{"id":"ba80a007-7f0c-5b70-b44c-8611c9034524","stable_key":"35ec55a7-323c-5c28-979e-3bdafe9d5769:barrier-mlc-cyanidin-3-glucoside","predicate":"decreases_in_recorded_experiment","statement":"The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.","claim_class":"observational","status":"source_derived_draft","evidence_grade":"ungraded","direction":"negative","is_public":true,"mechanism_event_id":"a7867f00-26f6-5b1e-ac03-6c406afcd46f","mechanism_event_label":"The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.","subject":{"id":"75149db0-02f7-5d32-8c7a-5c111d90d8ee","slug":"cyanidin-3-glucoside","display_name":"Cyanidin 3-O-beta-D-glucopyranoside","entity_type_key":"small_molecule"},"object":{"id":"d4deaea4-7433-5288-ae1d-8d9d23620e47","slug":"human-caco2-mlc-phosphorylation","display_name":"Myosin light-chain phosphorylation in human Caco-2 cells","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"a7867f00-26f6-5b1e-ac03-6c406afcd46f","stable_key":"35ec55a7-323c-5c28-979e-3bdafe9d5769:barrier-mlc-cyanidin-3-glucoside-event","event_type":"experimental_observation","label":"The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.","description":"**Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).","status":"provisional","compartment":null,"participants":[{"entity":{"id":"75149db0-02f7-5d32-8c7a-5c111d90d8ee","slug":"cyanidin-3-glucoside","display_name":"Cyanidin 3-O-beta-D-glucopyranoside","entity_type_key":"small_molecule"},"role":"tested factor","stoichiometry":null,"state_label":"cyanidin-3-glucoside plus TNF","sequence_order":0,"notes":""},{"entity":{"id":"d4deaea4-7433-5288-ae1d-8d9d23620e47","slug":"human-caco2-mlc-phosphorylation","display_name":"Myosin light-chain phosphorylation in human Caco-2 cells","entity_type_key":"cellular_process"},"role":"measured outcome","stoichiometry":null,"state_label":"decrease","sequence_order":1,"notes":""},{"entity":{"id":"fed11f0e-a497-5f77-8d68-7756e1c4b112","slug":"human-rela","display_name":"Human NF-kappa-B subunit RelA / RELA","entity_type_key":"protein"},"role":"reported NF-kappa-B pathway component","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""},{"entity":{"id":"600d5b09-e092-5146-af1e-2510cf17bac6","slug":"tnf","display_name":"Tumor necrosis factor","entity_type_key":"cytokine"},"role":"joint challenge","stoichiometry":null,"state_label":"","sequence_order":3,"notes":""}]},"contexts":[{"dimension":"evidence_access","value_text":"Full text retrieved; relevant methods/results/figure text reviewed. No independent raw-data verification.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_condition","value_text":"present","comparator":"TNF alone","unit":null,"notes":"Condition belongs to the full experimental contrast; do not separate a joint intervention.","entity":{"slug":"cyanidin-3-glucoside","display_name":"Cyanidin 3-O-beta-D-glucopyranoside","entity_type_key":"small_molecule"}},{"dimension":"experimental_condition","value_text":"present","comparator":"TNF alone","unit":null,"notes":"Condition belongs to the full experimental contrast; do not separate a joint intervention.","entity":{"slug":"tnf","display_name":"Tumor necrosis factor","entity_type_key":"cytokine"}},{"dimension":"experimental_contrast","value_text":"{\"intervention\": \"cyanidin-3-glucoside plus TNF\", \"comparator\": \"TNF alone\", \"endpoint\": \"The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.\", \"effect_direction\": \"decrease\", \"combination\": \"joint\", \"conditions\": [{\"entity_slug\": \"cyanidin-3-glucoside\", \"state\": \"present\"}, {\"entity_slug\": \"tnf\", \"state\": \"present\"}]}","comparator":null,"unit":null,"notes":"Explicit extracted experimental comparison; source-derived draft.","entity":null},{"dimension":"experimental_model","value_text":"Human Caco-2 monolayers; 0.25-1 uM glucosides; NF-kappa-B and MLC signaling studied.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"interpretation_status","value_text":"Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Pathway evidence in cultured intestinal epithelium, not systemic NF-kappa-B suppression.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"The active glucoside reduced TNF-triggered downstream myosin-light-chain phosphorylation in the barrier experiment.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity. | 2017 | DOI 10.1039/c7fo00625j | PMID 28740990 | https://pubmed.ncbi.nlm.nih.gov/28740990/ | https://doi.org/10.1039/c7fo00625j | https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"source_locator","value_text":"Reviewed reference lines 78-78; exact primary location described in quoted passage where extracted.","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"87dfac0e-4f76-52a8-aff3-6e1ff601bc24","evidence_kind":"source_excerpt","locator":"Lines 78-78","start_line":78,"end_line":78,"excerpt":"**Barrier protection is compound-selective.** In TNF-challenged human Caco-2 monolayers, cyanidin and delphinidin O-glucosides at 0.25–1 µM limited the fall in electrical resistance and rise in FITC-dextran permeability. Tested malvidin, peonidin and petunidin glucosides did not provide the same protection. NF-κB activation and downstream myosin-light-chain phosphorylation were reduced by the active compounds. This experiment measured functional permeability, not just more ZO-1 or occludin. It does not establish a clinical treatment for intestinal disease or a universal anthocyanin effect. [Cremonini et al., 2017](https://pubs.rsc.org/en/content/articlehtml/2017/fo/c7fo00625j).","model_system":"Human Caco-2 monolayers; 0.25-1 uM glucosides; NF-kappa-B and MLC signaling studied.","directness":"reported_statement","verification_status":"source_derived_draft","notes":"Exact excerpt of the retained AI-assisted reviewed reference; primary sources are cited in primary_references and access scope is retained. Not a verbatim quotation from a primary paper.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"b08e7f7d-4d34-56d7-a185-2124f8d72b3c","stable_key":"import-35ec55a7-323c-5c28-979e-3bdafe9d5769","title":"Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026)","document_type":"imported_text","citation_label":"Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication.","file_path":"","sha256":"7cff1a47fbd9c625412b84162b1c823004b4162b7c009f9a11d5807fb8e04ef9","revision_id":"1bd4fa42-bfeb-5148-8250-fc363d8c1de0","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}