Effects of dexpanthenol on acetic acid-induced colitis in rats

Çağın, Yasir Furkan; Parlakpınar, Hakan; Vardı, Nigar; Polat, Alaadin; Atayan, Yahya; Erdoğan, Mehmet Ali; Tanbek, Kevser

doi:10.3892/etm.2016.3728

Cited by 53 publications

(21 citation statements)

References 42 publications

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“…There is some evidence for therapeutic potential of B5 in IBD, its supplementation showed anti‐oxidative, anti‐inflammatory and anti‐apoptotic effects leading to decreased tissue damage in a rat model for acute colitis. [ 67 ] Interestingly, dietary‐induced B5 deficiency in pigs induced spontaneous colitis that histologically resembled human UC. [ 68 ] Due to the direct link between B5 and CoA‐related SCFA production, increasing dietary B5 intake may enhance colonic SCFA levels and induce colitis recovery.…”

Section: Vitaminsmentioning

confidence: 99%

Role of Dietary Micronutrients on Gut Microbial Dysbiosis and Modulation in Inflammatory Bowel Disease

Kundra¹,

Rachmühl²,

Lacroix³

et al. 2021

Molecular Nutrition Food Res

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In patients with inflammatory bowel diseases (IBD), dietary micronutrient intake is low and deficiencies are common. Besides the host, also the gut microbiota require micronutrients and low levels may disturb its functioning. Multi‐omics studies indeed detected shifts in micronutrient‐dependent microbial pathways in IBD. It is however not clear whether micronutrients may alleviate inflammation directly, by modulating the immune system, or also indirectly, by modulating the structure and function of the gut microbiota. The latter seems of particular interest, since the gut microbiota is one of the future therapeutic targets in IBD. A review of the most recent available literature on relevant micronutrients in context of IBD and gut microbiota was conducted. An overview per relevant micronutrient on its role on gut bacterial growth, metabolism and host–microbe interactions during gut inflammation is provided. Dietary micronutrients have potential to be part of future personalized microbiome‐targeted therapies in IBD, considering both the micronutrient status of the host and the gut microbiota. However, cohort studies together with integrated multi‐scale studies are needed to understand the mechanisms of micronutrient–microbiome–host interactions in IBD and to evaluate efficacy and safety of dietary micronutrient treatment strategies.

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Section: Vitaminsmentioning

confidence: 99%

Role of Dietary Micronutrients on Gut Microbial Dysbiosis and Modulation in Inflammatory Bowel Disease

Kundra¹,

Rachmühl²,

Lacroix³

et al. 2021

Molecular Nutrition Food Res

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“…Myloperoxidase is a hemoprotein enzyme abdudantly released from the neutrophils granules by inflammatory stimuli that catalyzes the formation of a number of reactive species (40). Studies have indicated that oxidative stress results from the shift of equilibrium between the prooxidant and anti-oxidant systems in favor of the pro-oxidant system which result of excessive production of free oxygen radicals and neutrophil infiltration (41,42). The study has also shown that administration of cinnarizine significantly reduce the expression of immunohistochemistry for markers of oxidative stress (myeloperoxidase and malondialdehyde) in colonic mucosa of experimentally induced colitis in rats.…”

Section: Discussionmentioning

confidence: 99%

Comparative treatment of induced ulcerative colitis in male rat model by using cinnarizine and sulfasalazine

Atarbashe¹,

Abu-Raghif²

2020

IJVS

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Ulcerative colitis is a chronic and intermittent illness. The current treatment failed to cure the disease which requires to investigate other drug with minimal side effects. The goal of the research is to assess the histological outcome, antioxidant and anti-inflammatory effects of cinnarizine in comparison with that of sulfasalazine (salazosulfapyridine) in experimentally induced colitis in rats. Acetic acid 4% (vol/vol) was used rectally to induce experimental colitis in rats. After induction, rats were administered either sulfasalazine 100mg/kg or cinnarizine 20 mg/kg as a therapeutic dose in rats orally for one week. The duration of treatment was depended on previous studies. There were estimation of histopathological and clinical parameters also the expression of cytokines (tumor necrosis factor alpha (TNF-α) and interleukin-4 (IL-4)), oxidative stress markers (malondialdehyde (MDA) and myeloperoxidase (MPO)), and adhesion molecules (intercellular adhesion molecule-1 (ICAM-1) and endothelial (E)-Selectin) in the colonic tissue. Results showed that both cinnarizine and sulfasalazine significantly reduced the clinical and histological injury in colon that induced by acetic acid. In addition to the down regulation of the increased colonic cytokines, MDA, MPO parameters and adhesive molecules. These results concluded that cinnarizine had an effective therapeutic role which is comparable with sulfasalazine on the experimental colitis through anti-inflammatory and antioxidant actions with down regulation the colonic adhesion molecule.

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“…The slides were then washed with cold PBS and incubated with anti-rabbit secondary antibody (KeyGen). The histological examination was performed following the standard procedures described previously ( 19 ).…”

Section: Methodsmentioning

confidence: 99%

Fisetin inhibits liver cancer growth in a mouse model: Relation to dopamine receptor

et al. 2017

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Fisetin (3,3′,4′,7-tetrahydroxyflavone), a natural abundant flavonoid, is produced in different vegetables and fruits. Fisetin has been reported to relate to various positive biological effects, including anti-proliferative, anticancer, anti-oxidative and neuroprotective effects. Dopamine receptors (DRs) belonging to G protein-coupled receptor family, are known as the target of ~50% of all modern medicinal drugs. DRs consist of various proteins, functioning as transduction of intracellular signals for extracellular stimuli. We found that fisetin performed as DR2 agonist to suppress liver cancer cells proliferation, migration and invasion. Caspase-3 signaling was activated to induce apoptosis for fisetin administration. Furthermore, TGF-β1 was also inhibited in fisetin-treated liver cancer cells, reducing epithelial-mesenchymal transition (EMT). Additionally, fisetin downregulated VEGFR1, p-ERK1/2, p38 and pJNK, ameliorating liver cancer progression. In vivo, the orthotopically implanted tumors from mice were inhibited by fisetin adminisatration accompanied by prolonged survival rate and higher levels of dopamine. Together, the results indicated a novel therapeutic strategy to suppress liver cancer progression associated with DR2 regulation, indicating that dopamine might be of importance in liver cancer progression.

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Effects of dexpanthenol on acetic acid-induced colitis in rats

Cited by 53 publications

References 42 publications

Role of Dietary Micronutrients on Gut Microbial Dysbiosis and Modulation in Inflammatory Bowel Disease

Role of Dietary Micronutrients on Gut Microbial Dysbiosis and Modulation in Inflammatory Bowel Disease

Comparative treatment of induced ulcerative colitis in male rat model by using cinnarizine and sulfasalazine

Fisetin inhibits liver cancer growth in a mouse model: Relation to dopamine receptor

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