Bee venom protects SH-SY5Y human neuroblastoma cells from 1-methyl-4-phenylpyridinium-induced apoptotic cell death

Doo, Ah-Reum; Kim, Seung-Nam; Kim, Seung-Tae; Park, Ji-Yeun; Chung, Sung-Hyun; Choe, Bo-Young; Chae, Younbyoung; Lee, Hyejung; Yin, Chang-Shik; Park, Hi-Joon

doi:10.1016/j.brainres.2011.10.003

Cited by 34 publications

(20 citation statements)

References 39 publications

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“…Apamin, the BV protein, prevents apoptosis indirectly by blocking SK channels on dopamine neurons (Salthun-Lassalle et al, 2004). In addition, BV was reported to directly inhibit apoptosis in SH-SY5Y human neuroblastoma cells (Doo et al, 2012). Furthermore, previous studies reported direct neuroprotective effect of BV on MPP + or MPTP/probenecid-induced apoptotic cell death (Alvarez-Fischer et al, 2013;Doo et al, 2012) supporting the current observation.…”

Section: Discussionsupporting

confidence: 73%

“…In subsequent events, BV decreased the expression level of Bax gene induced by rotenone treatment and hence suppressed the apoptotic pathway, which was further demonstrated by alleviated DNA fragmentation and suppressed caspase-3 activation induced by rotenone. Bcl-2 and Bax play an important role in the mitochondria-dependent apoptotic pathway (Doo et al, 2012). Induction of apoptosis factors would generate activation of the caspase cascade (Miller et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, BV acupuncture (BVA) has been shown to protect dopaminergic neurons effectively against MPTP-induced toxicity due to inhibition of microglial activation in mice (Doo et al, 2010;Kim et al, 2011). Moreover, BV has a direct neuroprotective effect on SH-SY5Y human neuroblastoma cells from MPP + -induced apoptotic cell death (Doo et al, 2012). However, such therapeutic uses are not supported by convincing evidence to date, and the underlying mechanism of BV amelioration of neurodegenerative diseases of the CNS, such as PD, remains to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective effects of bee venom acupuncture therapy against rotenone-induced oxidative stress and apoptosis

Khalil

Assaf

ElShebiney³

et al. 2015

Neurochemistry International

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neuroprotective effects of bee venom acupuncture therapy against rotenone-induced oxidative stress and apoptosis

Khalil

Assaf

ElShebiney³

et al. 2015

Neurochemistry International

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“…In addition, it contains biologically active amines (histamine and epinephrine) and a few non-peptide components including lipids, carbohydrates and free amino acids (Lariviere & Melzack, 1996). These components have been reported to exert anti-inflammatory (Jang et al, 2005;Kwon et al, 2002) and neuroprotective effects (Doo et al, 2012;Yang et al, 2010). BV is also known to be involved in antibacterial action (Han, Lee, Park, & Pak, 2013).…”

Section: Discussionmentioning

confidence: 97%

“…Hence, downregulation of these enzymes decreases overall melanin synthesis (Hearing & Tsukamoto, 1991). Treatment using bee venom (BV) from the honeybee (Apis mellifera L.) is a traditional therapeutic modality in East Asian countries (Yin, Lee, Hong, Chung, & Koh, 2005), that is especially known for its pain relieving (Billingham, Morley, Hanson, Shipolini, & Vernon, 1973;Kwon et al, 2001), anti-inflammatory (Kwon et al, 2002;Lee et al, 2004), anti-apoptotic (Doo et al, 2012) and anti-carcinogenic effects (Moon et al, 2007). BV has also been used as a cosmetic ingredient due to its anti-ageing and antimicrobial properties (Han, Lee, Yeo, Kweon, Woo, Baek, et al, 2007;Piek, 1986).…”

Section: Introductionmentioning

confidence: 99%

Anti-melanogenic properties of honeybee (Apis melliferaL.) venom in α-MSH-stimulated B16F1 cells

Han

Kim

Pak

2014

Food and Agricultural Immunology

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Since ancient times, honeybee (Apis mellifera L.) venom (BV) has been applied to the skin as an anti-ageing remedy. To further access BV as an effective whitening agent for cosmetics and potential external treatment for topical use, we investigated its ability to inhibit tyrosinase activity and subsequent melanin biosynthesis. B16F1 melanoma cells were treated with 10 nM α-melanocyte stimulating hormone (α-MSH) and then with various doses of BV. BV inhibited direct tyrosinase activity and cellular tyrosinase activity, which decreased melanin synthesis in α-MSH-stimulated B16F1 melanoma cells. In addition, we used reverse transcription-polymerase chain reaction and Western blotting for melanogenesis-related genes such as tyrosinase-related protein (TRP)-1 and TRP-2 to examine the mechanisms underlying the inhibitory effects of BV on melanogensis. BV decreased the mRNA and protein expression of TRP-1 and TRP-2. These findings suggest that BV induced the downregulation of melanogenesis by inhibiting TRP-1 and TRP-2 activation.

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CRHR1 Mediates the Up-Regulation of Synapsin I Induced by Nesfatin-1 Through ERK 1/2 Signaling in SH-SY5Y Cells

Chen

et al. 2017

Cell Mol Neurobiol

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The anorexigenic molecule nesfatin-1 has recently been taken as a potential mood regulator, but the potential mechanisms remain unknown. Results of our previous study have demonstrated that nesfatin-1 could induce anxiety- and depression-like behaviors in rats, accompanied by the hyperactivity of the hypothalamic-pituitary-adrenal axis and the imbalanced mRNA expression of synaptic vesicle proteins. To explore the potential neurobiological mechanism underlying the effect of nesfatin-1 on the synaptic plasticity, the human neuroblastoma SH-SY5Y cells were cultured and treated with different concentrations of nesfatin-1 in the present study. The mRNA and protein expressions of corticotropin-releasing hormone (CRH) were measured via real-time fluorescent quantitative PCR and western blot, respectively. The protein expressions of extracellular signal-regulated kinase 1/2 (ERK1/2), phosphorylated-ERK1/2 (p-ERK1/2), and synapsin I were detected via western blot. The results confirmed that nesfatin-1 (10~10 mol/L) could up-regulate the expression of CRH. Moreover, nesfatin-1 (10~10 mol/L) could also increase the protein expressions of p-ERK1/2 and synapsin I, and these effects could be blocked by CP376395, a selective antagonist of CRH type 1 receptor (CRHR1). Furthermore, the increased expression of synapsin I induced by nesfatin-1 could also be reversed by PD98059, a specific inhibitor of the p-ERK. These results indicated that CRHR1 might mediate the effect of nesfatin-1 on the expressions of synapsin I via ERK1/2 signaling pathway.

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Bee venom protects SH-SY5Y human neuroblastoma cells from 1-methyl-4-phenylpyridinium-induced apoptotic cell death

Cited by 34 publications

References 39 publications

Neuroprotective effects of bee venom acupuncture therapy against rotenone-induced oxidative stress and apoptosis

Neuroprotective effects of bee venom acupuncture therapy against rotenone-induced oxidative stress and apoptosis

Anti-melanogenic properties of honeybee (Apis melliferaL.) venom in α-MSH-stimulated B16F1 cells

CRHR1 Mediates the Up-Regulation of Synapsin I Induced by Nesfatin-1 Through ERK 1/2 Signaling in SH-SY5Y Cells

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