p38 mitogen-activated protein kinase family

evidence_span

{"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}

experimental_model

Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis

exposure

Increased NaCl in culture or high-salt mouse diet

limitations

NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.

nutrient_topic

Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium

organism

Human and mouse T cells; mouse disease model

plain_language

Blocking p38/MAPK interrupted this particular salt-sensitive immune response.

primary_references

[sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868

tissue_or_cell_type

T-helper cells and experimental CNS autoimmunity

Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 499–510

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft

### sodium-th17-p38 Silencing or chemical inhibition of p38/MAPK blocked the high-salt enhancement of TH17 differentiation in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking p38/MAPK interrupted this particular salt-sensitive immune response. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868

duration

Acute

evidence_access

Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

experimental_model

RAW 264.7 murine macrophages

exposure

SB239063 with (+)-lariciresinol

limitations

Inhibitor dependence establishes that p38 is required, not that lariciresinol binds or acts on p38 directly.

organism

RAW 264.7 murine macrophages

plain_language

The p38 inhibitor SB239063 suppressed the (+)-lariciresinol-induced response, placing p38 upstream of it.

primary_references

Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035

route

In vitro

tissue

p38 dependence of the antioxidant response

Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 22–31

Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

## p38-required-for-the-nrf2-response The p38 inhibitor SB239063 suppressed the (+)-lariciresinol-induced response, placing p38 upstream of it. Model/species: RAW 264.7 murine macrophages Tissue/system: p38 dependence of the antioxidant response Exposure: SB239063 with (+)-lariciresinol Route: In vitro Duration: Acute Limits: Inhibitor dependence establishes that p38 is required, not that lariciresinol binds or acts on p38 directly. Primary reference: Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

duration

Acute

evidence_access

Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

experimental_model

RAW 264.7 murine macrophages

exposure

(+)-Lariciresinol isolated from Rubia philippinensis

limitations

The abstract states p38 activation without giving concentrations or timing; those appear only in the full text and figures and were not read here.

organism

RAW 264.7 murine macrophages

plain_language

(+)-Lariciresinol activated p38 in murine macrophages.

primary_references

Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035

route

In vitro

tissue

Mitogen-activated protein kinase phosphorylation

Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 11–20

Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

## plus-lariciresinol-activates-p38 (+)-Lariciresinol activated p38 in murine macrophages. Model/species: RAW 264.7 murine macrophages Tissue/system: Mitogen-activated protein kinase phosphorylation Exposure: (+)-Lariciresinol isolated from Rubia philippinensis Route: In vitro Duration: Acute Limits: The abstract states p38 activation without giving concentrations or timing; those appear only in the full text and figures and were not read here. Primary reference: Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

duration

Not stated here

evidence_access

Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.

experimental_model

RAW 264.7 murine macrophages

exposure

(+)-Lariciresinol, dose-dependent, without cytotoxicity

limitations

Measured as transcript and protein level rather than as nuclear translocation in the abstract.

organism

RAW 264.7 murine macrophages

plain_language

(+)-Lariciresinol increased Nrf2 at both transcriptional and translational levels.

primary_references

Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035

route

In vitro

tissue

Nrf2 transcription factor abundance

Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 33–42

Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft

## plus-lariciresinol-raises-nrf2 (+)-Lariciresinol increased Nrf2 at both transcriptional and translational levels. Model/species: RAW 264.7 murine macrophages Tissue/system: Nrf2 transcription factor abundance Exposure: (+)-Lariciresinol, dose-dependent, without cytotoxicity Route: In vitro Duration: Not stated here Limits: Measured as transcript and protein level rather than as nuclear translocation in the abstract. Primary reference: Antioxidant efficacy and the upregulation of Nrf2-mediated HO-1 expression by (+)-lariciresinol, a lignan isolated from Rubia philippinensis, through the activation of p38. (2017). https://pubmed.ncbi.nlm.nih.gov/28378774/ DOI: 10.1038/srep46035 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.