Neuroprotection of geniposide against hydrogen peroxide induced PC12 cells injury: involvement of PI3 kinase signal pathway

Liu, Jianhui; Yin, Fei; Guo, Lixia; Deng, Xingming; Hu, Yinhe

doi:10.1038/aps.2008.25

Cited by 135 publications

(91 citation statements)

References 33 publications

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“…27) In our previous works, we reported that geniposide, a novel agonist for GLP-1R, prevented PC12 cells from oxidative damage via activation of glucagons-like peptide 1 receptor (GLP-1R), and induced PC12 cell neuronal differentiation via MAP kinase pathway. [10][11][12] Recently, we found that in glp-1r knockout PC12 cells, the neuroprotection of geniposide was inhibited significantly, suggesting that GLP-1R plays a critical role in the neuroprotection of geniposide and attenuates oxidative insults in these cells. 32) These neurotrophic/neuroprotective actions are in accordance with previous findings establishing that GLP-1R stimulation protects hippocampal neurons from amyloid-b peptide, Fe 2ϩ , and glutamate induced toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…The cell viability was assessed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay as described before. 11,12) To determine whether PI3K signaling pathway is involved in the cytoprotective effect of geniposide, LY294002, a selective inhibitor of PI3K, was used, which was added to cell cultures 30 min before treatment with SIN-1. Control neurons were treated with the appropriate amount of vehicle.…”

Section: Methodsmentioning

confidence: 99%

“…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%

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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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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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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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“…Since previous studies have shown that geniposide possesses in vitro antioxidant activity under oxidative stress induced by hydrogen peroxide [27,28] , we first investigated whether geniposide inhibited high glucose-induced ROS overproduction. In our study, exposure of endothelial cells to high glucose resulted in increased levels of intracellular ROS.…”

Section: Discussionmentioning

confidence: 99%

Geniposide inhibits high glucose-induced cell adhesion through the NF-κB signaling pathway in human umbilical vein endothelial cells

Wang

Xü

et al. 2010

Acta Pharmacol Sin

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Aim: To investigate whether geniposide, an iridoid glucoside extracted from gardenia jasminoides ellis fruits, inhibits cell adhesion to human umbilical vein endothelial cells (HUVECs) induced by high glucose and its underlying mechanisms. Methods: HUVECs were isolated from human umbilical cords and cultured. The adhesion of monocytes to HUVECs was determined using fluorescence-labeled monocytes. The mRNA and protein levels of vascular cell adhesion molecule-1 (VCAM-1) and endothelial selectin (E-selectin) were measured using real-time RT-PCR and ELISA. Reactive oxygen species (ROS) production was measured using a fluorescent probe. The amounts of nuclear factor-kappa B (NF-κB) and inhibitory factor of NF-κB (IκB) were determined using Western blot analysis. The translocation of NF-κB from the cytoplasm to the nucleus was determined using immunofluorescence. Results: Geniposide (10-20 µmol/L) inhibited high glucose (33 mmol/L)-induced adhesion of monocytes to HUVECs in a dose-dependent manner. This compound (5-40 µmol/L) also inhibited high glucose-induced expression of VCAM-1 and E-selectin at the gene and protein levels. Furthermore, geniposide (5-20 µmol/L) decreased ROS production and prevented IκB degradation in the cytoplasm and NF-κB translocation from the cytoplasm to the nucleus in HUVECs. Conclusion: Geniposide inhibits the adhesion of monocytes to HUVECs and the expression of CAMs induced by high glucose, suggesting that the compound may represent a new treatment for diabetic vascular injury. The mechanism underlying this inhibitory effect may be related to the inhibition of ROS overproduction and NF-κB signaling pathway activation by geniposide.

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“…Several lines of evidence indicate that the Akt signaling pathway responds to oxidative stress [95] and exerts a neuroprotective function [96,97]. Moreover, a large number of studies in vitro have illustrated that pharmacological compounds that protect cells against oxidative stress exert their neuroprotective effects through activation of the Akt pathway [98][99][100][101][102]. www.fhc.viamedica.pl Activated Akt can modulate the expression of proteins influencing cell death, such as inhibitors of apoptosis Bcl-2 and Bcl-XL or inducers of apoptosis Bax, Bad [103,104].…”

Section: Discussionmentioning

confidence: 99%

Docosahexaenoic acid provides protective mechanism in bilaterally MPTP-lesioned rat model of Parkinson's disease

Hacioglu

Seval-Celik

Tanrıöver

et al. 2012

Folia Histochem Cytobiol.

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Docosahexaenoic acid (DHA), a major polyunsaturated fatty acid (PUFA) in the phospholipid fraction of the brain, is essential for normal cellular function. Neurodegenerative disorders such as Parkinson's disease (PD) often exhibit significant declines in PUFAs. The aim of this study was to observe the effects of DHA supplementation in an experimental rat model of PD created with '1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine' (MPTP). Adult male Wistar rats were divided into four groups: (1) Control; (2) DHA-treated; (3) MPTP-induced; and (4) MPTP-induced + DHA-treated. Motor activity was investigated using the 'vertical pole' and 'vertical wire' tests. The dopaminergic lesion was determined by immunohistochemical analysis for tyrosine hydroxylase (TH)-immunopositive cells in substantia nigra (SN). Immunoreactivities of Bcl-2, Akt and phosphorylated-Akt (p-Akt) in SN were evaluated by immunohistochemistry. MPTP-induced animals exhibited decreased locomotor activity, motor coordination and loss of equilibrium. Diminished Parkinsonism symptoms and decreased dopaminergic neuron death were detected in the MPTP-induced + DHA-treated group compared to the MPTP-induced group. Moderate decreases in Akt staining were found in the MPTP-induced and MPTP-induced + DHA-treated groups compared to controls. p-Akt immunoreactivity decreased dramatically in the MPTP-induced group compared to the control; however, it was increased in the MPTP-induced + DHA--treated group compared to the MPTP-induced group. The staining intensity for Bcl-2 decreased prominently in the MPTP-induced group compared to the control, while it was stronger in the MPTP-induced + DHA-treated group compared to the MPTP-induced group. In conclusion, DHA significantly protects dopaminergic neurons against cell death in an experimental PD model. Akt/p-Akt and Bcl-2 pathways are related to this protective effect

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Neuroprotection of geniposide against hydrogen peroxide induced PC12 cells injury: involvement of PI3 kinase signal pathway

Abstract: These results demonstrate that the PI3K signaling pathway is involved in the neuroprotection of geniposide in PC12 cells against the oxidative damage induced by H(2)O(2) in PC12 cells.

Cited by 135 publications

References 33 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

Geniposide inhibits high glucose-induced cell adhesion through the NF-κB signaling pathway in human umbilical vein endothelial cells

Docosahexaenoic acid provides protective mechanism in bilaterally MPTP-lesioned rat model of Parkinson's disease

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