dieckol and Disease-Models--Animal

Topics: Administration, Oral; Animals; Anti-Inflammatory Agents; Aquatic Organisms; Benzofurans; Diet, High-Fat; Disease Models, Animal; Energy Intake; Liver; Lymphatic Vessels; Male; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease; Phaeophyceae; Plant Extracts

Ulcerative colitis (UC) is the major type of inflammatory ailment with elevated prevalence worldwide. Dieckol (DEK) is a phlorotannin that is extensively found in marine algae and has been found to have different pharmacological properties. Nevertheless, the impact of DEK in UC has not been investigated earlier. Therefore, we appraised DEK's function in dextran sulfate sodium (DSS)-induced UC in the mouse. An overall of 30 mice was randomized into 5 equal groups. Control mice treated with a standard diet (group I), colitis mice challenged with 3% of DSS through drinking water for 7 consecutive days (group II), DEK was supplemented via oral gavage from day 1 to 10 at the dosages of 5, 10, and 15 mg/kg b.wt, respectively. All animals were sacrificed on the 11th day. The body weight (bwt), colon length, disease activity index, malondialdehyde (MDA), myeloperoxidase (MPO), and histological features were observed using suitable techniques, and COX-2 expression was investigated by immunohistochemistry. Moreover, TNF-α, IL-1β, p65, IκBα, HO-1, and Nrf2 expressions were measured using ELISA and RT-PCR techniques, respectively. DEK treatment to the colitis mice considerably lessened, DSS-challenged alterations in body weight, DAI, colonic length shortening and histological changes. DEK exhibited potent antioxidant effects due to the reduced MDA and MPO, and Nrf2 expression markers while the HO-1 marker was augmented. Additionally, DEK also suppressed the expression s of TNF-α, IL-1β, and the p-p65, p-IκBα, and p65 and augmented the expression of IκBα, which eventually proved the anti-inflammatory potential of DEK against the DSS-challenge. Based on these results, DEK has been found effective in mitigating colitis, conceivably alleviating colon inflammation through the NF-κB inhibition and triggering of Nrf2/HO-1 signaling cascade.

Topics: Animals; Benzofurans; Colitis; Dextran Sulfate; Disease Models, Animal; Mice; NF-E2-Related Factor 2; NF-kappa B; Signal Transduction

One of the well-known causes of hearing loss is noise. Approximately 31.1% of Americans between the ages of 20 and 69 years (61.1 million people) have high-frequency hearing loss associated with noise exposure. In addition, recurrent noise exposure can accelerate age-related hearing loss. Phlorofucofuroeckol A (PFF-A) and dieckol, polyphenols extracted from the brown alga

Topics: Animals; Antioxidants; Aquatic Organisms; Benzofurans; Cochlea; Dioxins; Disease Models, Animal; Evoked Potentials, Auditory, Brain Stem; Hair Cells, Auditory; Hearing Loss, Noise-Induced; Kelp; Male; Mice; Mice, Inbred C57BL; Phytotherapy; Plant Extracts

Topics: Administration, Topical; Animals; Benzofurans; Biopsy, Needle; Cells, Cultured; Cytokines; Dermatitis, Atopic; Disease Models, Animal; Immunohistochemistry; Keratinocytes; Mice; Mice, Inbred Strains; Random Allocation; Sensitivity and Specificity; Thymic Stromal Lymphopoietin

In the present study, the attenuation of type ІІ diabetes by dieckol, a phlorotannin derivative isolated from brown seaweed, Ecklonia cava was investigated in C57BL/KsJ-db/db, a type ІІ diabetes mouse model. Dieckol was administered intraperitoneal injection at doses of 10 and 20 mg/kg body weight diabetes mice for 14 days. The blood glucose level, serum insulin level and body weight were significantly reduced in the dieckol administered group, compared to that of the saline administered group. Furthermore, reduced thiobarbituric acid reactive substraces (TBARS), as well as increased activities of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-px) in liver tissues were observed in the dieckol administered group. In addition, increased levels of the phosphorylation of AMPK and Akt were observed in the muscle tissues of the dieckol administered group in a Western blotting analysis. According to the findings of this study, it could be suggested that, dieckol can be developed as a therapeutic agent for type ІІ diabetes.

Topics: AMP-Activated Protein Kinases; Animals; Benzofurans; Blood Glucose; Body Weight; Catalase; Diabetes Mellitus, Experimental; Disease Models, Animal; Glutathione Peroxidase; Hypoglycemic Agents; Insulin; Lipid Peroxidation; Mice; Mice, Inbred C57BL; Phaeophyceae; Phosphorylation; Proto-Oncogene Proteins c-akt; Seaweed; Signal Transduction; Superoxide Dismutase