Neuroprotective effects of icaritin against beta amyloid-induced neurotoxicity in primary cultured rat neuronal cells via estrogen-dependent pathway

Wang, Z.; Zhang, X.; Wang, H.; Li, Qi; Lou, Yijia

doi:10.1016/j.neuroscience.2006.12.059

Cited by 117 publications

(67 citation statements)

References 55 publications

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“…Primary rat cortical neuronal cell culture was carried out as previously described with minor modifications [9,32]. Briefly, neonatal Wistar rats were sacrificed; cortices were separated on ice and cut into pieces prior digestion in 0.25% trypsin for 15 min at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Ochratoxin A induces apoptosis in neuronal cells

et al. 2009

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The mycotoxin ochratoxin A (OTA), which is produced by Aspergillus and Penicillium subspecies, is a frequently present contaminant of food and feedstuffs. OTA exhibits a wide range of toxic activities including nephro-and hepatotoxicity. However, little is known regarding potential neurotoxic effects of OTA. In the present study primary neurons as well as SH-SY5Y neuronal cells were incubated with increasing concentrations of OTA (0.1-2.5 lmol/L). OTA treatment resulted in a dose-dependent increase in cytotoxicity in both neuronal cell types. Caspase-9 and caspase-3 were activated in response to OTA treatment. Furthermore, caspase inhibitors were effective in partly counteracting OTA induced neurocytotoxicity. OTA induced apoptosis was accompanied by a loss of mitochondria membrane potential. Overall, present data indicated that OTA is neurotoxic at relatively low concentrations. OTA induced neurotoxicity seems to be, at least party, mediated by apoptosis. OTA may contribute to the pathogenesis of neurodegenerative diseases (e.g. Alzheimer's and Parkinson's disease) in which apoptotic processes are centrally involved.

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Section: Methodsmentioning

confidence: 99%

Ochratoxin A induces apoptosis in neuronal cells

et al. 2009

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“…Icaritin (ICT, Fig. 1a, C21H20O6, molecular weight of 368.4), a major flavonoid component in Epimedium brevicornum Maxim., possesses estrogenic properties 2 and presents a variety of biological activities, including the stimulation of neuronal differentiation, 3 the improvement of cardiovascular function, 4 the inhibition of growth of human prostatic smooth muscle cells, 5 interference of osteoblastic/obsteclastic activity 6,7 as well as immunosuppression. 8 Also, ICT exerts potent effects on inhibiting the growth of human cancer cells, such as endometrial cancer cells 9 and breast cancer stem/progenitor cells via the inhibition of extracellular signal-regulated kinase (ERK) signaling.…”

Section: Introductionmentioning

confidence: 99%

Dynamic Biodistribution of Icaritin and Its Phase-II Metabolite in Rat Tissues by Ultra-High Performance Liquid Chromatography-Tandem Mass Spectrometry

Zhang

2016

ANAL. SCI.

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“…Icaritin, a prenylflavonoid derivative from the Chinese tonic herb Epimedium, has been shown to have many pharmacological and biological activities, such as antioxidant activity [1] , enhancement of the osteoblastic differentiation of mesenchymal stem cells [2][3][4] , inhibition of human prostate carcinoma growth [5,6] and neuroprotective effects [7][8][9] .…”

Section: Introductionmentioning

confidence: 99%

Icaritin suppresses the proliferation of human osteosarcoma cells in vitro by increasing apoptosis and decreasing MMP expression

Wang

2014

Acta Pharmacol Sin

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Aim: To explore whether icaritin, a prenylflavonoid derivative of the Chinese tonic herb Epimedium, could suppress the proliferation of human osteosarcoma cells in vitro, and to elucidate the mechanisms of the action. Methods: Human osteosarcoma SaOS 2 cell line was used in the present study. The proliferation of the cells was examined using MTT assay and immunofluorescence DAPI staining. Cell motility was studied with the scratch assay. Cell apoptosis was determined by Annexin V-FITC and PI double staining using flow cytometry. Western blotting and RT-PCR were used to measure the expression of mRNAs and proteins in the cells. Results: Icaritin (5-15 μmol/L) suppressed the proliferation of SaOS 2 cells in vitro in a dose-dependent manner. Furthermore, the cell motility was significantly decreased after exposure to icaritin. Moreover, icaritin (5 μmol/L) time-dependently induced the apoptosis of SaOS 2 cells, markedly suppressed MMP-2 and MMP-9 expression, upregulated caspase-3 and caspase-9 expression, and increased the level of cleaved caspase-3 in the cells. Co-exposure to the caspase-3 inhibitor zVAD-fmk (10 μmol/L) compromised the icaritininduced caspase-3 expression and apoptosis in SaOS 2 cells. Conclusion: Icaritin suppresses the proliferation of SaOS 2 human osteosarcoma cells by increasing apoptosis and downregulating MMP expression.

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Neuroprotective effects of icaritin against beta amyloid-induced neurotoxicity in primary cultured rat neuronal cells via estrogen-dependent pathway

Cited by 117 publications

References 55 publications

Ochratoxin A induces apoptosis in neuronal cells

Ochratoxin A induces apoptosis in neuronal cells

Dynamic Biodistribution of Icaritin and Its Phase-II Metabolite in Rat Tissues by Ultra-High Performance Liquid Chromatography-Tandem Mass Spectrometry

Icaritin suppresses the proliferation of human osteosarcoma cells in vitro by increasing apoptosis and decreasing MMP expression

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