Therapeutic Implications of Phenolic Acids for Ameliorating Inflammatory Bowel Disease
Abstract
:1. Introduction
2. Chemical Structures and Primary Dietary Sources of Phenolic Acids
3. Effect of Phenolic Acids on Intestinal Mucosal Barrier
4. Effect of Phenolic Acids on Oxidative Stress
5. Effect of Phenolic Acids on Immune System
6. Effect of Phenolic Acids on Gut Microbes
7. Conclusions and Future Perspectives
Author Contributions
Funding
Conflicts of Interest
References
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Phenolic Compounds | Substituent Group | |
---|---|---|
Benzoic acid | Salicylic acid | 2-OH |
3-Hydroxybenzoic acid | 3-OH | |
4-Hydroxybenzoic acid | 4-OH | |
2,3-Dihydroxybenzoic | 2,3-OH | |
Gentisic acid | 2,5-OH | |
Protocatechuic acid | 3,4-OH | |
Gallic acid | 3,4,5-OH | |
Vanillic acid | 4-OH, 3-OCH3 | |
Isovanillic Acid | 3-OH, 4-OCH3 | |
Syringic | 4-OH, 3,5-OCH3 | |
Cinnamic acid | Cinnamic acid | / |
o-Coumaric acid | 2-OH | |
p-Coumaric acid | 4-OH | |
Caffeic acid | 3,4-OH | |
Ferulic Acid | 4-OH, 3-OCH3 | |
Sinapic acid | 4-OH, 3,5-OCH3 | |
Chlorogenic acid | 3,4-OH, 1-Quinic |
Phenolic Acid Compounds | Model | Dose | Effect | Reference |
---|---|---|---|---|
4-Hydroxybenzoic acid | 2.5% DSS treated mice for 7 days | 10–40 mg/kg and 100 mg/kg, orally | reduced inflammatory cytokines; improved mucosal barrier | Xu X [15], Han X [16] |
10 ng/mL TNF-α treated Caco-2 cells | 3, 10 and 30 μM | decreased the expression of proinflammatory cytokines; increased the expression of tight junction proteins | Xu X [15] | |
Protocatechuic Acid | 3.5% DSS treated C57BL/6 mice for 7 days | 5, 10, and 20 mg/kg, orally | reduced inflammatory factors; increased occluding protein expression | Yang X [17] |
20 mg/mL of TNBS-treated BALB/c mice through the catheter | 30 and 60 mg/kg, intraperitoneally | prevented the macroscopic damage and the increase in myeloperoxidase activity; increased expression of antioxidant enzymes; reduced expression of proinflammatory cytokines | Crespo I [18] | |
5% DSS treated rat for 5 days | 10 mg/kg, orally | prevented the increase in proinflammatory cytokines in the plasma; suppressed the DSS-mediated elevation in colonic myeloperoxidase activity | Farombi EO [19] | |
Gallic acid | 2.5% DSS treated BALB/c mice for 7 days | 10 mg/kg, orally | reduced inflammation; improved oxidative stress; upregulated the expression of Nrf2 and its downstream targets | Pandurangan AK [20] |
2.5% DSS treated BALB/c mice for 7 days | 10 mg/kg, orally | reduced the expression of inflammatory mediators; suppressed p65-NF-κB and IL-6/p-STAT3 activation | Pandurangan AK [21] | |
TNBS treated BALB/c mice through the catheter. | 20, 40, 60 mg/kg, orally | reduced inflammation; suppressed NF-κB | Zhu L [22] | |
10 ng/mL IL-1β treated HIEC-6 cells | 20, 40, 60 mg/kg | inhibited apoptosis | Zhu L [22] | |
3.5% DSS treated BALB/c mice for 7 days | 40, 80, 120 mg/kg, orally | reduced inflammation; downregulated the expressions of NLRP3 | Yu T-Y [23] | |
2.5% DSS treated C56B/6L mice for 10 days | 200 mg/kg, orally | trapped deleterious metabolite ammonia; improved gut microbiota dysbiosis | Peng J [24] | |
Vanillic acid | 10 mg/kg LPS-treated weaned piglet | 4000 mg/kg in diet | decreased serum levels of proinflammatory factor; enhanced the expression of tight junction protein; modulated gut microbiota | Hu R [25] |
5% DSS treated BALB/c mice for 7 days | 200 mg/kg, orally | relieved colitis; reduced IL-6 | Kim S-J [26] | |
Syringic Acid | OGD/R-stimulated cell injury in Caco-2 cell | 0.1, 1.0 and 10.0 μM | inhibited intestinal barrier disruption; ameliorated apoptosis; attenuated oxidant stress; suppressed the release of inflammatory cytokines | Xiang S [27] |
3.5% DSS treated BALB/c mice for 7 days | 25 mg/kg, orally | suppressed proinflammatory cytokine; prevented DSS-induced colon damage; reduced the activity of MPO | Fang W [28] | |
2.5% DSS treated C56BL/6 mice for 7 days | 50 mg/kg, orally | regulated oxidative stress; alleviated inflammatory response; relieved proptosis | Luo Q [29] | |
0.8 mL of 7% acetic acid was instilled into the rat colon through the cannula | 10, 25, and 50 mg/kg | decreased the mean macroscopic ulcer score; increased HO-1, Nrf2, and NQO1 mRNA expression; decreased the tissue levels of TNF-α and IL-1β | Ekhtiar M [30] | |
Cinnamic acid | 2.5% DSS treated albino mice for 7 days | 25 and 50 mg/kg, orally | reduced the levels of TNF-α and IL-6 | Habboby M [31] |
0.4 mL 120 mg/mL DNBS was instilled into the rat colon through the cannula | 30 mg/kg, orally | activated GPR109A in the inflamed colon | Kang C [32] | |
Coumaric acid | 0.8 mL 7% acetic acid was rectally injected into rats | 50, 100, and 150 mg/kg, orally | improved oxidative stress; improved the inflammation | Ghasemi-Dehnoo M [33] |
0.8 mL 7% acetic acid was rectally injected into rats | 100 and 150 mg/kg | decreased the mean macroscopic ulcer score; increased HO-1, Nrf2, and NQO1 mRNA expression; decreased the tissue levels of TNF-α and IL-1β | Ekhtiar M [30] | |
Caffeic acid | 3.5% DSS treated C57BL mice t for 7 days | 50 mg/kg, orally | suppressed the production of inflammatory cytokines; interfered with the infiltration and function of mononuclear macrophages | Xiang C [34] |
3.5% DSS treated ICR mice for 7 days | 250 mg/kg, orally | decreased proinflammatory cytokines; increased the level of IL-10; altered the gut microbiome composition | Wan F [35] | |
1 ng/mL IL-1β treated CCD-18Co cells | 10 and 50 μM | reduced the biosynthesis of IL-8 and MCP1, | Zielinska D [36] | |
Ferulic acid | 0.8 mL 7% acetic acid was rectally injected into rats | 20, 40, and 60 mg/kg, orally | inhibited inflammatory, apoptotic, and production of MDA and NO; increased the activity of antioxidant factors | Ghasemi-Dehnoo M [37] |
1% DSS treated C57BL mice t for 16 days | 50 mg/kg, orally | improved histopathologic score and MPO activity | Islam MS [38] | |
100 mg/kg TNBS was rectally injected into rats | 20 and 40 mg/kg, orally | suppression of oxidative stress, apoptosis, production of proinflammatory cytokines, and inhibition of COX-2 synthesis | Sadar SS [39] | |
100 mg/kg TNBS was rectally injected into rats | 10, 20 and 250 mg/kg, orally | inhibited the inflammatory injury of endothelial cells; | Yu S [40] | |
10 ng/mL TNF-α treated HIMECs | 125, 250, 500 μM | reduced the expression of inflammatory factors; improved cell viability | Yu S [40] | |
Sinapic acid | 30 mg/kg TNBS was rectally injected into BABL/c mice | 10, 30, and 100 mg/kg, orally | improved the macroscopic changes of colonic damage; improved the changes in expression of biochemical mediators of inflammation | Lee JY [41] |
20 μg/mL LPS and 20 ng/mL TNF-α treated Caco-2 cells | 12.5, 25 and 50 μM | suppressed impairment of intestinal permeability and cellular reorganization of tight junction proteins | Jang S [42] | |
2% DSS treated C57BL mice for 7 days | 2 and 10 mg/kg, orally | alleviated DSS-induced IBD; modified gut microbiota | Jang S [42] | |
20 μg/mL LPS-treated Caco-2 cells | 5, 10 and 15 μM | reduced the expression of proinflammatory cytokines; improved tight junction mRNA levels | Lan H [43] | |
2 mL 4% acetic acid was rectally injected into rats | 40 mg/kg, orally | suppressed inflammation, oxidative stress, and apoptosis | Shahid M [44] | |
2% DSS treated Kunming mice for 7 days | 10 and 50 mg/kg, orally | attenuated intestinal permeability; reduced inflammatory; attenuated oxidative damage; reduced the activation of the NLRP3 inflammasome | Qian B [45] | |
Chlorogenic acid | 2.5% DSS treated C57BL/6 mice for 8 days | 1 mM, orally | suppressed inflammation; modified gut microbiota; promoted the growth of Akkermansia | Zhang Z [46] |
BALB/c mice intracolonic administration of 4 mg in 0.1 mL of 30% ethanol TNBS | 20 mg/kg, orally | anti-inflammatory; decreased neutrophil infiltration and suppression of NF-κB-dependent pathways. | Zatorski H [47] | |
5% DSS treated C57BL/6 mice for 7 days | 30, 60, and 120 mg/kg, orally | reduced mucosal damage; inhibited colonic mucosal inflammation; improved colitis through MAPK/ERK/JNK signaling pathway | Gao W [48] | |
2 mM H2O2 and 10 ng/mL of TNF-α treated Caco-2 cells | 0.5, 1 and 2 mM | reduced IL-8 secretion | Shin HS [49] | |
3% DSS treated C57BL/6 mice for 8 days | 1 mM, orally | reduced proinflammatory cytokines | Shin HS [49] | |
2.5% DSS treated C57BL/6 mice for 5 days | 2% in diet | decreased the production of proinflammatory cytokines; and restored intestinal microbial diversity. | Zhang P [50] | |
5 mg/kg indomethacin treated C57BL/6 mice for 5 days | 50 mg/kg, orally | prevented inflammation; prevented intestinal barrier dysfunction; decreased Bacteroides-derived LPS | Yan Y [51] | |
IL-10 KO mice | 1 mg/kg, orally | increased the ratio of CD4+/CD8+ T cell subsets; prevented inflammation | Lee YM [52] | |
3% DSS treated BALB/c mice for 7 days | 20 and 40 mg/kg, orally | prevented inflammation | Zeng J [53] | |
0.5 ug/mL LPS and 2 nM ATP induced Raw264.7 cells | 15.63, 31.25, 62.5, 125 and 250 μM | improved the cellular vitality | Zeng J [53] |
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Lu, Y.; Han, X. Therapeutic Implications of Phenolic Acids for Ameliorating Inflammatory Bowel Disease. Nutrients 2024, 16, 1347. https://doi.org/10.3390/nu16091347
Lu Y, Han X. Therapeutic Implications of Phenolic Acids for Ameliorating Inflammatory Bowel Disease. Nutrients. 2024; 16(9):1347. https://doi.org/10.3390/nu16091347
Chicago/Turabian StyleLu, Yanan, and Xue Han. 2024. "Therapeutic Implications of Phenolic Acids for Ameliorating Inflammatory Bowel Disease" Nutrients 16, no. 9: 1347. https://doi.org/10.3390/nu16091347