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The water extract of Samultang protects the Lipopolysaccharide (LPS)/Phorbol 12-myristate 13-acetate (PMA)-induced damage and nitric oxide production of C6 glial cells via down-regulation of NF-κB

Samultang has been traditionally used for treatment of ischemic heart and brain diseases in oriental medicine. However, little is known about the mechanism by which Samultang rescues the myocardial and neuronal cells from ischemic damage. This study was designed to evaluate whether the water extract...

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Published in:General pharmacology 2000-05, Vol.34 (5), p.303-310
Main Authors: So, Hong-Seob, Oh, Jaymin, Chung, Yeun-Tai, Moon, Yeon-Ja, Kim, Do-Hwan, Moon, Byung-Soon, Lee, Ho-Seob, Baek, Seung-Wha, Park, Channy, Lim, Yun Sook, Kim, Myung-Sunny, Park, RaeKil
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cited_by cdi_FETCH-LOGICAL-c366t-76f55923b2f9f58c3156acef717597250659bcec3f22dade6b3cd736fb9e8a963
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container_issue 5
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container_title General pharmacology
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creator So, Hong-Seob
Oh, Jaymin
Chung, Yeun-Tai
Moon, Yeon-Ja
Kim, Do-Hwan
Moon, Byung-Soon
Lee, Ho-Seob
Baek, Seung-Wha
Park, Channy
Lim, Yun Sook
Kim, Myung-Sunny
Park, RaeKil
description Samultang has been traditionally used for treatment of ischemic heart and brain diseases in oriental medicine. However, little is known about the mechanism by which Samultang rescues the myocardial and neuronal cells from ischemic damage. This study was designed to evaluate whether the water extract of Samultang may modulate the production of nitric oxide (NO) in LPS and PMA treated-C6 glial cells to protect the cells from NO-induced cytotoxicity. C6 glial cells treated with both LPS and PMA significantly produced a large amount of NO compared to untreated, PMA, or LPS-treated cells. In parallel with NO production, cotreatment of LPS and PMA induced the severe apoptotic death of C6 glial cells. However, Samultang significantly reduced both cell death and NO production by LPS/PMA in a dose-dependent manner. In addition, the modulatory effects of Samultang on LPS/PMA-induced cytotoxicity and NO production could be mimicked by exogenous treatments of N GMMA, a nitric oxide synthase (NOS) inhibitor, and pyrrolidine dithiocarbamate (PDTC), a strong NF-κB inhibitor. Treatment of C6-glial cells with LPS/PMA induced the transcriptional activation of NF-κB, which was markedly inhibited by Samultang. Taken together, we suggest that the protective effects of Samultang against LPS/PMA-induced cytotoxicity may be mediated by the suppression of NO synthesis via down-regulation of NF-κB activation.
doi_str_mv 10.1016/S0306-3623(00)00073-2
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Treatment of C6-glial cells with LPS/PMA induced the transcriptional activation of NF-κB, which was markedly inhibited by Samultang. Taken together, we suggest that the protective effects of Samultang against LPS/PMA-induced cytotoxicity may be mediated by the suppression of NO synthesis via down-regulation of NF-κB activation.</description><subject>Biological and medical sciences</subject><subject>General pharmacology</subject><subject>LPS</subject><subject>Medical sciences</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>NF-^KB protein</subject><subject>NF-κB</subject><subject>Nitric oxide</subject><subject>Pharmacognosy. Homeopathy. Health food</subject><subject>Pharmacology. 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ispartof General pharmacology, 2000-05, Vol.34 (5), p.303-310
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subjects Biological and medical sciences
General pharmacology
LPS
Medical sciences
Neuropharmacology
Neuroprotective agent
NF-^KB protein
NF-κB
Nitric oxide
Pharmacognosy. Homeopathy. Health food
Pharmacology. Drug treatments
PMA
Samultang
title The water extract of Samultang protects the Lipopolysaccharide (LPS)/Phorbol 12-myristate 13-acetate (PMA)-induced damage and nitric oxide production of C6 glial cells via down-regulation of NF-κB
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