Neuroprotective effects of lotus seedpod procyanidins on extremely low frequency electromagnetic field-induced neurotoxicity in primary cultured hippocampal neurons.
← Research streamCompared with control, ELF-EMF exposure decreased cell viability and increased apoptotic cells in primary cultured rat hippocampal neurons. Lotus seedpod procyanidins (LSPCs) protected against ELF-EMF-induced damage, including reducing ROS and Ca(2+) elevatio…
Study snapshot
Abstract
The present study investigated the protective effects of lotus seedpod procyanidins (LSPCs) on extremely low frequency electromagnetic field (ELF-EMF)-induced neurotoxicity in primary cultured rat hippocampal neurons and the underlying molecular mechanism. The results of MTT, morphological observation, superoxide dismutase (SOD) and malondialdehyde (MDA) assays showed that compared with control, incubating neurons under ELF-EMF exposure significantly decreased cell viability and increased the number of apoptotic cells, whereas LSPCs evidently protected the hippocampal neurons against ELF-EMF-induced cell damage. Moreover, a certain concentration of LSPCs inhibited the elevation of intracellular reactive oxygen species (ROS) and Ca(2+) level, as well as prevented the disruption of mitochondrial membrane potential induced by ELF-EMF exposure. In addition, supplementation with LSPCs could alleviate DNA damage, block cell cycle arrest at S phase, and inhibit apoptosis and necrosis of hippocampal neurons under ELF-EMF exposure. Further study demonstrated that LSPCs up-regulated the activations of Bcl-2, Bcl-xl proteins and suppressed the expressions of Bad, Bax proteins caused by ELF-EMF exposure. In conclusion, these findings revealed that LSPCs protected against ELF-EMF-induced neurotoxicity through inhibiting oxidative stress and mitochondrial apoptotic pathway.
AI evidence extraction
Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.
Main findings
Compared with control, ELF-EMF exposure decreased cell viability and increased apoptotic cells in primary cultured rat hippocampal neurons. Lotus seedpod procyanidins (LSPCs) protected against ELF-EMF-induced damage, including reducing ROS and Ca(2+) elevation, preventing mitochondrial membrane potential disruption, alleviating DNA damage, blocking S-phase arrest, and inhibiting apoptosis/necrosis; LSPCs also increased Bcl-2/Bcl-xl activation and suppressed Bad/Bax changes associated with ELF-EMF exposure.
Outcomes measured
- Cell viability (MTT)
- Morphological changes
- Apoptosis
- Superoxide dismutase (SOD)
- Malondialdehyde (MDA)
- Reactive oxygen species (ROS)
- Intracellular Ca(2+) level
- Mitochondrial membrane potential
- DNA damage
- Cell cycle arrest (S phase)
- Necrosis
- Bcl-2, Bcl-xl activation
- Bad, Bax expression
Limitations
- In vitro primary neuron culture model (rat), limiting direct generalization to in vivo or humans
- Exposure parameters (e.g., frequency, intensity, duration) not reported in the abstract
- Sample size and replication details not reported in the abstract
View raw extracted JSON
{
"study_type": "in_vitro",
"exposure": {
"band": "ELF",
"source": null,
"frequency_mhz": null,
"sar_wkg": null,
"duration": null
},
"population": "Primary cultured rat hippocampal neurons",
"sample_size": null,
"outcomes": [
"Cell viability (MTT)",
"Morphological changes",
"Apoptosis",
"Superoxide dismutase (SOD)",
"Malondialdehyde (MDA)",
"Reactive oxygen species (ROS)",
"Intracellular Ca(2+) level",
"Mitochondrial membrane potential",
"DNA damage",
"Cell cycle arrest (S phase)",
"Necrosis",
"Bcl-2, Bcl-xl activation",
"Bad, Bax expression"
],
"main_findings": "Compared with control, ELF-EMF exposure decreased cell viability and increased apoptotic cells in primary cultured rat hippocampal neurons. Lotus seedpod procyanidins (LSPCs) protected against ELF-EMF-induced damage, including reducing ROS and Ca(2+) elevation, preventing mitochondrial membrane potential disruption, alleviating DNA damage, blocking S-phase arrest, and inhibiting apoptosis/necrosis; LSPCs also increased Bcl-2/Bcl-xl activation and suppressed Bad/Bax changes associated with ELF-EMF exposure.",
"effect_direction": "mixed",
"limitations": [
"In vitro primary neuron culture model (rat), limiting direct generalization to in vivo or humans",
"Exposure parameters (e.g., frequency, intensity, duration) not reported in the abstract",
"Sample size and replication details not reported in the abstract"
],
"evidence_strength": "low",
"confidence": 0.78,
"peer_reviewed_likely": "yes",
"keywords": [
"extremely low frequency",
"ELF-EMF",
"neurotoxicity",
"hippocampal neurons",
"oxidative stress",
"mitochondrial apoptotic pathway",
"lotus seedpod procyanidins",
"LSPCs",
"ROS",
"Ca2+",
"DNA damage",
"cell cycle arrest",
"Bcl-2",
"Bax"
],
"suggested_hubs": []
}AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.
Identifiers and source
DOI: 10.1016/j.biopha.2016.05.032
PubMed: 27470406
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