Sulfasalazine attenuates ulcerative colitis in rats via downregulation of mirna-31, metalloproteinase-3 and high mobility group box1
By: Boshra, Sylvia A
.
Publisher: M P Innovare Academic Sciences Pvt Ltd 2021Edition: Vol.13(10).Description: 74-80p.Subject(s): PHARMACEUTICSOnline resources: Click here
In:
International journal of pharmacy and pharmaceutical scienceSummary: Objective: This study targets the inhibition of inflammatory mediators and the enhancement of gastrointestinal mucosa healing in ulcerative colitis in rats through sulfasalazine.
Methods: Twenty four female albino rats were divided into 3 groups: normal control, colitis group (rats received 5% dextran sodium sulfate (DSS) in their drinking water for 7 d), sulfasalazine group (500 mg/kg/day was administrated orally one week ahead of DSS and parallel with its administration). The impact of sulfasalazine on intestinal inflammation was investigated via estimation of some inflammatory mediators, namely; serum Leucine rich α 2 Glycoprotein (LRG) as well as colon cAMP, Myloperoxidase (MPO) and TNF-α using ELISA technique as well as gene expression of Trefoil Factor 3 (TFF3), High mobility group box1 (HMGB1), Nuclear factor kappa B (NF-κB) and metalloproteinase-3 (MMP3) and miRNA-31 levels using RT-PCR.
Results: Sulfasalazine substantially decreases the release of LRG, MPO and TNF-α and the expression of HMGB1, NF-κB, MMP3, TFF3 and miRNA31 at p≤ 0.05 compared to colitis group in vivo. Moreover, Sulfasalazine significantly increases the colonic cAMP at p≤ 0.05 in groups of rats treated with DSS.
Conclusion: Sulfasalazine has a protective effect on inflammatory bowel disease causing mucosal healing within the gastrointestinal tract. Additional studies are warranted to explore the molecular mechanism of sulfasalazine in ulcerative colitis and its clinical application.
| Item type | Current location | Call number | Status | Date due | Barcode | Item holds |
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Articles Abstract Database
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School of Pharmacy Archieval Section | Not for loan | 2022-0416 |
Objective: This study targets the inhibition of inflammatory mediators and the enhancement of gastrointestinal mucosa healing in ulcerative colitis in rats through sulfasalazine.
Methods: Twenty four female albino rats were divided into 3 groups: normal control, colitis group (rats received 5% dextran sodium sulfate (DSS) in their drinking water for 7 d), sulfasalazine group (500 mg/kg/day was administrated orally one week ahead of DSS and parallel with its administration). The impact of sulfasalazine on intestinal inflammation was investigated via estimation of some inflammatory mediators, namely; serum Leucine rich α 2 Glycoprotein (LRG) as well as colon cAMP, Myloperoxidase (MPO) and TNF-α using ELISA technique as well as gene expression of Trefoil Factor 3 (TFF3), High mobility group box1 (HMGB1), Nuclear factor kappa B (NF-κB) and metalloproteinase-3 (MMP3) and miRNA-31 levels using RT-PCR.
Results: Sulfasalazine substantially decreases the release of LRG, MPO and TNF-α and the expression of HMGB1, NF-κB, MMP3, TFF3 and miRNA31 at p≤ 0.05 compared to colitis group in vivo. Moreover, Sulfasalazine significantly increases the colonic cAMP at p≤ 0.05 in groups of rats treated with DSS.
Conclusion: Sulfasalazine has a protective effect on inflammatory bowel disease causing mucosal healing within the gastrointestinal tract. Additional studies are warranted to explore the molecular mechanism of sulfasalazine in ulcerative colitis and its clinical application.
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