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From a natural polyphenol, Tannic acid (TA), poly(TA) nanoparticles were readily prepared using a single step approach with three different biocompatible crosslinkers; trimethylolpropane triglycidyl ether (TMPGDE), poly(ethylene glycol) diglycidyl ether (PEGGE), and trisodium trimetaphosphate (STMP). P(TA) particles were obtained with controllable diameters between 400 to 800nm with -25mV surface charge. The effect of synthesis conditions, such as the emulsion medium, pH values of TA solution, and the type of crosslinker, on the shape, size, dispersity, yield, and degradability of poly(Tannic Acid) (p(TA)) nanoparticles was systematically investigated. The hydrolytic degradation amount in physiological pH conditions of 5.4, 7.4, and 9.0 at 37.5°C were found to be in the order TMPGDE

A novel resourceful bulk poly(Tannic Acid) (p(TA)) hydrogel was prepared by crosslinking TA molecules with an epoxy crosslinker, trimethylolpropane triglycidyl ether (TMPGDE), in an autoclave at 90°C for 2h. The obtained p(TA) hydrogels were in disk form and have highly porous morphology. The swelling characteristics of p(TA) hydrogels were investigated in wound healing pH conditions of pH 5.4, 7.4, and 9 at 37.5°C, and the hydrogels showed good swelling and moisture content behavior. Especially, p(TA) hydrogels were found to be sensitive to pH 9 with 1669% maximum swelling. P(TA) hydrogels were completely degraded at pH 9 hydrolytically in 9 days. Total phenol contents and the effects of scavenging ABTS(+) radicals of degraded p(TA) hydrogels at pH 5.4, 7.4, and 9 were evaluated and calculated in terms of gallic acid equivalent and trolox equivalent antioxidant capacity, respectively, and found to be very effective. Moreover, degraded p(TA) hydrogels display strong antimicrobial behavior against gram positive Staphylococcus aureus, Bacillus subtilis, gram negative Pseudomonas aeruginosa bacteria strains and Candida albicans fungus strain. The WST-1 results indicated that bulk p(TA) hydrogels have no cyctotoxicity to the L929 fibroblast cell line in vitro., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Humic acid is an antioxidant molecule used in agriculture and livestock breeding, as well as in medicine. Our aim was to investigate the potential renoprotective effects of humic acid in a renal ischemia reperfusion model. Twenty-one rats were randomly divided into three equal groups. Intraperitoneal serum or humic acid was injected at 1, 12, and 24 h. Non-ischemic group I was evaluated as sham. The left renal artery was clamped in serum (group II) and intraperitoneal humic acid (group III) to subject to left renal ischemic reperfusion procedure. Ischemia and reperfusion time was 60 min for each. Total antioxidant status, total oxidative status, oxidative stress index, and ischemia-modified albumin levels were analyzed biochemically from the serum samples. Kidneys were evaluated histopatologically and immunohistochemically. Biochemical results showed that total oxidative status, ischemia-modified albumin, and oxidative stress index levels were significantly decreased, but total antioxidant status was increased in the humic acid group (III) compared with the ischemia group (II) On histopathological examination, renal tubular dilatation, tubular cell damage and necrosis, dilatation of Bowman's capsule, hyaline casts, and tubular cell spillage were decreased in the humic acid group (III) compared with the ischemia group (II). Immunohistochemical results showed that apoptosis was deteriorated in group III. Renal ischemia reperfusion injury was attenuated by humic acid administration. These observations indicate that humic acid may have a potential therapeutic effect on renal ischemia reperfusion injury by preventing oxidative stress.

Many studies of brain ischemia have shown the role played by massive ischemia-induced production of reactive oxygen species, the main mechanism of neuronal death. However, currently, there is no treatment choice to prevent cell death triggered by reactive oxygen species. In our study, we researched the effects of tannic acid, an antioxidant, on the ischemic tissue of rats with induced middle cerebral artery occlusion. The animals were divided into three groups of eight animals. The sham group were only administered 10 % ethanol intraperitoneally, the second group had middle cerebral artery occlusion induced and were given 10 % ethanol intraperitoneally, while the third group had middle cerebral artery occlusion with 10 mg/kg dose tannic acid dissolved in 10 % ethanol administered within half an hour intraperitoneally. The rats were sacrificed 24 h later, and brain tissue was examined biochemically and histopathologically. Biochemical evaluation of brain tissue found that comparing the ischemic group with no treatment with the tannic acid-treated ischemia group; the superoxide dismutase (SOD) levels were higher, malondialdehyde (MDA) levels were lower, and nuclear respiratory factor-1 (NRF-1) was higher in the tannic acid-treated group. Histopathological examination showed that the histopathological results of the tannic acid group were better than the group not given tannic acid. Biochemical and histopathological results showed that tannic acid administration had an antioxidant effect on the negative effects of ischemia in brain tissue.

We aimed to demonstrate the potential protective effects of pyrrolidine dithiocarbamate (PDTC) on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH). Adult male rats were randomly assigned to 4 groups: control group, MCT-treated rats only, MCT-injected rats treated with PDTC, and PDTC-treated rats only. Blood and tissue samples were collected after the sacrifice. Levels of malondialdehyde (MDA) were measured by using the thiobarbituric acid method. Total antioxidant status (TAS) was determined using a commercially available ImAnOx kit. A histopathological evaluation was accomplished by scoring the degree of severity. Endothelial damage of the main pulmonary artery was evaluated by immunohistochemical labeling of endothelial cells using anti-rat endothelial cell antigen 1 (RECA-1) antibody. MCT-induced right ventricular hypertrophy (RVH) was reduced significantly in the MCT+PDTC-treated group. MDA levels were significantly lowered in the MCT+PDTC-treated group. TAS was significantly higher in the MCT+PDTC-treated group when compared with the rats with PAH. Histopathological examination demonstrated that PDTC treatment reduced the development of inflammation, hemorrhage and congestion, and collagen deposition. In conclusion, PDTC attenuated PAH and protected pulmonary endothelium in rats administered MCT. These findings suggest that PDTC treatment may provide a new effective therapeutic approach in the treatment of PAH., (Copyright © 2013 Elsevier GmbH. All rights reserved.)

In this study, we aimed to investigate the possible protective effect of resveratrol on gentamicin induced nephrotoxicity. Experiments were carried out in male Wistar rats weighing 200-250 g. Gentamicin sulfate (80 mg/kg per day i.p.), resveratrol (10 mg/kg per day i.p.) and gentamicin together with resveratrol were administered for 6 d. The animals were sacrificed 24 h after the last injection. Urine, blood samples and tissue samples were collected from the animals on the seventh day of the treatment before they were sacrificed. Kidneys were collected for histopathological studies and fixed in 10% buffered formalin solution. Tissue samples were stored at -70 degrees C in liquid nitrogen for the determination of glutathione (GSH), glutathione-S-transferase (GST), malondialdehyde (MDA) and catalase (CAT). Glutathione assay was determined by the method of Beutler et al. GST amounts were measured by the method of Habig et al. Catalase activity was tested by Aebi's method and MDA was determined according to Thayer's method. Blood urea level was significantly increased in the gentamicin treated group. The study showed lowered levels of urea and creatinine levels in resveratrol administered groups when compared with gentamicin administered rats, and the difference was statistically significant. It has been determined that resveratrol caused statistically significant decrease in lipid peroxidation and reduced the level of catalase. Histopathological examination showed that resveratrol prevented partly gentamicin induced tubular damage. The results histopathologically demonstrated that resveratrol has a protective effect against gentamicin induced nephrotoxicity, lipid peroxidation and cellular damage in rats.

Free radical-mediated injury to lung and pulmonary vasculature is an important mechanism in hypoxia-induced lung damage. In this study, we aimed to investigate the potential protective effects of erdosteine as an antioxidant agent on hypobaric hypoxia-induced pulmonary hypertension. Adult male rats were assigned randomly to three groups. The first group of rats was exposed to hypobaric-hypoxia and the second group was treated with erdosteine (20mg/kg, daily) for 2 weeks, during which time they were in a hypoxic chamber. These groups were compared with normoxic controls. All rats were sacrificed after 2 weeks. The hypoxia-induced increase in right ventricle to left ventricle plus septum weight ratio (from 0.20+/-0.01 to 0.26+/-0.01) was reduced significantly in the erdosteine-treated group (0.23+/-0.01). Malondialdehyde levels were elevated (from 0.33+/-0.11 to 0.59+/-0.02) and total antioxidant status was not changed significantly (from 1.77+/-0.42 to 2.61+/-0.23) by hypoxia. In contrast to the hypoxia-exposed group, malondialdehyde levels were significantly decreased in the erdosteine-treated group (0.37+/-0.02). Total antioxidant status (4.03+/-0.22) was significantly higher in erdosteine-treated rats when compared to non-treated rats. Histopathological examination demonstrated that erdosteine prevented inflammation and protected lung parenchyma and pulmonary endothelium of hypoxia-exposed rats.