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Yazar "Bag, H. G." seçeneğine göre listele

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    Neuroprotection against CCl4 induced brain damage with crocin in Wistar rats
    (Taylor & Francis Ltd, 2018) Altinoz, E.; Erdemli, M. E.; Gul, M.; Aksungur, Z.; Gul, S.; Bag, H. G.; Kaya, G. B.
    Owing to its lipophilic property, carbon tetrachloride (CCl4) is rapidly absorbed by both the liver and brain. We investigated the protective effects of crocin against brain damage caused by CCl4. Fifty rats were divided into five groups of ten: control, corn oil, crocin, CCl4 and CCl4 + crocin. CCl4 administration decreased glutathione (GSH) and total antioxidant status (TAS) levels, and catalase (CAT) activity, while significant increases were observed in malondialdehyde (MDA) and total oxidant status (TOS) levels and superoxide dismutase (SOD) activity. The cerebral cortex nuclear lamina developed a spongy appearance, neuronal degeneration was observed in the hippocampus, and heterochromatic and pyknotic neurons with increased cytoplasmic eosinophilia were observed in the hippocampus after CCl4 treatment. Because crocin exhibits strong antioxidant properties, crocin treatment increased GSH and TAS levels and CAT activities, and decreased MDA and TOS levels and SOD activity; significant improvements also were observed in histologic architecture. We found that crocin administration nearly eliminated CCl4 induced brain damage by preventing oxidative stress.
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    Protective effects of crocin on biochemistry and histopathology of experimental periodontitis in rats
    (Taylor & Francis Ltd, 2019) Kocaman, G.; Altinoz, E.; Erdemli, M. E.; Gul, M.; Erdemli, Z.; Gul, S.; Bag, H. G.
    We investigated the effectiveness of crocin for preventing oxidative damage in experimentally produced periodontitis. We used three groups of 10 female Wistar rats divided into: control (C); experimental periodontitis (EP), experimental periodontitis + crocin (Cr-EP). Malondialdehyde (MDA), glutathione (GSH), total antioxidant status (TAS), total oxidant status (TOS) and superoxide dismutase (SOD) and catalase (CAT) enzyme activities were measured. We examined histopathology and inflammatory cell infiltration in gingiva and periodontal ligament. MDA and TOS levels, and SOD and CAT activities increased significantly in rats with induced periodontitis compared to the control group, while GSH and TAS levels were decreased significantly compared to the control group. Histopathologic examination revealed inflammatory cell infiltration in gingiva epithelium and subepithelial connective tissue in the EP group. Histological damage was reduced significantly after crocin treatment compared to the EP group. Crocin supplementation may help reduce oxidative damage to periodontal tissues.
  • Küçük Resim Yok
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    Saffron (its active constituent, crocin) supplementation attenuates lipid peroxidation and protects against tissue injury
    (Comenius Univ, 2016) Altinoz, E.; Ozmen, T.; Oner, Z.; Elbe, H.; Erdemli, M. E.; Bag, H. G.
    The aim of the current study was to investigate the outcomes in a rat model of an acute swimming exercise induced oxidative stress in brain, kidney, liver, skeletal and cardiac muscles using supplementation with crocin. Rats were divided into the eight groups; Normal Control (NC: Untreated and did not swim), Crocin Control (CC: Received crocin and did not swim), Exercise-1 (E-1: Untreated and swam), Exercise-24 (E-24: Untreated and swam), Exercise-48 (E-48: Untreated and swam), Exercise+Crocin-1 (EC-1: Received crocin and swam), Exercise+Crocin-24 (EC-24: Received crocin and swam), Exercise+Crocin-48 (EC-48: Received crocin and swam). The malondialdehyde (MDA) and xanthine oxidase (XO) enzymes levels increased after swimming in untreated and crocin treated groups, but there was a lower increase in crocin treated groups. The highest MDA levels in all tissues were observed in E-1 compared to all other groups. There were significant differences between control and exercise groups in MDA levels of tissues (p < 0.001). In contrast, there were significant differences between control and exercise groups in glutathione (GSH) levels of tissues. In addition, the crocin supplementation significantly increased GSH levels and decreased MDA and XO enzyme levels when compared to untreated exercise groups. Crocin can protect the tissues against exercise induced oxidative stress by enhancing antioxidant activity (Tab. 3, Fig. 1, Ref. 37). Text in PDF www.elis.sk.
  • Küçük Resim Yok
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    Thymoquinone is protective against 2,3,7,8-tetrachlorodibenzo-p-dioxin induced hepatotoxicity
    (Taylor & Francis Ltd, 2018) Erdemli, M. E.; Yigitcan, B.; Gul, M.; Bag, H. G.; Gul, S.; Aksungur, Z.
    We investigated changes in rat liver tissues following administration of thymoquinone (TQ) against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced hepatotoxicity. Fifty rats were assigned randomly to five groups of 10 as follows: control, corn oil, TCDD, TQ and TCDD + TQ. Biochemical and histopathological analyses were conducted on liver tissue. We found that 30 day TCDD administration caused histopathological changes in liver including thickening of Glisson's capsule, intracytoplasmic vacuolization in hepatocytes, sinusoidal dilation, vascular and sinusoidal congestion and inflammatory cell infiltration. TCDD administration increased malondialdehyde (MDA), total oxidant status (TOS), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels in rat liver tissue and reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and total antioxidant status (TAS) levels compared to all other groups. In the TQ treated group, GSH, SOD, CAT and TAS levels increased compared to all other groups. MDA, TOS, ALT, AST, ALP levels decreased compared to all other groups. Our histological findings were consistent with the biochemical findings. The oxidative and histologic effects of TCDD were eliminated by TQ treatment. TCDD administration caused oxidative stress in rat liver and TQ administered with TCDD prevented TCDD induced hepatotoxicity. TQ could be considered an alternative anti-TCDD toxicity agent.

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