ArticleNeural regeneration research2014
Geniposide, the component of the Chinese herbal formula Tongluojiunao, protects amyloid-β peptide (1-42-mediated death of hippocampal neurons via the non-classical estrogen signaling pathway.
Article in Neural regeneration research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Estrogen Receptors: A New Frontier in Alzheimer's Disease Therapy.International journal of molecular sciences · 2024Review
- Patchouli alcohol as a selective estrogen receptor β agonist ameliorates AD-like pathology of APP/PS1 model mice.Acta pharmacologica Sinica · 2022Article
- Exploring the Therapeutic Potential of Phytochemicals in Alzheimer's Disease: Focus on Polyphenols and Monoterpenes.Frontiers in pharmacology · 2022Review
- Effects of three different formulae of Gamisoyosan on lipid accumulation induced by oleic acid in HepG2 cells.Integrative medicine research · 2017Article
- Beta 2-adrenergic receptor activation enhances neurogenesis in Alzheimer's disease mice.Neural regeneration research · 2016Article
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14 authors.
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Abstract
Tongluojiunao (TLJN) is an herbal medicine consisting of two main components, geniposide and ginsenoside Rg1. TLJN has been shown to protect primary cultured hippocampal neurons. However, its mechanism of action remains unclear. In the present study, primary cultured hippocampal neurons treated with Aβ1-42 (10 µmol/L) significantly increased the release of lactate dehydrogenase, which was markedly reduced by TLJN (2 µL/mL), specifically by the component geniposide (26 µmol/L), but not ginsenoside Rg1 (2.5 µmol/L). The estrogen receptor inhibitor, ICI182780 (1 µmol/L), did not block TLJN- or geniposide-mediated decrease of lactate dehydrogenase under Aβ1-42-exposed conditions. However, the phosphatidyl inositol 3-kinase or mitogen-activated protein kinase pathway inhibitor, LY294002 (50 µmol/L) or U0126 (10 µmol/L), respectively blocked the decrease of lactate dehydrogenase mediated by TLJN or geniposide. Therefore, these results suggest that the non-classical estrogen pathway (i.e., phosphatidyl inositol 3-kinase or mitogen-activated protein kinase) is involved in the neuroprotective effect of TLJN, specifically its component, geniposide, against Aβ1-42-mediated cell death in primary cultured hippocampal neurons.
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