 |
Recommended Citation GB/T 7714 | Ren Guiru,Kong Jingjing,Jia Ning,et al. Luteolin attenuates neuronal apoptosis in the hippocampi of diabetic encephalopathy rats[J]. NEURAL REGENERATION RESEARCH,2013,8(12):1071-1080. |
APA | Ren Guiru,Kong Jingjing,Jia Ning,&Shang Xiuli.(2013).Luteolin attenuates neuronal apoptosis in the hippocampi of diabetic encephalopathy rats.NEURAL REGENERATION RESEARCH,8(12),1071-1080. |
MLA | Ren Guiru,et al."Luteolin attenuates neuronal apoptosis in the hippocampi of diabetic encephalopathy rats".NEURAL REGENERATION RESEARCH 8.12(2013):1071-1080. |
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