Hesperidin modulates dextran sulfate sodium‐induced ulcerative colitis in rats: Targeting sphingosine kinase‐1‐ sphingosine 1 phosphate signaling pathway, mitochondrial biogenesis, inflammation, and apoptosis

Shafik, Noha M.; Gaber, Rasha A.; Mohamed, Dareen Abd El-Aziz; Ebeid, Abla M.

doi:10.1002/jbt.22312

Cited by 14 publications

(9 citation statements)

References 33 publications

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“…The antioxidants SOD and NQO-1 directly eliminate free superoxide radicals to protect against lipid peroxidation [50,51]. Previous reports of acute gut inflammation in the DSS model observed a significant increase in lipid peroxidation and reduced levels of antioxidant enzymes (NQO-1 and SOD) [18,19,[52][53][54][55][56], which were replicated in the present study. We also observed a significant reduction in MDA levels after treatment with idebenone, which is consistent with a previous report where idebenone effectively suppressed lipid peroxidation in brain mitochondria [57].…”

Section: Discussionsupporting

confidence: 87%

Idebenone Protects against Acute Murine Colitis via Antioxidant and Anti-Inflammatory Mechanisms

Shastri

Shinde

Sohal

et al. 2020

IJMS

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Oxidative stress is a key player of the inflammatory cascade responsible for the initiation of ulcerative colitis (UC). Although the short chain quinone idebenone is considered a potent antioxidant and a mitochondrial electron donor, emerging evidence suggests that idebenone also displays anti-inflammatory activity. This study evaluated the impact of idebenone in the widely used dextran sodium sulphate (DSS)-induced mouse model of acute colitis. Acute colitis was induced in C57BL/6J mice via continuous exposure to 2.5% DSS over 7 days. Idebenone was co-administered orally at a dose of 200 mg/kg body weight. Idebenone significantly prevented body weight loss and improved the disease activity index (DAI), colon length, and histopathological score. Consistent with its reported antioxidant function, idebenone significantly reduced the colonic levels of malondialdehyde (MDA) and nitric oxide (NO), and increased the expression of the redox factor NAD(P)H (nicotinamide adenine dinucleotide phosphate) dehydrogenase quinone-1 (NQO-1) in DSS-exposed mice. Immunohistochemistry revealed a significantly increased expression of tight junction proteins, which protect and maintain paracellular intestinal permeability. In support of an anti-inflammatory activity, idebenone significantly attenuated the elevated levels of pro-inflammatory cytokines in colon tissue. These results suggest that idebenone could represent a promising therapeutic strategy to interfere with disease pathology in UC by simultaneously inducing antioxidative and anti-inflammatory pathways.

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Section: Discussionsupporting

confidence: 87%

Idebenone Protects against Acute Murine Colitis via Antioxidant and Anti-Inflammatory Mechanisms

Shastri

Shinde

Sohal

et al. 2020

IJMS

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“…Studies revealed that apoptosis is a marker of active UC. [ 40,41 ] TUNEL assay showed more TUNEL‐positive cells in the DSS + DB group of male animals as compared to female animals. NLR family pyrin domain‐containing 3 (NLRP3) inflammasome, found in the intestinal epithelial cells and its downstream effector proteins, caspase‐1 and IL‐1β are responsible for intestinal inflammation.…”

Section: Discussionmentioning

confidence: 97%

Association of Type 1 diabetes with ulcerative colitis in BALB/c mice: Investigations on sex‐specific differences

Singla

Sahu

Jena

2021

J Biochem & Molecular Tox

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Diabetes comorbidity in ulcerative colitis (UC) has relevant clinical and therapeutic implications. The link between hyperglycemia and intestinal barrier function with respect to infection and inflammation consequences exists in diabetes. The present study was designed to decipher the molecular mechanisms associated with Type 1 Diabetes mellitus and the UC in both male and female BALB/c mice. Dextran sulfate sodium (DSS; 2.5%w/v) dissolved in drinking water was given for three cycles (each cycle; 7 days) with 7 days recovery period in‐between to both male and female BALB/c mice. At the first recovery period, Streptozotocin (40 mg/kg; i.p.) was administered for 5 consecutive days in the case of male BALB/c mice; whereas the same procedure was repeated at the beginning of each recovery period in female animals. In the DSS + DB group of male animals, disease activity index, myeloperoxidase activity, nitrite level, plasma lipopolysaccharides, interleukin‐1β, histological score, % fibrotic area, % TUNEL positive cells were significantly increased. Furthermore, protein expression of phosphorylated nuclear factor kappa light chain enhancer of activated B cells (pNFκB65), proliferating cell nuclear antigen, interleukin‐6, apoptosis‐associated speck‐like protein containing a caspase‐recruitment domain, and cysteine‐containing aspartate‐specific proteases‐1 (caspase‐1) significantly increased in the DSS + DB group of male animals as compared to female. The present study findings proved that hyperglycemic conditions exacerbated the pathological conditions in UC of male animals; whereas milder conditions developed in females.

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“…Mitochondria are intracellular double-membrane-bound organelles that play a key role in inflammatory diseases such as rheumatoid arthritis and UC [37,38]. The maintenance of mitochondrial function might counteract the inflammation, oxidative stress, and epithelial barrier damage in colitis [39,40].…”

Section: Discussionmentioning

confidence: 99%

Atractylenolide III Improves Mitochondrial Function and Protects Against Ulcerative Colitis by Activating AMPK/SIRT1/PGC-1α

Han

Shi

et al. 2022

Mediators of Inflammation

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Ulcerative colitis (UC) is a complex inflammatory bowel disease (IBD) associated with mitochondrial function. Atractylenolide III (AT III) is a natural product with anti-inflammatory effects. The aim of this work is to investigate the protective effect of AT III on UC and its underlying mechanisms. Herein, dextran sulfate sodium- (DSS-) induced mice and lipopolysaccharide- (LPS-) stimulated intestinal epithelial cells (IEC-6) were employed to mimic UC pathologies in vivo and in vitro. The results showed that in DSS-induced mice, AT III significantly reversed the body weight loss, colon length reduction, disease activity index (DAI) increase, and histological damage. The production of proinflammatory factors and reduction of antioxidants in colitis were suppressed by AT III. In addition, we demonstrated that AT III attenuated the intestinal epithelial barrier destruction and mitochondrial dysfunction induced by DSS, which was similar to the in vitro results in LPS-treated IEC-6 cells. The protein levels of p-AMPK, SIRT1, and PGC-1α along with acetylated PGC-1α were also upregulated by AT III in vivo and in vitro. In conclusion, these findings support that AT III may protect against mitochondrial dysfunction by the activation of the AMPK/SIRT1/PGC-1α signaling pathway during UC development.

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Hesperidin modulates dextran sulfate sodium‐induced ulcerative colitis in rats: Targeting sphingosine kinase‐1‐ sphingosine 1 phosphate signaling pathway, mitochondrial biogenesis, inflammation, and apoptosis

Cited by 14 publications

References 33 publications

Idebenone Protects against Acute Murine Colitis via Antioxidant and Anti-Inflammatory Mechanisms

Idebenone Protects against Acute Murine Colitis via Antioxidant and Anti-Inflammatory Mechanisms

Association of Type 1 diabetes with ulcerative colitis in BALB/c mice: Investigations on sex‐specific differences

Atractylenolide III Improves Mitochondrial Function and Protects Against Ulcerative Colitis by Activating AMPK/SIRT1/PGC-1α

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