Table 1.
The protective effects of C3G against IBD.
| Year; Author | Study Type | Subjects (Animal/Cell Models/Individuals) | Dose | IBD Indicators | Related Molecular Mechanisms in Regulation of IBD |
|---|---|---|---|---|---|
| [125] | In vitro | CM stimulated T84 cells | 25, 50, 100 μM for 4 h | NA | ↓ IP-10 (CXCL10) |
| [115] | In vitro | Cytokine stimulated HT-29 cells | 12.5 to 50 μM for 24 h | NA | ↓ NO,↓ PGE2, ↓ IL-8, ↓ iNOS ↓ COX-2↓ STAT1 |
| [116] | In vitro | Cytokine stimulated HT-29 cells | 25 μM, for 1 h | ↑ Nrf2 pathway, ↑ HO-1,↑ GCLC and GCLM ↑ GSH/GSSG |
↓ Reactive species |
| [114] | In vitro | Caco-2 cells + TNF-α | 20–40 μM for24 h | ↑ Nrf2 pathway, ↑ GSH ↑ HO-1 and NQO-1 mRNA Levels |
↓ TNF-α, ↓ IKKα/β phosphorylation/activation and IκBα, ↓ NF-κB pathway ↓ Il-6 induced by TNF-α, COX-2, PGE2 and TXB2 |
| [118] | In vitro | Caco-2 cells | 0.25, 0.5 and 1 μM for 24 h | ↑ FITC-dextran permeability | ↓ IKKα, ↓ p65 phosphorylation, ↓ MLC, ↓ TNFα, ↓ NF-kB pathway, ↓ TEER |
| [121] | In vitro | Caco-2-HUVECs | 20 or 40 μM for 24 h | NA | ↓ NF-κB pathway, ↓ TNF-α, ↓ IL-8 ↓ endothelial cells activation: ↓ E-selectin, ↓ VCAM-1 mRNA, ↓ leukocyte adhesion |
| [39] | In vivo and in vitro | BALB/c TNBS-induced colitic mice Caco-2 cell monolayer model +LPS |
200 μL for 12 h before TNBS injection 24.2–96.8 g/kgBW daily for 3 days |
NA | ↓ MPO, ↓ TEER, ↓ LY flux values. ↓ NO, ↓ TNF-α, ↓ IL-1b, ↓ IL-6, ↓ IFN-γ ↓ histological damage |
| [117] | In vitro | (Cell culture: RAW 264.7 cells+ IFNα+ IFNβ, 24 h) Naïve mouse peritoneal macrophages, lymphocytes removed + 1 ug/mL LPS, 24 h |
1 ug/mL for 24 h | NA | Direct inhibition of CD80 and CD86 Inhibition of CD169 Expression induced by Type I IFN ↓ IL-1β, IL-18, IL-6, IL-17, and TNF-α |
| [36] | In vitro | Caco-2 cells + 100 μM PA (basolateral side) |
10 or 20 μM for 24 h | ↑ Nrf2/EpRE pathway ↑ NQO-1 |
↓ NF-κB pathway ↓ IL-6 and IL-8 mRNA levels ↓ COX-2 ↓ ROS |
| [113] | In vitro | Caco-2 cells+ LPS ± HPP | C3G-BP complexes (100–100 μg/mL) | ↑ IL-10 | ↓ depolarization of mitochondria, ↓ ROS ↓ IL-1β, TNF-α, and IL-8 ↓ iNOS, COX-2, Bcl-2 and cleaved caspase-3 levels Inhibition of apoptosis |
| [119] | In vitro | Caco-2 cells +TNF- α | 0.18, 0.37, 0.75, 1.5 μg C3G eq./mL for 24 h (ACN-rich purified and standardized bilberry and blackcurrant extract (BBE)) |
Activation of Nrf2/ Keap1 pathway | Inhibition of NF-κB pathway activated by TNF-α ↓ IL-8 and ↓ IL-6 mRNA levels |
| [124] | In vivo | DSS-induced colitic UC mice + HHP treatment | HPP 200 mg/kg C3G+ blueberry pectin complex (Oral administration) | ↑ protein levels of the ratio Bcl-2/Bax and caspase-3/cleaved caspase-3 genes ↑ Bacteroidetes, Verrucomicrobia Candidatus Saccharibacteria. |
↓ mRNA expression of pro-inflammatory factors ↓ NF-κB P65, ↓ NF-κB pathway ↓ Firmicutes, Proteobacteria, ↓ Firmicutes to Bacteroidetes (F/B) ratio |
| [126] | Cohort study | 47 IBD patients Administration of a purple corn supplement to IBD patients receiving infliximab |
Purple corn supplement composed by 2 mg GAE/g DW (gallic acid equivalents per g of dry weight) and total anthocyanin content of 0.5 mg cyanidin 3-glucoside (C3G) |
NA |
CD group only, not UC: ↓ CRP, ↓ IFN-γ ↓ TNF-α, IL-5, IL-9, IL-10, IL-12p70, and IL-17A |
PA: palmitic acid, HHP: high hydrostatic pressure treatment, BP: blueberry pectin, HUVECs: human umbilical vein endothelial cells, TEER: transepithelial electrical resistance, LY flux: Lucifer yellow flux, TNF-α: tumor necrosis factor-a, IL-6: interleukin-6, IL1b: interleukin-1b, IFN-γ: interferon-γ, PGE2: prostaglandin E2, iNOS: nitric oxide synthase, COX-2: cyclooxygenase-2, HO-1: hemoxygenase-1, MLC: phosphorylation of myosin light chain. GCLM: glutamate cysteine ligase mRNA; ↑, increase; ↓, decrease.