ArticleJournal of molecular neuroscience : MN2015
Cannabinoid receptor CB1 is involved in nicotine-induced protection against Aβ1-42 neurotoxicity in HT22 cells.
Article in Journal of molecular neuroscience : MN, 2015. 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, 12 citations in OpenAlex.
- Differential Effects of Endocannabinoids on Amyloid-Beta Aggregation and Toxicity.International journal of molecular sciences · 2023Article
- Pseudopeptide Amyloid Aggregation Inhibitors: In Silico, Single Molecule and Cell Viability Studies.International journal of molecular sciences · 2021Article
- Mel1c Mediated Monochromatic Light-Stimulated IGF-I Synthesis through the Intracellular GInternational journal of molecular sciences · 2019Article
- Curcumin Alleviates β Amyloid-Induced Neurotoxicity in HT22 Cells via Upregulating SOD2.Journal of molecular neuroscience : MN · 2019Article
- Cannabinoid CB2 Receptor Mediates Nicotine-Induced Anti-Inflammation in N9 Microglial Cells Exposed to β Amyloid via Protein Kinase C.Mediators of inflammation · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidences suggest that nicotine exerts a neuroprotective effect on Alzheimer's disease (AD), yet the precise mechanism is not fully elucidated. Here, HT22 cells were exposed to amyloid beta protein fragment (Aβ)1-42 to mimic the pathological process of neuron in AD. We hypothesized that cannabinoid receptor CB1 is involved in the nicotine-induced neuroprotection against Aβ1-42 injury in HT22 cells. CB1 expression in HT22 cells was investigated by immunocytochemistry and Western blot. The injury of HT22 cells was evaluated by cellular morphology, cell viability, and lactate dehydrogenase (LDH) release. The apoptosis of HT22 cells was assessed by flow cytometry and expressions of Bcl-2 and Bax. The results demonstrated that nicotine markedly upregulated CB1 expression, increased cell viability, ameliorated cellular morphology, decreased LDH release, and reduced the apoptotic rate of HT22 cells exposed to Aβ1-42 for 24 h, while the blockade of CB1 or the inhibition of protein kinase C (PKC) partially reversed the neuroprotection. Furthermore, the blockade of CB1 reversed nicotine-induced PKC activation in HT22 cells exposed to Aβ1-42. These results suggest that CB1 is involved in the nicotine-induced neuroprotection against Aβ1-42 neurotoxicity, and the neuroprotection may be dependent on the activation of PKC.
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