Yüzme egzersizi ve yaşlanmaya bağlı vasküler disfonksiyon: irisin peptidinin rolü

ÖZETÇalışmada doğal yaşlanma sürecinde ya da D-galaktoz ile taklit edilenyaşlanma modelinde ABSTRACTThe aim of this study is to investigate possible effect of exerciseon endothelial function of thoracic aortae in both natural aging and D-galactosemimetic ageing models

Yüzme egzersizi ve yaşlanmaya bağlı vasküler disfonksiyon: irisin peptidinin rolü

Çalışmada doğal yaşlanma sürecinde ya da D-galaktoz ile taklit edilen yaşlanma modelinde; ABSTRACT The aim of this study is to investigate possible effect of exercise on endothelial function of thoracic aortae in both natural aging and D-galactose mimetic ageing models

Potential Effect of 1,25 Dihydroxyvitamin D-3 on Thioacetamide-Induced Hepatotoxicity in Rats

Background: 1,25 Dihydroxyvitamin D-3 (1,25(OH)(2)D-3) modulates inflammation and immune responses. Deficiency of 1,25(OH)(2)D-3 was found to be associated with the risk of cancer, cardiovascular disease, osteoarthritis, infections, and autoimmune diseases. This study evaluated the effect of 1,25 dihydroxyvitamin D-3 1,25(OH)(2)D-3 on thioacetamide (TAA)-induced acute liver injury in rats. Materials and methods: Rats were treated with either saline or 1,25(OH)(2)D-3 (0.30 mg/kg; orogastrically) for 15 d. Starting from day 13, TAA (200 mg/kg; intraperitoneally) was given for 3 d. On day 15, all rats were euthanized. Liver and blood samples were collected. Results: TAA caused severe damage, increased lipid peroxidation with reductions in endogenous antioxidants, increased apoptosis, increased production of reactive oxygen species, and elevated inducible nitric oxide synthase (iNOS), and nuclear factor kappa B (NF-kappa B) expression in liver. Extent of damage was decreased by 1,25(OH)(2)D-3 (P < 0.01). 1,25(OH)(2)D-3 attenuated the increase in malondialdehyde (P < 0.01), increase in myeloper-oxidase (P < 0.01), increase in chemiluminescence levels (P < 0.05) and apoptotic activity (P < 0.001). Elevated liver iNOS and NF-kappa B expression in TAA group was also reduced by 1,25(OH)(2)D-3 (P < 0.001, for iNOS; P < 0.001, for NF-kappa B). TAA group revealed high serum aspartate transaminase and alanine transaminase (ALT) activities (P < 0.01, for aspartate transaminase; P = 0.08, for ALT) and reduced albumin levels (P < 0.01) compared with control. 1,25(OH)(2)D-3 had no statistically significant effect on these parameters. Conclusions: 1,25(OH)(2)D-3 provides protection against hepatic injury in a rat model of TAA-induced hepatotoxicity via suppression of inflammatory reaction, oxidative stress, and apoptosis. (C) 2019 Elsevier Inc. All rights reserved

Nesfatin-1 alleviates gastric damage via direct antioxidant mechanisms

Background: Indomethacin is a nonsteroidal anti-inflammatory drug, which is known to produce serious side effects, causing ulcerative lesions. Nesfatin-1, a newly identified anorexigenic peptide, was recently shown to have neuroprotective effects. The aim of the study was to investigate the anti-inflammatory effects of nesfatin-1 on indomethacin-induced gastric ulcer. Materials and methods: After a 24-h starvation period, ulcer was induced in Sprague-Dawley rats by subcutaneous administration of indomethacin (25 mg/kg), whereas control group received vehicle. Fifteen minutes after ulcer induction, rats were treated with either saline or nesfatin-1 (0.1, 0.3, or 1 mu g/kg, intraperitoneally). At the fourth hour, all rats were decapitated and their trunk blood was collected for tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 measurements. Stomach samples were examined microscopically and analyzed for myeloperoxidase (MPO) activity, malondialdehyde (MDA), glutathione (GSH), luminol-, and lucigenin-enhanced chemiluminescence (CL) levels. Results: Ulcer induction increased serum TNF-alpha; and IL-6 levels, gastric CL and MDA levels and MPO activity but decreased gastric GSH content (P < 0.05-0.001). On the other hand, 0.1 mu g/kg dose of nesfatin-1 reduced microscopic and macroscopic damage scores, decreased MPO activity and MDA levels, CL and IL-6 levels, whereas gastric GSH was replenished (P < 0.01). However, indomethacin-induced increase in TNF-alpha level was abolished at only 1 mu g/kg dose of nesfatin-1 (P < 0.01). Conclusions: Nesfatin-1 alleviated indomethacin-induced gastric injury, suggesting that the anti-inflammatory and gastroprotective effects of nesfatin-1 on oxidative gastric damage could be implemented by supporting the balance in oxidant and antioxidant systems while inhibiting the generation of pro-inflammatory mediators. (C) 2015 Elsevier Inc. All rights reserved

Estrogen Alleviates Acetic Acid-Induced Gastric or Colonic Damage via Both ER alpha- and ER beta-Mediated and Direct Antioxidant Mechanisms in Rats

In order to demonstrate the possible protective effects of estrogen receptor (ER)-alpha and ER beta receptor subtypes in the pathogenesis of colonic and gastric oxidant damage, experimental ulcer and colitis were induced by acetic acid, and the animals were randomly divided as colitis, ulcer, and their corresponding non-ulcer and non-colitis control groups. Each group of rats was treated intramuscularly with the vehicle, selective ER alpha agonist propylpyrazole-triol (1 mg/kg), ER beta agonist diarylpropionitrile (1 mg/kg), non-selective ER agonist 17 beta estradiol (E2; 1 mg/kg), or E2 plus non-selective ER antagonist ICI-182780 (1 mg/kg). The results revealed that induction of ulcer or colitis resulted in systemic inflammation as assessed by increased levels of plasma TNF-alpha and IL-6 levels. In both tissues, the presence of oxidant damage was verified by histological analysis and elevated myleoperoxidase activity. In the colitis and ulcer groups, both ER agonists and the non-selective E2 reversed the oxidative damage in a similar manner. These findings indicate that estrogen acts via both ER alpha- and ER beta-mediated and direct antioxidant mechanisms, where both ER subtypes play equal and efficient roles in the anti-inflammatory action of estrogen, in limiting the migration of neutrophils to the inflamed tissue, reducing the release and activation of cytokines and thereby alleviating tissue damage

Nesfatin-1 Ameliorates Sepsis-Induced Remote Organ Injury: The Role of Oxidant-Antioxidant Status and Neutrophils

Purpose: Protective effects of nesfatin-1 was studied in sepsis-induced injury of remote organs. Methods: Male rats were randomly divided as control and sepsis (cecal ligation-perforation) groups, treated with either saline or nesfatin-1 (10 mu g/kg). At 16 h following surgery, samples of brain, kidney, liver and lung tissues were removed and myeloperoxidase (MPO) activity, glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured in these tissues. Results: In saline-treated septic rats, elevated MDA and MPO activities were accompanied with depleted CAT, SOD and GSH levels in the brain, kidney, liver and lung tissues, implicating extensive oxidative damage in all remote organs. Nesfatin-1 reduced MDA levels (brain, lung) and MPO activities (brain, kidney), and preserved antioxidant GSH (brain, lung), CAT (brain) and SOD (kidney) levels. Severe hepatocyte degeneration, neuronal damage, glomerulotubular degeneration and alveolar disturbance in saline-treated septic rats were replaced with regular tissue morphologies in nesfatin-1-treated rats. Conclusion: Nesfatin-1 alleviates oxidative damage by enhancing endogenous antioxidant systems and inhibiting recruitment of neutrophils, suggesting that nesfatin-1 may be have a potential therapeutic impact on the treatment of septic shock to reduce subsequent remote organ failure