{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kang C"],"funding":["National Research Foundation of Korea"],"pagination":["41"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9865397"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["We designed colon-targeted trans-cinnamic acid (tCA) and synthesized its conjugates with glutamic acid (tCA-GA) and aspartic acid (tCA-AA). We evaluated the anti-colitic activity of colon-targeted tCA using a dinitrobenzenesulfonic acid-induced rat colitis model. The conjugates lowered the distribution coefficient and Caco-2 cell permeability of tCA and converted to tCA in the cecum, with higher rates and percentages with tCA-GA than with tCA-AA. Following oral gavage, tCA-GA delivered a higher amount of tCA to the cecum and exhibited better anti-colitic effects than tCA and sulfasalazine (SSZ), which is the current treatment for inflammatory bowel disease. In the cellular assay, tCA acted as a full agonist of GPR109A (EC50: 530 µM). The anti-colitic effects of tCA-GA were significantly compromised by the co-administration of the GPR109A antagonist, mepenzolate. Collectively, colon-targeted tCA potentiated the anti-colitic activity of tCA by effectively activating GPR109A in the inflamed colon, enabling tCA to elicit therapeutic superiority over SSZ."],"journal":["Pharmaceutics"],"pubmed_title":["Colon-Targeted Trans-Cinnamic Acid Ameliorates Rat Colitis by Activating GPR109A."],"pmcid":["PMC9865397"],"funding_grant_id":["2021R1I1A3A0403710411"],"pubmed_authors":["Cho H","Yoon IS","Kang C","Kim HY","Jung Y","Yoo JW","Kim J","Ju S"],"additional_accession":[]},"is_claimable":false,"name":"Colon-Targeted Trans-Cinnamic Acid Ameliorates Rat Colitis by Activating GPR109A.","description":"We designed colon-targeted trans-cinnamic acid (tCA) and synthesized its conjugates with glutamic acid (tCA-GA) and aspartic acid (tCA-AA). We evaluated the anti-colitic activity of colon-targeted tCA using a dinitrobenzenesulfonic acid-induced rat colitis model. The conjugates lowered the distribution coefficient and Caco-2 cell permeability of tCA and converted to tCA in the cecum, with higher rates and percentages with tCA-GA than with tCA-AA. Following oral gavage, tCA-GA delivered a higher amount of tCA to the cecum and exhibited better anti-colitic effects than tCA and sulfasalazine (SSZ), which is the current treatment for inflammatory bowel disease. In the cellular assay, tCA acted as a full agonist of GPR109A (EC50: 530 µM). The anti-colitic effects of tCA-GA were significantly compromised by the co-administration of the GPR109A antagonist, mepenzolate. Collectively, colon-targeted tCA potentiated the anti-colitic activity of tCA by effectively activating GPR109A in the inflamed colon, enabling tCA to elicit therapeutic superiority over SSZ.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2025-04-22T01:05:33.536Z","creation":"2025-04-05T19:51:43.135Z"},"accession":"S-EPMC9865397","cross_references":{"pubmed":["36678670"],"doi":["10.3390/pharmaceutics15010041"]}}