Protective Effects of Hericium erinaceus Mycelium and  Its Isolated Erinacine A against Ischemia-Injury-Induced Neuronal Cell Death via the Inhibition of iNOS/p38 MAPK  and Nitrotyrosine

Lee, Kam-Fai; Chen, Jiann-Hwa; Teng, Chiao-Fang; Shen, Chien-Heng; Hsieh, Meng‐Che; Lu, Chun‐Wei; Lee, Ko‐Chao; Lee, Li-Ya; Chen, Wanping; Chen, Chin‐Chu; Huang, Wen‐Shih; Kuo, Hsing‐Chun

doi:10.3390/ijms150915073

Cited by 92 publications

(86 citation statements)

References 40 publications

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“…Stroke is the primary cause of long-term disability and death worldwide (Iadecola & Anrather 2011;Lee et al 2014). Ischemic stroke caused by arterial occlusions constitutes approximately 80% of all stroke cases (Wang et al 2010a).…”

Section: Introductionmentioning

confidence: 99%

SMND-309 promotes neuron survival through the activation of the PI3K/Akt/CREB-signalling pathway

Wang

Zhang

Han

et al. 2016

Pharmaceutical Biology

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Context In clinical practice, the promotion of neuron survival is necessary to recover neurological functions after the onset of stroke. Objective This study aimed to investigate the post-ischaemic neuroprotective effect of SMND-309, a novel metabolite of salvianolic acid, on differentiated SH-SY5Y cells. Materials and methods SH-SY5Y cells were differentiated by pre-treating with 5 mM all-transretinoic acid for 6 d. The differentiated SH-SY5Y cells were exposed to oxygen-glucose deprivation (OGD) for 2 h and reperfusion (R) for 24 h to induce OGD/R injury. After OGD injury, differentiated SH-SY5Y cells were treated with or without SMND-309 (5, 10, 20 mM) for another 24 h. Cell viability was detected through Cell counting kit-8 assay and lactate dehydrogenase leakage assay. Apoptosis was evaluated through flow cytometry, caspase-3 activity assay. Changes in protein levels were assessed through Western blot. Results SMND-309 ameliorated the degree of injury in the differentiated SH-SY5Y cells by increasing cell viabilities (5 mM, 65.4% ± 4.1%; 10 mM, 69.8% ± 3.7%; 20 mM, 75.3% ± 5.1%) and by reducing LDH activity (20 mM, 2.5 fold) upon OGD/R stimulation. Annexin V-fluorescein isothiocyanate/propidium iodide staining results suggested that apoptotic rate of differentiated SH-SY5Y cells decreased from 43.8% induced by OGD/R injury to 19.2% when the cells were treated with 20 mM SMND-309. SMND-309 significantly increased the Bcl-2 level of the injured differentiated SH-SY5Y cells but decreased the caspase-3 activity of these cells by 1.6-fold. In contrast, SMND-309 did not affect the Bax level of these cells. SMND-309 evidently increased the protein expression of BDNF when Akt and CREB were activated. This function was antagonized by the addition of LY294002. Conclusion SMND-309 can prevent neuronal cell death in vitro. This process may be related to the activation of the PI3K/Akt/CREB-signalling pathway.ARTICLE HISTORY

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Section: Introductionmentioning

confidence: 99%

SMND-309 promotes neuron survival through the activation of the PI3K/Akt/CREB-signalling pathway

Wang

Zhang

Han

et al. 2016

Pharmaceutical Biology

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“…The analytical column used was a COSMOSIL 5C18-AR-II (250 × 4.6 mm; particle size 5 µm, Nacalai USA, Inc., Kyoto, Japan). Extraction of 5 mg/kg H. erinaceus erinacine A with 85% ethanol was confirmed and quantified by HPLC [10, 11]. The erinacine A chemical compounds reported in this article (PubChem CID: 10410568) are shown in Fig.…”

Section: Methodsmentioning

confidence: 99%

“…Erinacine A (Fig. 1)-enriched H. erinaceous mycelia, which exhibit well-known anti-inflammatory and anticancer effects [10-13], have been extensively investigated and proposed to promote a decrease in cell viability and enhance apoptosis in various cancer cells. Moreover, our previous studies indicated that H. erinaceus mycelium and extracted erinacine A could be used to investigate the in vitro and in vivo antitumor activity through cell cycle arrest in the G1 phase of the human colorectal cancer cells involved in the generation of ROS and the activation of the p70S6K/NF-kB signaling pathway, which leads to p21 expression and inactivation of cdk2/cyclin E and cdk4/cyclin D1 [12].…”

Section: Introductionmentioning

confidence: 99%

A Comparative Proteomic Analysis of Erinacine A’s Inhibition of Gastric Cancer Cell Viability and Invasiveness

Kuo

Lee

et al. 2017

Cell Physiol Biochem

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Background / Aims: Erinacine A, isolated from the ethanol extract of the Hericium erinaceus mycelium, has been demonstrated as a new alternative anticancer medicine. Drawing upon current research, this study presents an investigation of the molecular mechanism of erinacine A inhibition associated with gastric cancer cell growth. Methods: Cell viability was determined by Annexin V–FITC/propidium iodide staining and migration using a Boyden chamber assay to determine the effects of erinacine A treatment on the proliferation capacity and invasiveness of gastric cancer cells. A proteomic assay provided information that was used to identify the differentially-expressed proteins following erinacine A treatment, as well as the mechanism of its targets in the apoptotic induction of erinacine A. Results: Our results demonstrate that erinacine A treatment of TSGH 9201 cells increased cytotoxicity and the generation of reactive oxygen species (ROS), as well as decreased the invasiveness. Treatment of TSGH 9201 cells with erinacine A resulted in the activation of caspases and the expression of TRAIL. Erinacine A induction of apoptosis was accompanied by sustained phosphorylation of FAK/AKT/p70S6K and the PAK1 pathways, as well as the generation of ROS. Furthermore, the induction of apoptosis and anti-invasion properties by erinacine A could involve the differential expression of the 14-3-3 sigma protein (1433S) and microtubule-associated tumor suppressor candidate 2 (MTUS2), with the activation of the FAK/AKT/p70S6K and PAK1 signaling pathways. Conclusions: These results lead us to speculate that erinacine A may generate an apoptotic cascade in TSGH 9201 cells by activating the FAK/AKT/p70S6K/PAK1 pathway and upregulating proteins 1433S and MTUS2, providing a new mechanism underlying the anti-cancer effects of erinacine A in human gastric cancer cells.

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“…Bioactive compounds extracted from its fruiting body or mycelium ( Figure 1) have been demonstrated to possess antioxidative [20], antidiabetic [21], anticancer [22,23], anti-inflammatory [24], antimicrobial [23], antihyperglycemic [25], and hypolipidemic properties [26]. Moreover, H. erinaceus has been used to treat cognitive impairments [27], Alzheimer's disease [28], Parkinson's disease [29], ischemic stroke [30], and presbycusis [14]. Recently, the present research on H. erinaceus has been focused on its antidepressant-like effects for the treatment of depressive disorder [31][32][33].…”

Section: Introductionmentioning

confidence: 99%

Therapeutic Potential of Hericium erinaceus for Depressive Disorder

Chong

Fung

Wong

et al. 2019

IJMS

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Depression is a common and severe neuropsychiatric disorder that is one of the leading causes of global disease burden. Although various anti-depressants are currently available, their efficacies are barely adequate and many have side effects. Hericium erinaceus, also known as Lion’s mane mushroom, has been shown to have various health benefits, including antioxidative, antidiabetic, anticancer, anti-inflammatory, antimicrobial, antihyperglycemic, and hypolipidemic effects. It has been used to treat cognitive impairment, Parkinson’s disease, and Alzheimer’s disease. Bioactive compounds extracted from the mycelia and fruiting bodies of H. erinaceus have been found to promote the expression of neurotrophic factors that are associated with cell proliferation such as nerve growth factors. Although antidepressant effects of H. erinaceus have not been validated and compared to the conventional antidepressants, based on the neurotrophic and neurogenic pathophysiology of depression, H. erinaceus may be a potential alternative medicine for the treatment of depression. This article critically reviews the current literature on the potential benefits of H. erinaceus as a treatment for depressive disorder as well as its mechanisms underlying the antidepressant-like activities.

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Protective Effects of Hericium erinaceus Mycelium and Its Isolated Erinacine A against Ischemia-Injury-Induced Neuronal Cell Death via the Inhibition of iNOS/p38 MAPK and Nitrotyrosine

Cited by 92 publications

References 40 publications

SMND-309 promotes neuron survival through the activation of the PI3K/Akt/CREB-signalling pathway

SMND-309 promotes neuron survival through the activation of the PI3K/Akt/CREB-signalling pathway

A Comparative Proteomic Analysis of Erinacine A’s Inhibition of Gastric Cancer Cell Viability and Invasiveness

Therapeutic Potential of Hericium erinaceus for Depressive Disorder

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