Protective effects of Gastrodia elata Blume on MPP+-induced cytotoxicity in human dopaminergic SH-SY5Y cells

Hua, An; Kim, In Su; Koppula, Sushruta; Kim, Byung‐Wook; Park, Pyo Jam; Lim, Beong Ou; Choi, Wahn Soo; Lee, Kwang Ho; Choi, Dong Kug

doi:10.1016/j.jep.2010.05.006

Cited by 74 publications

(46 citation statements)

References 71 publications

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“…Then, cDNA was amplified by PCR using specific primers as mentioned previously (20,22). The PCR was performed using the above-prepared cDNA as a template for respective targets, as described previously (25,26). PCR products were analyzed on 1% agarose gels.…”

Section: Isolation Of Total Rna and Reverse Transcription-polymerase mentioning

confidence: 99%

Anti-neuroinflammatory Activity of a Novel Cannabinoid Derivative by Inhibiting the NF-κB Signaling Pathway in Lipopolysaccharide-Induced BV-2 Microglial Cells

Park

Kim

et al. 2013

J Pharmacol Sci

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Abstract. Microglial-mediated neuroinflammation has recently been implicated as one of the important mechanisms responsible for the progression of neurodegenerative diseases. Activated microglia cells produce various neurotoxic factors that are harmful to neurons. Therefore, suppression of the inflammatory response elicited by activated microglia is considered a potential therapeutic target for neurodegenerative diseases. The cannabinoid (CB) system is widespread in the central nervous system and is very crucial for modulating a spectrum of neurophysiological functions such as pain, appetite, and cognition. In the present study, we synthesized and investigated a novel CB derivative (CD-101) for its ability to suppress lipopolysaccharide (LPS)-mediated activation of BV-2 microglial cells and subsequent release of various inflammatory mediators. CD-101 significantly inhibited the production of inflammatory markers such as nitric oxide, cyclooxygenase-2, and pro-inflammatory cytokines such as tumor necrosis factor-α, interleukin-1β, and interleukin-6. The anti-neuroinflammatory effect of this novel cannabinoid derivative occurred by inhibiting p38MAPK phosphorylation and by decreasing nuclear translocation of p65 subunit of nuclear factor kappa-B in LPS-stimulated BV-2 microglial cells. These results suggest that the use of the cannabinoid derivative CD-101 might be a potential therapeutic target against neuroinflammatory disorders.

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Section: Isolation Of Total Rna and Reverse Transcription-polymerase mentioning

confidence: 99%

Anti-neuroinflammatory Activity of a Novel Cannabinoid Derivative by Inhibiting the NF-κB Signaling Pathway in Lipopolysaccharide-Induced BV-2 Microglial Cells

Park

Kim

et al. 2013

J Pharmacol Sci

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“…The primer sequences used are presented in Table 1. PCR was performed using the above-prepared cDNA as a template as described previously (16,17).…”

Section: Isolation Of Total Rna and Rt-pcrmentioning

confidence: 99%

Anti-neuroinflammatory Activity of Kamebakaurin From Isodon japonicus via Inhibition of c-Jun NH2-Terminal Kinase and p38 Mitogen-Activated Protein Kinase Pathway in Activated Microglial Cells

et al. 2011

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Abstract.Compelling evidence supports the notion that the majority of neurodegenerative diseases are associated with microglia-mediated neuroinflammation. Therefore, quelling of microglial activation may lead to neuronal cell survival. The present study investigated the effects of Kamebakaurin (KMBK), a kaurane diterpene isolated from Isodon japonicus HARA (Labiatae), on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated cytotoxicity in rat primary microglial cultures and the BV-2 cell line. KMBK significantly inhibited the LPSinduced production of nitric oxide (NO) in a concentration-dependent fashion in activated microglial cells. The mRNA and protein levels of inducible nitric oxide synthase (iNOS) and cyclooxycenase-2 (COX-2) were also decreased dose-dependently. Furthermore KMBK inhibited the JNK and p38 mitogen-activated protein kinases (MAPKs) in LPS-stimulated BV-2 microglial cells. Considering the results obtained, the present study authenticated the potential benefits of KMBK as a therapeutic target in ameliorating microglia-mediated neuroinflammatory diseases.

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“…with the function of "calming liver and stopping wind" are frequently used in herbal formulations for the treatment of PD in China . The in vitro or in vivo anti-Parkinsonian activities of these two herbal materials have also been reported in neurotoxic models of PD (Shim et al, 2009;An et al, 2010;Kim et al, 2011). Another example is the green tea polyphenols (GTPs) which is under phase II clinical investigation (Meissner et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Anti-Parkinsonian drug discovery from herbal medicines: What have we got from neurotoxic models?

Song

Sze

et al. 2012

Journal of Ethnopharmacology

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Protective effects of Gastrodia elata Blume on MPP+-induced cytotoxicity in human dopaminergic SH-SY5Y cells

Cited by 74 publications

References 71 publications

Anti-neuroinflammatory Activity of a Novel Cannabinoid Derivative by Inhibiting the NF-κB Signaling Pathway in Lipopolysaccharide-Induced BV-2 Microglial Cells

Anti-neuroinflammatory Activity of a Novel Cannabinoid Derivative by Inhibiting the NF-κB Signaling Pathway in Lipopolysaccharide-Induced BV-2 Microglial Cells

Anti-neuroinflammatory Activity of Kamebakaurin From Isodon japonicus via Inhibition of c-Jun NH2-Terminal Kinase and p38 Mitogen-Activated Protein Kinase Pathway in Activated Microglial Cells

Anti-Parkinsonian drug discovery from herbal medicines: What have we got from neurotoxic models?

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