Sinapic Acid Ameliorates Acetic Acid-Induced Ulcerative Colitis in Rats by Suppressing Inflammation, Oxidative Stress, and Apoptosis

• Published in: Molecules (Basel, Switzerland) Switzerland), 2022-06, Vol.27 (13), p.4139
• Main Authors: Shahid, Mudassar, Raish, Mohammad, Ahmad, Ajaz, Bin Jardan, Yousef A, Ansari, Mushtaq Ahmad, Ahad, Abdul, Alkharfy, Khalid M, Alaofi, Ahmed L, Al-Jenoobi, Fahad I
• Format: Article
• Language: English
• Subjects: Acetic acid; Acetic Acid - metabolism; Acids; Animals; Antibodies; Antioxidants; Apoptosis; BAX protein; Bcl-2 protein; bcl-2-Associated X Protein - metabolism; Caspase 3 - metabolism; Caspase-3; Catalase; Colitis, Ulcerative - chemically induced; Colitis, Ulcerative - drug therapy; Colitis, Ulcerative - metabolism; Colon; Colon - metabolism; Coumaric Acids; Cytokines; Diarrhea; Disease; Gene expression; Inflammation; Inflammation - metabolism; Inflammatory bowel disease; Inflammatory bowel diseases; inflammatory markers; Inspection; Interleukin 6; Laboratory animals; Markers; NF-κB protein; Nitric oxide; Oxidants; Oxidative Stress; Oxidizing agents; Pain; Polyphenols; Prednisolone; Prostaglandin E2; Proteins; Proto-Oncogene Proteins c-bcl-2 - metabolism; Rats; Rectum; Sinapic acid; Statistical analysis; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Ulcerative colitis; Ulcers; Variance analysis
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules27134139

: Ulcerative colitis (UC) is a long-term condition which results in inflammation and ulcers of the colon and rectum. The key indications of active disease are abdominal pain and diarrhea mixed with blood. : We explore the underlying colon protective mechanism of sinapic acid (SA) against acetic acid (AA) induced ulcerative colitis in rats. The implications of inflammation, oxidative stress, and apoptosis are studied. : Twenty-four rats were distributed into four categories, normal control (NC), ulcerative colitis (UC), ulcerative Colitis with SA 40 mg/kg (SA 40 mg/kg + AA), and ulcerative colitis with prednisolone (PRDL 10 mg/kg + AA), and were pretreated orally with saline, saline and SA (40 mg/kg/day) or PRDL (10 mg/kg/day) respectively, for 7 days. UC was prompted by trans-rectal administration of 4% AA on the 5th day, colon tissues were surgically removed for gross morphology and histological inspection, oxidative stress, and inflammatory markers and immunoblot analysis of Bax, caspase-3, and Bcl-2. : Macroscopic and histological inspection demonstrated that both SA 40 mg/kg and PRDL (10 mg/kg/day) significantly ameliorates colonic injuries. In addition, both pretreatments significantly ameliorates AA-induced UC, oxidative stress, as indicated by suppressed malondialdehyde (MDA), nitric oxide (NO) levels and restoring antioxidant/oxidant balance as indicated by catalase and glutathione levels, suppressed inflammation via inhibiting cytokines TNF-α, IL-6, inflammatory markers MPO, PGE , COX-2 and NF-κB and inhibiting the protein expression of Bax and caspase-3 apoptotic protein and increasing the anti-apoptotic protein, Bcl-2 thereby inhibiting apoptosis. : Sinapic acid significantly ameliorates AA induced UC in rats by suppressing inflammation, oxidative stress, and apoptosis in colonic tissues which exhibits its potential for the management of UC.