Gastrodia elata BL mediates the suppression of nnos and microglia activation to protect against neuronal damage in kainic acid-treated rats

Ching Liang Hsieh, Chi Long Chen, Nou Ying Tang, Chin Min Chuang, Ching Tou Hsieh, Su Yin Chiang, Jaung Geng Lin, Sheng Feng Hsu

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

Our previous studies showed that Gastrodia elata (GE), an herb used in traditional Chinese medicine, has both anti-convulsive and free radical-scavenging activities in kainic acid (KA)-treated rats. The aim of the present study was to further investigate possible physiological mechanisms of GE against activities of neuronal nitric oxide synthase (nNOS) and microglia in KA-treated rats; 0.5 g/kg and 1.0 g/kg of GE extract were administered orally, whereas 20 mg/kg of N-nitro-L-arginine methyl ester (L-NAME) was administered intraperitoneally (ip), both at 30 minutes prior to KA (2 μg/2 μl) being injected into the right hippocampus region of rats. ED1-staining, apoptotic, inducible nitric oxide synthase (iNOS), and nNOS-staining cells were observed in the hippocampus region. The results indicated that 1.0 g/kg of GE and 20 mg/kg of L-NAME reduced the counts of ED1-stained cells, and 0.5 g/kg and 1.0 g/kg of GE, and 20 mg/kg of L-NAME reduced the numbers of apoptotic cells and nNOS-staining cells. In addition, 20 mg/kg of L-NAME also reduced the numbers of iNOS-staining cells, but 0.5 g/kg and 1.0 g/kg of GE did not. This study demonstrated that GE was able to reduce nNOS, microglia activation and apoptosis, suggesting that GE has a protective effect against neuronal damage in KA-treated rats.

Original languageEnglish
Pages (from-to)599-611
Number of pages13
JournalAmerican Journal of Chinese Medicine
Volume33
Issue number4
DOIs
Publication statusPublished - 2005

Fingerprint

Gastrodia
Kainic Acid
Microglia
Nitric Oxide Synthase Type I
NG-Nitroarginine Methyl Ester
Staining and Labeling
Nitric Oxide Synthase Type II
Hippocampus
Chinese Traditional Medicine
Free Radicals
Cell Count
Apoptosis

Keywords

  • Apoptosis
  • Gastrodia elata
  • Kainic acid
  • Microglia
  • Nitric oxide synthase (NOS)

ASJC Scopus subject areas

  • Complementary and alternative medicine

Cite this

Gastrodia elata BL mediates the suppression of nnos and microglia activation to protect against neuronal damage in kainic acid-treated rats. / Hsieh, Ching Liang; Chen, Chi Long; Tang, Nou Ying; Chuang, Chin Min; Hsieh, Ching Tou; Chiang, Su Yin; Lin, Jaung Geng; Hsu, Sheng Feng.

In: American Journal of Chinese Medicine, Vol. 33, No. 4, 2005, p. 599-611.

Research output: Contribution to journalArticle

Hsieh, Ching Liang ; Chen, Chi Long ; Tang, Nou Ying ; Chuang, Chin Min ; Hsieh, Ching Tou ; Chiang, Su Yin ; Lin, Jaung Geng ; Hsu, Sheng Feng. / Gastrodia elata BL mediates the suppression of nnos and microglia activation to protect against neuronal damage in kainic acid-treated rats. In: American Journal of Chinese Medicine. 2005 ; Vol. 33, No. 4. pp. 599-611.
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abstract = "Our previous studies showed that Gastrodia elata (GE), an herb used in traditional Chinese medicine, has both anti-convulsive and free radical-scavenging activities in kainic acid (KA)-treated rats. The aim of the present study was to further investigate possible physiological mechanisms of GE against activities of neuronal nitric oxide synthase (nNOS) and microglia in KA-treated rats; 0.5 g/kg and 1.0 g/kg of GE extract were administered orally, whereas 20 mg/kg of N-nitro-L-arginine methyl ester (L-NAME) was administered intraperitoneally (ip), both at 30 minutes prior to KA (2 μg/2 μl) being injected into the right hippocampus region of rats. ED1-staining, apoptotic, inducible nitric oxide synthase (iNOS), and nNOS-staining cells were observed in the hippocampus region. The results indicated that 1.0 g/kg of GE and 20 mg/kg of L-NAME reduced the counts of ED1-stained cells, and 0.5 g/kg and 1.0 g/kg of GE, and 20 mg/kg of L-NAME reduced the numbers of apoptotic cells and nNOS-staining cells. In addition, 20 mg/kg of L-NAME also reduced the numbers of iNOS-staining cells, but 0.5 g/kg and 1.0 g/kg of GE did not. This study demonstrated that GE was able to reduce nNOS, microglia activation and apoptosis, suggesting that GE has a protective effect against neuronal damage in KA-treated rats.",
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AU - Chen, Chi Long

AU - Tang, Nou Ying

AU - Chuang, Chin Min

AU - Hsieh, Ching Tou

AU - Chiang, Su Yin

AU - Lin, Jaung Geng

AU - Hsu, Sheng Feng

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N2 - Our previous studies showed that Gastrodia elata (GE), an herb used in traditional Chinese medicine, has both anti-convulsive and free radical-scavenging activities in kainic acid (KA)-treated rats. The aim of the present study was to further investigate possible physiological mechanisms of GE against activities of neuronal nitric oxide synthase (nNOS) and microglia in KA-treated rats; 0.5 g/kg and 1.0 g/kg of GE extract were administered orally, whereas 20 mg/kg of N-nitro-L-arginine methyl ester (L-NAME) was administered intraperitoneally (ip), both at 30 minutes prior to KA (2 μg/2 μl) being injected into the right hippocampus region of rats. ED1-staining, apoptotic, inducible nitric oxide synthase (iNOS), and nNOS-staining cells were observed in the hippocampus region. The results indicated that 1.0 g/kg of GE and 20 mg/kg of L-NAME reduced the counts of ED1-stained cells, and 0.5 g/kg and 1.0 g/kg of GE, and 20 mg/kg of L-NAME reduced the numbers of apoptotic cells and nNOS-staining cells. In addition, 20 mg/kg of L-NAME also reduced the numbers of iNOS-staining cells, but 0.5 g/kg and 1.0 g/kg of GE did not. This study demonstrated that GE was able to reduce nNOS, microglia activation and apoptosis, suggesting that GE has a protective effect against neuronal damage in KA-treated rats.

AB - Our previous studies showed that Gastrodia elata (GE), an herb used in traditional Chinese medicine, has both anti-convulsive and free radical-scavenging activities in kainic acid (KA)-treated rats. The aim of the present study was to further investigate possible physiological mechanisms of GE against activities of neuronal nitric oxide synthase (nNOS) and microglia in KA-treated rats; 0.5 g/kg and 1.0 g/kg of GE extract were administered orally, whereas 20 mg/kg of N-nitro-L-arginine methyl ester (L-NAME) was administered intraperitoneally (ip), both at 30 minutes prior to KA (2 μg/2 μl) being injected into the right hippocampus region of rats. ED1-staining, apoptotic, inducible nitric oxide synthase (iNOS), and nNOS-staining cells were observed in the hippocampus region. The results indicated that 1.0 g/kg of GE and 20 mg/kg of L-NAME reduced the counts of ED1-stained cells, and 0.5 g/kg and 1.0 g/kg of GE, and 20 mg/kg of L-NAME reduced the numbers of apoptotic cells and nNOS-staining cells. In addition, 20 mg/kg of L-NAME also reduced the numbers of iNOS-staining cells, but 0.5 g/kg and 1.0 g/kg of GE did not. This study demonstrated that GE was able to reduce nNOS, microglia activation and apoptosis, suggesting that GE has a protective effect against neuronal damage in KA-treated rats.

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