Impaired neural stem/progenitor cell proliferation in streptozotocin-induced and spontaneous diabetic mice

Guo, Jun; Yu, Caiyong; Li, Hongzeng; Liu, Fangfang; Feng, Rui; Wang, Hui; Meng, Yanyan; Li, Zhuyi; Ju, Gong; Wang, Jian

doi:10.1016/j.neures.2010.08.012

Cited by 50 publications

(45 citation statements)

References 74 publications

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“…This finding is in agreement with previous studies (Guo et al 2010;Navaratna et al 2011). Moreover, reduced neurogenesis and lower BDNF levels are observed in animal models of depression (Hurley et al 2013;Liu et al 2014).…”

Section: Notesupporting

confidence: 94%

Anti-depressant effect of hesperidin in diabetic rats

El-Marasy

Abdallah

El‐Shenawy

et al. 2014

Can. J. Physiol. Pharmacol.

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This study aimed to investigate the anti-depressant effect of hesperidin (Hsp) in streptozotocin (STZ)-induced diabetic rats. Additionally, the effect of Hsp on hyperglycaemia, oxidative stress, inflammation, brain-derived neurotrophic factor (BDNF), and brain monoamines in diabetic rats was also assessed. The Wistar rats in the experimental groups were rendered hyperglycaemic with a single dose of STZ (52.5 mg·(kg body mass)(-1), by intraperitoneal injection). The normal group received the vehicle only. Hyperglycaemic rats were treated with Hsp (25.0, 50.0, or 100.0 mg·(kg body mass)(-1)·day(-1), per oral) and fluoxetine (Flu) (5.0 mg·(kg body mass)(-1)·day(-1), per oral) 48 h after the STZ injection, for 21 consecutive days. The normal and STZ control groups received the vehicle (distilled water). Behavioral and biochemical parameters were then assessed. When Hsp was administered to the STZ-treated rats, this reversed the STZ-induced increase in immobility duration in the forced swimming test (FST) and attenuated hyperglycaemia, decreased malondialdehyde (MDA), increased reduced glutathione (GSH) decreased interleukin-6 (IL-6), and increased BDNF levels in the brain. Treatment with Hsp attenuated STZ-induced neurochemical alterations, as indicated by increased levels of monoamines in the brain, namely, norepinephrine (NE), dopamine (DA), and serotonin (5-hydroxytryptamine; 5-HT). All of these effects of Hsp were similar to those observed with the established anti-depressant Flu. This study shows that Hsp exerted anti-depressant effect in diabetic rats, which may have been partly mediated by its amelioration of hyperglycaemia as well as its anti-oxidant and anti-inflammatory activities, the enhancement of neurogenesis, and changes in the levels of monoamines in the brain.

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Section: Notesupporting

confidence: 94%

Anti-depressant effect of hesperidin in diabetic rats

El-Marasy

Abdallah

El‐Shenawy

et al. 2014

Can. J. Physiol. Pharmacol.

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“…The high glucose condition has been reported to decrease the proliferation of embryonic neural stem cells by altering the expression of genes involved in proliferation and cell fate-specification (Fu et al, 2006). In the adult brain, diabetes results in a significant reduction in the proliferation of neural stem/progenitor cells in the dentate gyrus of the hippocampus (Jackson- Guilford et al, 2000;Stranahan et al, 2008) and, or in the SVZ of the lateral ventricle (Guo et al, 2010). Furthermore, in db/db mice, focal ischemia worsened the ischemic white matter lesions, with a reduction of the NG2-positive OPCs, and high glucose culture conditions also reduced the proliferation and survival of oligodendrocytes (Chen et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Type 2 diabetes reduces the proliferation and survival of oligodendrocyte progenitor cells in ishchemic white matter lesions

et al. 2015

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“…As for the role of hyperglycemia in neurogenesis, some studies indicate that long-term hyperglycemia suppresses proliferation of hippocampus NSPCs using streptozotocin-(STZ) induced type 1 diabetes model (Jackson-Guilford et al, 2000;Saravia et al, 2004;Beauquis et al, 2006;Zhang et al, 2008;Guo et al, 2010) or spontaneous type 1 diabetes model (Beauquis et al, 2008;Guo et al, 2010), while other researches find an enhanced proliferation of NSPCs employing type 2 diabetes model (Lang et al, 2009;Ramos-Rodriguez et al, 2014). The discrepancy among studies may be attributed to different hyperglycemic models and target blood glucose levels.…”

Section: Discussionmentioning

confidence: 99%