Protective effect of diallyl disulfide on oxidative stress-injured neuronally differentiated PC12 cells

Koh, Seong‐Ho; Kwon, Hyugsung; Park, Kee Hyung; Ko, Jin Kyung; Kim, Joo Hwan; Hwang, Myung-Sil; Yum, Young Na; Kim, Ok-Hee; Kim, Juhan; Kim, Hee-Tae; Do, Byung-Rok; Kim, Kyung Suk; Kim, Haekwon; Roh, Hee-Tae; Yu, Hyun-Jeung; Jung, Hai Kwan; Kim, Seung Hyun

doi:10.1016/j.molbrainres.2004.10.006

Cited by 63 publications

(49 citation statements)

References 54 publications

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“…Confluent cells were detached, counted, and seeded into Petri dishes (10-cm diameter) at a density of 1 ϫ 10 6 cells/ml and allowed to adhere 24 h at 37°C. For neuronal differentiation, the cells were cultured with appropriate concentration of rat NGF (Koh et al, 2005). Thereafter, the medium was replaced with fresh medium, and cells were treated with A␤ (1 g/ml) in the presence or absence of sage, rosmarinic acid, or TDZD-8, both given 10 min before A␤42.…”

Section: Methodsmentioning

confidence: 99%

The Spice Sage and Its Active Ingredient Rosmarinic Acid Protect PC12 Cells from Amyloid-β Peptide-Induced Neurotoxicity

Iuvone

Filippis

Esposito

et al. 2006

J Pharmacol Exp Ther

221

120

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Traditional use and clinical reports suggest that the culinary herb sage (Salvia officinalis) may be effective for patients with mild to moderate Alzheimer's disease (AD). In this study, we evaluated the effect of a standardized extract from the leaves of S. officinalis (SOE) and its active ingredient rosmarinic acid on Alzheimer amyloid-␤ peptide (A␤)-induced toxicity in cultured rat pheochromocytoma (PC12) cells. Incubation of PC12 cells with A␤ (fragment 1-42) for 24 h caused cell death, and this effect was reduced by SOE and its active ingredient, rosmarinic acid. Rosmarinic acid reduced a number of events induced by A␤. These include reactive oxygen species formation, lipid peroxidation, DNA fragmentation, caspase-3 activation, and tau protein hyperphosphorylation. Moreover, rosmarinic acid inhibited phosphorylated p38 mitogen-activated protein kinase but not glycogen synthase kinase 3␤ activation. These data show the neuroprotective effect of sage against A␤-induced toxicity, which could validate the traditional use of this spice in the treatment of AD. Rosmarinic acid could contribute, at least in part, for sage-induced neuroprotective effect.

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Section: Methodsmentioning

confidence: 99%

The Spice Sage and Its Active Ingredient Rosmarinic Acid Protect PC12 Cells from Amyloid-β Peptide-Induced Neurotoxicity

Iuvone

Filippis

Esposito

et al. 2006

J Pharmacol Exp Ther

221

120

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“…Recently, Kim et al (2005) and Koh et al (2005) have reported that low concentration of DADS (<25 μM) induces anti-apoptotic patterns in gene and protein expressions and high concentration induces pro-apoptotic patterns in neuronal cells. The present work demonstrated that DADS (1-5 μM) did not significantly increase the percentage of apoptosis in both cell lines in the absence of N-nitrosamines [ Fig.…”

Section: Discussionmentioning

confidence: 99%

“…The large majority of cancer chemopreventive agents induce spontaneous apoptosis in the absence of any apoptosis inducers (D'Agostini et al, 2005), whereas there are limited research papers with regard to its anti-apoptotic effects Koh et al, 2005). Recently, Revel et al (2001Revel et al ( , 2003 have reported that the protective role of resveratrol towards adverse effects of benzo(a)pyrene in sperm and lung could be related to a reduction of benzo(a)pyrene-induced DNA damage and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Antiapoptotic effects of dietary antioxidants towards N‐nitrosopiperidine and N‐nitrosodibutylamine‐induced apoptosis in HL‐60 and HepG2 cells

García

Morales

Arranz

et al. 2009

J of Applied Toxicology

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The aim of this work was to determine the effect of vitamin C, diallyl disulfide (DADS) and dipropyl disulfide (DPDS) towards N-nitrosopiperidine (NPIP) and N-nitrosodibutylamine (NDBA)-induced apoptosis in human leukemia (HL-60) and hepatoma (HepG2) cell lines using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay. None of the vitamin C (5-50 microm), DADS and DPDS (1-5 microm) concentrations selected induced a significant percentage of apoptosis. In simultaneous treatments, vitamin C, DADS and DPDS reduced the apoptosis induced by NPIP and NDBA in HL-60 and HepG2 cells (around 70% of reduction). We also investigated its scavenging activities towards reactive oxygen species (ROS) produced by NPIP and NDBA using 2',7'-dichlorodihydrofluorescein diacetate in both cell lines. ROS production induced by both N-nitrosamine was reduced to control levels by vitamin C (5-50 microm) in a dose-dependent manner. However, DADS (5 microm) increased ROS levels induced by NPIP and NDBA in HL-60 (40 and 20% increase, respectively) and HepG2 cells (18% increase), whereas DPDS was more efficient scavenger of ROS at the lowest concentration (1 microm) in both HL-60 (52 and 25% reduction, respectively) and HepG2 cells (24% reduction). The data demonstrated that the scavenging ability of vitamin C and DPDS could contribute to inhibition of the NPIP- and NDBA-induced apoptosis. However, more than one mechanism, such as inhibition of phase I and/or induction of phase II enzymes, could be implicated in the protective effect of dietary antioxidants towards NPIP- and NDBA-induced apoptosis in HL-60 and HepG2 cells.

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“…Moreover, PC12 cells can be considered as dopaminergic-like neurons because they synthesize and release dopamine [24]. PC12 cells (American Tissue Type Collection CRL-1721) were cultured in 10-cm Petri dishes in DMEM supplemented with 5% FBS, 15% HS, 2 mM glutamine, 100 U/mL penicillin and 100 μg/mL streptomycin at 37°C in 5% CO 2 /95% air and differentiated with retinoic acid as described by Koh et al [25]. Depending on the experiments, PC12 cells were treated with a MPTPconditioned C6 cell medium, with S100B protein (Sigma Aldrich; 0.005-5 μM) or co-cultured with C6 cells.…”

Section: Methodsmentioning

confidence: 99%

Cannabinoid CB1 receptor stimulation affords neuroprotection in MPTP-induced neurotoxicity by attenuating S100B up-regulation in vitro

et al. 2007

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In this study, we investigated the mechanism of S100B neurotoxicity and the effect of cannabinoids, in C6 cells treated with 1-methyl-4-phenyl 1,2,3,6 tetrahydropyridine (MPTP) and co-cultured with differentiated PC12 cells. MPTP concentration-and time-dependently increased S100B density in C6 cells. This effect was followed by increased C6 cell proliferation and decreased cell viability of co-cultured PC12 cells. An antibody against S100B, given to PC12 cells before co-culture, led to their survival. Treatment with arachidonyl-2-chloroethylamide, a CB 1 agonist, significantly inhibited MPTP-induced S100B density in C6 cells and protected co-cultured PC12 cells from cell death. Because MPTP selectively increased the levels of anandamide in C6 cells, the involvement of the endocannabinoid system was investigated by using selective inhibitors of endocannabinoid inactivation (cellular re-uptake or enzymatic hydrolysis) and selective cannabinoid CB 1 and CB 2 receptor antagonists and by silencing the CB 1 receptor. Our data suggest that selective activation of CB 1 receptors by either exogenous or endogenous cannabinoids might afford neuroprotection in MPTP-induced neurotoxicity also by controlling S100B up-regulation in activated glial cells.

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Protective effect of diallyl disulfide on oxidative stress-injured neuronally differentiated PC12 cells

Cited by 63 publications

References 54 publications

The Spice Sage and Its Active Ingredient Rosmarinic Acid Protect PC12 Cells from Amyloid-β Peptide-Induced Neurotoxicity

The Spice Sage and Its Active Ingredient Rosmarinic Acid Protect PC12 Cells from Amyloid-β Peptide-Induced Neurotoxicity

Antiapoptotic effects of dietary antioxidants towards N‐nitrosopiperidine and N‐nitrosodibutylamine‐induced apoptosis in HL‐60 and HepG2 cells

Cannabinoid CB1 receptor stimulation affords neuroprotection in MPTP-induced neurotoxicity by attenuating S100B up-regulation in vitro

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