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Protective effects of ginseng saponins on 3-nitropropionic acid-induced striatal degeneration in rats.
Neuropharmacology. 2005 Apr; 48(5):743-56.N

Abstract

The precise cause of neuronal cell death in Huntington's disease (HD) is not known. Systemic administration of 3-nitropropionic acid (3-NP), an irreversible succinate dehydrogenase inhibitor, not only induces a cellular ATP depletions but also causes a selective striatal degeneration similar to that seen in HD. Recent accumulating reports have shown that ginseng saponins (GTS), the major active ingredients of Panax ginseng, have protective effects against neurotoxin insults. In the present study, we examined in vitro and in vivo effects of GTS on striatal neurotoxicity induced by repeated treatment of 3-NP in rats. Here, we report that systemic administration of GTS produced significant protections against systemic 3-NP- and intrastriatal malonate-induced lesions in rat striatum with dose-dependent manner. GTS also improved significantly 3-NP-caused behavioral impairment and extended survival. However, GTS itself had no effect on 3-NP-induced inhibition of succinate dehydrogenase activity. To explain the mechanisms underlying in vivo protective effects of GTS against 3-NP-induced striatal degeneration, we examined in vitro effect of GTS against 3-NP-caused cytotoxicity using cultured rat striatal neurons. We found that GTS inhibited 3-NP-induced intracellular Ca(2+) elevations. GTS restored 3-NP-caused mitochondrial transmembrane potential reduction in cultured rat striatal neurons. GTS also prevented 3-NP-induced striatal neuronal cell deaths with dose-dependent manner. The EC(50) was 12.6 +/- 0. 7microg/ml. These results suggest that in vivo protective effects of GTS against 3-NP-induced rat striatal degeneration might be achieved via in vitro inhibition of 3-NP-induced intracellular Ca(2+) elevations and cytotoxicity of striatal neurons.

Authors+Show Affiliations

Research Laboratory for the Study of Ginseng Signal Transduction and Department of Physiology and Anatomy, College of Veterinary Medicine, Konkuk University, Seoul, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15814108

Citation

Kim, Jong-Hoon, et al. "Protective Effects of Ginseng Saponins On 3-nitropropionic Acid-induced Striatal Degeneration in Rats." Neuropharmacology, vol. 48, no. 5, 2005, pp. 743-56.
Kim JH, Kim S, Yoon IS, et al. Protective effects of ginseng saponins on 3-nitropropionic acid-induced striatal degeneration in rats. Neuropharmacology. 2005;48(5):743-56.
Kim, J. H., Kim, S., Yoon, I. S., Lee, J. H., Jang, B. J., Jeong, S. M., Lee, J. H., Lee, B. H., Han, J. S., Oh, S., Kim, H. C., Park, T. K., Rhim, H., & Nah, S. Y. (2005). Protective effects of ginseng saponins on 3-nitropropionic acid-induced striatal degeneration in rats. Neuropharmacology, 48(5), 743-56.
Kim JH, et al. Protective Effects of Ginseng Saponins On 3-nitropropionic Acid-induced Striatal Degeneration in Rats. Neuropharmacology. 2005;48(5):743-56. PubMed PMID: 15814108.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective effects of ginseng saponins on 3-nitropropionic acid-induced striatal degeneration in rats. AU - Kim,Jong-Hoon, AU - Kim,Sunoh, AU - Yoon,In-Soo, AU - Lee,Jong-Hwan, AU - Jang,Byung-Jun, AU - Jeong,Sang Min, AU - Lee,Jun-Ho, AU - Lee,Byung-Hwan, AU - Han,Jin-Soo, AU - Oh,Sekwan, AU - Kim,Hyung-Chun, AU - Park,Tae Kyu, AU - Rhim,Hyewhon, AU - Nah,Seung-Yeol, PY - 2004/07/15/received PY - 2004/10/14/revised PY - 2004/12/10/accepted PY - 2005/4/9/pubmed PY - 2005/6/25/medline PY - 2005/4/9/entrez SP - 743 EP - 56 JF - Neuropharmacology JO - Neuropharmacology VL - 48 IS - 5 N2 - The precise cause of neuronal cell death in Huntington's disease (HD) is not known. Systemic administration of 3-nitropropionic acid (3-NP), an irreversible succinate dehydrogenase inhibitor, not only induces a cellular ATP depletions but also causes a selective striatal degeneration similar to that seen in HD. Recent accumulating reports have shown that ginseng saponins (GTS), the major active ingredients of Panax ginseng, have protective effects against neurotoxin insults. In the present study, we examined in vitro and in vivo effects of GTS on striatal neurotoxicity induced by repeated treatment of 3-NP in rats. Here, we report that systemic administration of GTS produced significant protections against systemic 3-NP- and intrastriatal malonate-induced lesions in rat striatum with dose-dependent manner. GTS also improved significantly 3-NP-caused behavioral impairment and extended survival. However, GTS itself had no effect on 3-NP-induced inhibition of succinate dehydrogenase activity. To explain the mechanisms underlying in vivo protective effects of GTS against 3-NP-induced striatal degeneration, we examined in vitro effect of GTS against 3-NP-caused cytotoxicity using cultured rat striatal neurons. We found that GTS inhibited 3-NP-induced intracellular Ca(2+) elevations. GTS restored 3-NP-caused mitochondrial transmembrane potential reduction in cultured rat striatal neurons. GTS also prevented 3-NP-induced striatal neuronal cell deaths with dose-dependent manner. The EC(50) was 12.6 +/- 0. 7microg/ml. These results suggest that in vivo protective effects of GTS against 3-NP-induced rat striatal degeneration might be achieved via in vitro inhibition of 3-NP-induced intracellular Ca(2+) elevations and cytotoxicity of striatal neurons. SN - 0028-3908 UR - https://www.unboundmedicine.com/medline/citation/15814108/Protective_effects_of_ginseng_saponins_on_3_nitropropionic_acid_induced_striatal_degeneration_in_rats_ DB - PRIME DP - Unbound Medicine ER -