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

Abstract

Background: 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. Aims: 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. Methodology: 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. Results: 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, PGE2, 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. Conclusion: 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.

Sinapic acid alleviates 5-fluorouracil-induced nephrotoxicity in rats via Nrf2/HO-1 signalling

“…Sinapic acid (SA, 3,5-dimethoxy-4-hydroxycinnamic acid) is an orally bioavailable phytochemical with antioxidative, anticancer, antimutagenic, anti-inflammatory, neuroprotective, anti-glycaemic, and antibacterial properties ( Chen, 2016 , Nićiforović and Abramovič, 2014a ). Through a variety of mechanisms, such as activating and safeguarding intracellular antioxidant enzymes or interacting with ROS, SA exerts a chemoprotective effect by inhibiting the pathways of oxidative stress, apoptosis, and NF-κB, and activating the Nrf2/HO-1 pathway( Altindag and Ozdek, n.d. , Ansari et al, 2021 , Huang et al, 2018 ; Nićiforović and Abramovič, 2014b; Raish et al, 2018 , Rezaei et al, 2021 , Shahid et al, 2022 , Verma et al, 2020 , Yun and Yang, 2020 , Zhao et al, 2021 ).…”

Sishen Pill Ameliorates Dextran Sulfate Sodium (DSS)-Induced Colitis with Spleen-Kidney Yang Deficiency Syndromes: Role of Gut Microbiota, Fecal Metabolites, Inflammatory Dendritic Cells, and TLR4/NF-κB Pathway

“…KEGG enrichment analysis of 13 common differential metabolites further demonstrates that the sphingolipid signaling pathway, sphingolipid metabolism, and phenylpropanoid biosynthesis were significantly enriched. Some studies have confirmed that sinapic acid significantly ameliorates acetic acid-induced UC in rats by suppressing cytokines TNF- α and IL-6 in colonic tissues [ 51 ]. Sphingolipids have an indispensable role in intestinal inflammation [ 52 – 54 ], including ceramide, ceramide 1-phosphate, sphingomyelin, and sphingosine 1-phosphate.…”

Identification of Doxorubicin as Repurposing Inhibitory Drug for MERS-CoV PLpro

“…Western blotting was performed for monoclonal-His antibody to confirm the presence of N-terminal 6xHis-Tag, as described previously [ 38 , 39 ]. Whole cell protein (10 μL) isolated by sonication was mixed with 2X Laemmli dye and electrophoresed on 10% SDS−polyacrylamide gel, after which it was transferred onto nitrocellulose membranes using a transblot turbo machine (BioRad), then blocked in Every Blot Blocking Buffer at room temperature for 10 min (BioRad).…”