Neurotrophic property of geniposide for inducing the neuronal differentiation of PC12 cells

Liu, Jianhui; Zheng, Xiangkuo; Yin, Fei; Hu, Yinhe; Guo, Lixia; Deng, Xingming; Chen, Gang; Jiajia, Jing; Zhang, Heng

doi:10.1016/j.ijdevneu.2006.08.009

Cited by 82 publications

(63 citation statements)

References 20 publications

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“…9) Our previous works showed that geniposide was a novel agonist for glucagon-like peptide 1 receptor (GLP-1R), which induced the neuronal differentiation of PC12 cells and prevented PC12 cells from oxidative stress. [10][11][12] However, the mechanisms involved in these cytoprotective effects of geniposide remain to be fully established.…”

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confidence: 99%

Geniposide Induces the Expression of Heme Oxygenase-1 via PI3K/Nrf2-Signaling to Enhance the Antioxidant Capacity in Primary Hippocampal Neurons

Yin

Liu

Zheng

et al. 2010

Biological & Pharmaceutical Bulletin

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Oxidative stress in brain is emerging as a potential causal factor in aging and age-related neurodegenerative disorders. A large body of evidence shows that induction of endogenous antioxidative proteins seems to be a reasonable strategy for delaying the progression of cell injury. In this study, geniposide upregulates the expression of heme oxygenase-1 (HO-1) to attenuate the cell apoptosis induced by 3-morpholinosydnonimine hydrochloride (SIN-1) in primary cultured hippocampal neurons. Furthermore, geniposide induces the nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and activation of phosphatidylinositol 3-kinase (PI3K) in the presence of oxidative stress, and both LY294002 (a specific inhibitor of PI3K) and Zinc protoporphyrin (ZnPP, an inhibitor of HO-1) decrease the cytoprotective action of geniposide in hippocampal neurons. Taken together, the novel cytoprotective mechanism of geniposide to antagonize oxidative stress may be involved in PI3K-and Nrf2-mediated upregulation of the antioxidative enzyme HO-1.

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mentioning

confidence: 99%

Geniposide Induces the Expression of Heme Oxygenase-1 via PI3K/Nrf2-Signaling to Enhance the Antioxidant Capacity in Primary Hippocampal Neurons

Yin

Liu

Zheng

et al. 2010

Biological & Pharmaceutical Bulletin

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“…A significant increase on the GAP-43 protein level in parallel with neurite outgrowth was observed after the treatment with geniposide. The data also demonstrate that geniposide induces the neuronal differentiation of PC12 cells via the MAPK pathway (Liu et al, 2006). Therefore, geniposide has neuroprotective effects due to the activation of GLP-1R in cells without nNOS.…”

Section: Neurite Outgrowth Promoted By Geniposidementioning

confidence: 57%

“…Its protective effect from memory impairment and the normalization of objection recognition has been shown in animal behavioral experiments (Gao et al, 2014;Lv et al, 2014). Using a high-throughput screen for GLP-1R agonists, geniposide was identified as an agonist for GLP-1R (Liu et al, 2006). It has been shown that the activation of GLP-1R by geniposide induces neurotrophic and neuroprotective effects in cells .…”

Section: Introductionmentioning

confidence: 98%

Neuroprotective effects of geniposide on Alzheimer’s disease pathology

Liu

Hölscher³

et al. 2015

Reviews in the Neurosciences

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AbstractA growing body of evidence has linked two of the most common aged-related diseases: type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD). It has led to the notion that drugs developed for the treatment of T2DM may be beneficial in modifying the pathophysiology of AD. As a receptor agonist of glucagon-like peptide-1 (GLP-1R), which is a newer drug class to treat T2DM, geniposide shows clear effects in inhibiting pathological processes underlying AD, such as promoting neurite outgrowth. In the present article, we review the possible molecular mechanisms of geniposide to protect the brain from pathologic damages underlying AD: reducing amyloid plaques, inhibiting τ phosphorylation, preventing memory impairment and loss of synapses, reducing oxidative stress and the chronic inflammatory response, and promoting neurite outgrowth via the GLP-1R signaling pathway. In summary, the Chinese herb geniposide shows great promise as a novel treatment for AD.

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“…In several neuronal cell line studies, GLP‐1 induced neurite outgrowth24, 25. One study found that ICV infusion of GIP stimulated progenitor cell proliferation in the rat hippocampus26.…”

Section: Biology Of Incretin Hormones In Peripheral Organs and The Brainmentioning

confidence: 99%

Potentials of incretin‐based therapies in dementia and stroke in type 2 diabetes mellitus

Groeneveld

Kappelle

Biessels

2015

J of Diabetes Invest

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Patients with type 2 diabetes mellitus are at risk for accelerated cognitive decline and dementia. Furthermore, their risk of stroke is increased and their outcome after stroke is worse than in those without diabetes. Incretin‐based therapies are a class of antidiabetic agents that are of interest in relation to these cerebral complications of diabetes. Two classes of incretin‐based therapies are currently available: the glucagon‐like‐peptide‐1 agonists and the dipeptidyl peptidase‐4 ‐inhibitors. Independent of their glucose‐lowering effects, incretin‐based therapies might also have direct or indirect beneficial effects on the brain. In the present review, we discuss the potential of incretin‐based therapies in relation to dementia, in particular Alzheimer's disease, and stroke in patients with type 2 diabetes. Experimental studies on Alzheimer's disease have found beneficial effects of incretin‐based therapies on cognition, synaptic plasticity and metabolism of amyloid‐β and microtubule‐associated protein tau. Preclinical studies on incretin‐based therapies in stroke have shown an improved functional outcome, a reduction of infarct volume as well as neuroprotective and neurotrophic properties. Both with regard to the treatment of Alzheimer's disease, and with regard to prevention and treatment of stroke, randomized controlled trials in patients with or without diabetes are underway. In conclusion, experimental studies show promising results of incretin‐based therapies at improving the outcome of Alzheimer's disease and stroke through glucose‐independent pleiotropic effects on the brain. If these findings would indeed be confirmed in large clinical randomized controlled trials, this would have substantial impact.

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Neurotrophic property of geniposide for inducing the neuronal differentiation of PC12 cells

Cited by 82 publications

References 20 publications

Geniposide Induces the Expression of Heme Oxygenase-1 via PI3K/Nrf2-Signaling to Enhance the Antioxidant Capacity in Primary Hippocampal Neurons

Geniposide Induces the Expression of Heme Oxygenase-1 via PI3K/Nrf2-Signaling to Enhance the Antioxidant Capacity in Primary Hippocampal Neurons

Neuroprotective effects of geniposide on Alzheimer’s disease pathology

Potentials of incretin‐based therapies in dementia and stroke in type 2 diabetes mellitus

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