Neuroprotective effects of icariin on corticosterone-induced apoptosis in primary cultured rat hippocampal neurons

Liu, Baojun; Zhang, Hongying; Xu, Changqing; Yang, Guang; Jiang, Tao; Huang, Jianhua; Wu, Jinfeng; Duan, Xiaohong; Cao, Yuxue; Dong, Jingcheng

doi:10.1016/j.brainres.2010.12.053

Cited by 102 publications

(66 citation statements)

References 32 publications

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“…This process is essential for the initiation and progression of phosphate-induced vascular calcification [41], with apoptotic bodies exposing phosphatidylserine on the outer membranes, generating a potential calcium-binding site suitable for hydroxyapatite deposition [35], [40]. These results support previous reports demonstrating that glucocorticoids inhibit VSMC proliferation [22], [44] and induce apoptosis in a range of cell types including neuronal cells, growth plate chondrocytes and thymocytes [6], [7], [20], [21].…”

Section: Discussionsupporting

confidence: 87%

A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification

Zhu

Rashdan

Chapman

et al. 2016

Vascular Pharmacology

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Vascular calcification, which is common in the elderly and in patients with atherosclerosis, diabetes and chronic renal disease, increases the risk of cardiovascular morbidity and mortality. It is a complex, active and highly regulated cellular process that resembles physiological bone formation. It has previously been established that pharmacological doses of glucocorticoids facilitate arterial calcification. However, the consequences for vascular calcification of endogenous glucocorticoid elevation have yet to be established. Glucocorticoids (cortisol, corticosterone) are released from the adrenal gland, but can also be generated within cells from 11-keto metabolites of glucocorticoids (cortisone, 11-dehydrocorticosterone [11-DHC]) by the enzyme, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). In the current study we hypothesized that endogenous glucocorticoids facilitate vascular smooth muscle cell (VSMC) calcification and investigated the receptor-mediated mechanism underpinning this process.In vitro studies revealed increased phosphate-induced calcification in mouse VSMCs following treatment for 7 days with corticosterone (100 nM; 7.98 fold; P < 0.01), 11-DHC (100 nM; 7.14 fold; P < 0.05) and dexamethasone (10 nM; 7.16 fold; P < 0.05), a synthetic glucocorticoid used as a positive control. Inhibition of 11β-HSD isoenzymes by 10 μM carbenoxolone reduced the calcification induced by 11-DHC (0.37 fold compared to treatment with 11-DHC alone; P < 0.05). The glucocorticoid receptor (GR) antagonist mifepristone (10 μM) had no effect on VSMC calcification in response to corticosterone or 11-DHC. In contrast, the mineralocorticoid receptor (MR) antagonist eplerenone (10 μM) significantly decreased corticosterone- (0.81 fold compared to treatment with corticosterone alone; P < 0.01) and 11-DHC-driven (0.64 fold compared to treatment with 11-DHC alone; P < 0.01) VSMC calcification, suggesting this glucocorticoid effect is MR-driven and not GR-driven. Neither corticosterone nor 11-DHC altered the mRNA levels of the osteogenic markers PiT-1, Osx and Bmp2. However, DAPI staining of pyknotic nuclei and flow cytometry analysis of surface Annexin V expression showed that corticosterone induced apoptosis in VSMCs.This study suggests that in mouse VSMCs, corticosterone acts through the MR to induce pro-calcification effects, and identifies 11β-HSD-inhibition as a novel potential treatment for vascular calcification.

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Section: Discussionsupporting

confidence: 87%

A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification

Zhu

Rashdan

Chapman

et al. 2016

Vascular Pharmacology

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“…For central nervous system, icariin shows a potent neuronal protective activity to prevent neuronal degeneration in animal models, by inhibiting neuronal apoptosis and tau protein hyperphosphorylation (Wang et al, 2009;Urano and Tohda, 2010;Zhu et al, 2010;Liu et al, 2011;Zhang et al, 2012). Our previous studies confirmed that icariin protected neuron form ischemia (Li et al, 2005), protected rat from aluminum-induced learning and memory deficits (Luo et al, 2007), and elevated acetylcholinesterase and choline acetyltransferase in rat hippocampus .…”

Section: Introductionsupporting

confidence: 61%

Icariin decreases both APP and Aβ levels and increases neurogenesis in the brain of Tg2576 mice

Dong

Gong

et al. 2015

Neuroscience

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“…Icariin and its derivatives have been suggested to increase NO synthesis in the penis [56], inhibit PDE5 in cavernosal smooth muscle [57–59], have positive neurotrophic effect on nitrergic nerves [56], enhance smooth muscle proliferation [60], and decrease advanced glycation endproduct formation [60] and mimic endogenous androgens [61]. Icariin has also been suggested to have anti-inflammatory, antiosteoporotic, and neuroprotective properties [62–64]. …”

Section: Resultsmentioning

confidence: 99%

Sexual Enhancement Products for Sale Online: Raising Awareness of the Psychoactive Effects of Yohimbine, Maca, Horny Goat Weed, andGinkgo biloba

Corazza

Martinotti

Santacroce

et al. 2014

BioMed Research International

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Introduction. The use of unlicensed food and herbal supplements to enhance sexual functions is drastically increasing. This phenomenon, combined with the availability of these products over the Internet, represents a challenge from a clinical and a public health perspective. Methods. A comprehensive multilingual assessment of websites, drug fora, and other online resources was carried out between February and July 2013 with exploratory qualitative searches including 203 websites. Additional searches were conducted using the Global Public Health Intelligence Network (GPHIN). Once the active constitutes of the products were identified, a comprehensive literature search was carried out using PsycInfo and PubMed. Results. The most common sexual enhancement products available on the Internet were identified. Their active ingredients included yohimbine, maca, horny goat weed and Ginkgo biloba. These four substances were reported with the occurrence of adverse events and the induction of psychological symptoms, such as mood changes, anxiety, and hallucinations as well as addictive behaviours. Conclusions. Uncontrolled availability of sexual enhancement products that contain potentially harmful substances is a major public health concern. The possible impact on population health, particularly among subjects with psychiatric disorders, usually at risk for sexual dysfunction, may be significant. This new trend needs to be extensively studied and monitored.

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Neuroprotective effects of icariin on corticosterone-induced apoptosis in primary cultured rat hippocampal neurons

Cited by 102 publications

References 32 publications

A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification

A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification

Icariin decreases both APP and Aβ levels and increases neurogenesis in the brain of Tg2576 mice

Sexual Enhancement Products for Sale Online: Raising Awareness of the Psychoactive Effects of Yohimbine, Maca, Horny Goat Weed, andGinkgo biloba

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