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    Caffeic acid phenetyl ester accelerates cutaneous wound healing in a rat model and decreases oxidative stress
    (Wiley, 2007) Serarslan, G.; Altug, E.; Kontas, T.; Atik, E.; Avci, G.
    Background Cutaneous injury causes a depression in antioxidant status, as reactive oxygen species (ROS) are produced in response to injury. Aim To determine the effects of caffeic acid phenethyl ester (CAPE), an antioxidant and anti-inflammatory agent, on wound healing in rats. Methods In total, 40 male rats were divided into two groups: one group treated with CAPE (n = 20) and a second untreated control group (n = 20). A linear full-thickness incision was performed on the back of each rat and sutured. After incision, CAPE was given to the treatment group and saline to the control group. On days 1, 3, 7 and 14, five animals in each group were killed, and wound tissues dissected for biochemical and histopathological analysis. Results Wound tissues showed a significant increase in glutathione and nitric oxide levels, and a significant decrease in malondialdehyde levels and superoxide dismutase levels in the CAPE group compared with the control group. Histopathology of the wound tissues displayed rapid epithelium development in the CAPE group compared with the control group. Conclusions This study has demonstrated that CAPE partly accelerates full-thickness wound healing by its antioxidant and ROS-scavenging capabilities.
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    The Effects of Interferon ?2b on Chemically-induced Peritoneal Fibrosis and on Peritoneal Tissue MMP-2 and TIMP-2 Levels in Rats
    (Field House Publishing Llp, 2010) Ucar, E.; Borazan, A.; Semerci, E.; Binici, D. N.; Yaldiz, M.; Aysal, A.; Altug, E.
    This study investigated the effect of interferon alpha 2b on chlorhexidine gluconate (CH)-induced peritoneal fibrosis (PF) in rats and assessed peritoneal tissue levels of metalloproteinase (MMP)-2 and tissue inhibitors of metalloproteinases (TIMP)-2. Wistar albino rats (n = 8 per group) were treated as follows: control group, 3 ml/day of 0.9% saline intraperitoneally for 28 days; CH group, 0.1% CH (200 g [3 ml]/day) in 15% ethanol and 0.9% saline intra-peritoneally for 28 days; CH + interferon (IFN) group, CH (as above) plus pegylated IFN-alpha 2b 1.5 mu g/kg per week subcutaneously on days 0, 7, 14, 21 and 28; IFN group, pegylated IFN-alpha 2b (as above). Parietal peritoneum samples were obtained from the left anterior abdominal wall after 35 days. Parietal thickness, degree of vascular proliferation and inflammation, and MMP-2 and TIMP-2 levels were determined. The mean peritoneal thicknesses of the control, CH, CH + IFN and IFN groups were 7.02 +/- 3.89, 156.86 +/- 29.13, 59.88 +/- 22.1, 9.27 +/- 2.03 mu m, respectively. Pegylated IFN-alpha 2b decreased CH-induced expression of MMP-2 in the parietal peritoneum, but had no effect on TIMP-2 levels. Further studies are needed to determine the optimal dosage and duration for pegylated IFN-alpha 2b treatment.