In the published article, there was an error in the legend for
Table 1 Dietary phytochemicals and their restorative effects on mitochondrial function and lipid homeostasis as published. ↓ increase; ↑ decrease (on table footnotes). The corrected legend appears below.
Table 1.
Dietary phytochemicals and their restorative effects on mitochondrial function and lipid homeostasis.
| Phytochemical (Source) | Outcome | Proposed pathway | Model | Reference |
|---|---|---|---|---|
| Resveratrol (Grape, wine, peanut, and cranberry) | Anti-inflammatory protection and oxidative stress inhibition against intestinal inflammation. Anti-inflammatory effects. Protective effects against the alterations of mitochondrial function and oxidative stress. ↓Disease activity and ↑Quality of life in UC patients at least partially through the ↓Oxidative stress. Anti-atherosclerotic effects: ↓FA and MAG intestinal accumulation. Restoration of succinate and lactic acid levels. |
Nrf2 activation: ↑Oxygenase-1 (HO-1) mRNA, ↓ROS production, and ↑PPAR-γ accumulation. ↑Nrf2, ↓IL-1β, and ↑IL-11. ↑Intracellular ATP, protective effects against ↓Δψm induced by INDO. - Abolishes oleate-triggered lipid, total cholesterol, and esterified cholesterol accumulation by activating PPAR-α and PPAR-γ signaling. |
cytokine-stimulated (IL-1α, TNF-α, IFN-γ) HT-29 cells In vitro UC model in Caco-2 cells challenged with TNF-α. Intestinal epithelial Caco-2 cells induced by indomethacin (INDO). Prospective, randomized, double-blind, placebo-controlled study in UC patients. Supplements (containing 500 mg trans-resveratrol) or placebo capsules. ApoE null mice fed with a high-fat diet (HFD) (AS) and resveratrol intervention. RAW 264.7 mice Mø treated with oleate and resveratrol. |
(147) (148) (149) (150) (151) |
| Quercetin (onion, apple grape, and citrus fruits) | Protective effects against the alterations of mitochondrial function and oxidative stress. Mitochondrial protective effects against and maintenance of gastrointestinal mucosal renewing regulating apoptosis. ↓NLRP3 inflammasome activation and ↓Mitochondrial damage. Intestinal anti-inflammatory effects via Nrf2/HO-1 |
↑Intracellular ATP, protective effects against ↓Δψm induced by INDO, and inhibition of the inhibitory effects of INDO and rotenone on complex I. Prevents Ca2+ mobilization induced by INDO and its consequences, including ↑Caspase-3 and caspase-9 activation and cytochrome C release. ↓Activity of caspase-1 and ↓Secretion of IL-1β and ↓IL-18 via NLRP3 inflammasome. Improvement in Δψm, blocking cytochrome C release, ↓O2 consumption, ↓ mtDNA cytosolic content, and ↓ ROS level. ↓TNF-α, IFN-γ, and IL-6. Nuclear Nrf2 accumulation ↑ HO-1 expression in colonic Mø. |
Intestinal epithelial Caco-2 cells induced by INDO. Intestinal epithelial Caco-2 cells induced by INDO. Caco-2 cells infected by Escherichia coli O157:H7 T cell-dependent colitis model induced by the adoptive transfer of naive T cells into Rag1 null mice and DSS-induced colitis mice model. |
(149) (152) (153) (154) |
| Sulforaphane (cruciferous vegetables) |
Antioxidant and anti-inflammatory effects, ↑ Mitochondrial bioenergetic function upon cholesterol-induced pancreatic β-cell dysfunction. ↓Intestinal permeability upon LPS, ↓Oxidative stress, ↓Inflammation, and ↓apoptosis. |
Improving ATP turnover, spare capacity, and impairment of the electron flow at complexes I, II, and IV. ↓NFκB pathway. ↑SIRT1 and ↑PGC-1α expression. ↑ Antioxidant enzymes of the Nrf2 pathway and ↓Lipid peroxidation induced by cholesterol. Activating the AMPK/SIRT1/PGC-1 pathway. |
Min6 cells, a β-cell line exposed to high concentration of cholesterol. LPS-induced Caco-2 in vitro model. |
(155) (156) |
| Dried apple peel polyphenols (DAPP) | ↓DSS-induced damage, ↓Pro-inflammatory factors, ↓Oxidative markers, and ↓ROS. ↓Mitochondria-dependent cell death, ↑β-oxidation, ↑Mitochondrial bioenergetics, and ↓Alteration in mitochondrial morphology. | ↓TNF-α, COX-2, and iNOS. | In vivo model of DSS-induced colitis in male C57BL6 mice. | (157>) |
| Strawberry Ellagitannin-Rich Extract (S-ET) | ↓ HFD effects in rats, ↓Body weight, ↓Relative mass of the epididymal pad, ↓Hepatic fat, ↓Oxidized glutathione, ↓TG, ↓Total cholesterol, and ↓Thiobarbituric acid-reactive substances concentrations and improve blood plasma parameters. | ↓H2O2 and SOD2 protein expression and ↑8-oxoguanine DNA glycosylase 1 (OGG1) expression. ↑CPT-1 and ACADL, ATP production, and PGC-1α. ↓NF-kB and AP-1. | HFD supplemented with S-ET) in Male Wistar rats. In vivo model | (158) |
| Luteolin (carrot, pepper, celery, spinach, and parsley) | Antioxidants and anti-inflammatory effects. Anti-inflammatory effects. ↓Lipid accumulation. Reparative effects of intestinal barrier injury. |
↑ Nrf2 and ↓iNOS, IL-6, and TNF-α expression. ↓NLRP3 expression via disruption of IL-17A signaling. ↓LXR-dependent SREBP-1c expression and intracellular lipid levels. ↓LXR-induced ABCA1 expression in Mø. ↓MAPK/NF-κB/MLCK t activating indirectly Nrf2 signaling pathways. |
DSS-induced UC C57BL/6 mouse model. DSS-induced colitis C57BL/6 mice model. HepG2 cells and RAW264.7 Mø stimulated LXRα/β agonist (T0901317). Ethanol-induced intestinal barrier damage in a Caco-2 cell monolayer model. |
(159) (160) (161) (162) |
| Sesamin (Sesamum indicum seeds) | Anti-atherosclerotic effects: ↓oxLDL-elicited lipid accumulation and ↑ HDL-mediated cholesterol efflux. Antioxidants and anti-inflammatory effects. ↓Cholesterol absorption by enterocytes. ↓ Hepatic lipogenic genes expression. Antagonist ligand of LXRα. |
↑ PPARγ-dependent ABCG1 mRNA levels. Cytoprotective effect via Glutathione-S-transferase (GSH)-mediated ROS scavenger. Nrf2/ARE signaling activation dependent on ERK and AKT activation. ↑LXR-induced ABCA1/G1 expression. |
RAW264.7 Mø stimulated with oxLDL and sesamin. Caco-2 cells stimulated by H2O2 LS174T colonic epithelial cells with LXRα agonist (T090) treatment. |
(163) (164) (165) |
[↑ increase; ↓ decrease]
[↑ increase; ↓ decrease]
In the published article, there was an error in the Funding statement. This work was funded by the Agencia Nacional de Investigación y Desarrollo (ANID)/PhD fellowship #21220889 (JA), and #21200669 (NG), FONDECYT Grants #1120702 (MAH), #11201322 (FAU), MiBi: interdisciplinary group on mitochondrial targeting and bioenergetics ACT 210097 (FAU); FONDECYT postdoctoral grant #3210367 (KD-C). The correct Funding statement appears below.
FUNDING
This work was funded by the Agencia Nacional de Investigación y Desarrollo (ANID)/PhD fellowship #21220889 (JA), and #21200669 (NG), FONDECYT Grants #1220702 (MAH), #11201322 (FAU), MiBi: interdisciplinary group on mitochondrial targeting and bioenergetics ACT 210097 (FAU); FONDECYT postdoctoral grant #3210367 (KD-C).
The authors apologize for these errors and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
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