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KUMAŞ, MELTEM

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MELTEM
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KUMAŞ
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Author: EŞREFOĞLU, MUKADDES × Subject: Apoptosis ×

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    PublicationOpen Access
    Protective Effect of Curcumin on Cadmium-Induced Liver Apoptosis in Rats
    (2016-12-01T00:00:00Z) Bayindir, Nihan; EŞREFOĞLU, MUKADDES; Kumas, Meltem; Iraz, Meryem; Kesgin, Siddika; Kilic, Elif; BAYINDIR, NİHAN; EŞREFOĞLU, MUKADDES; KUMAŞ, MELTEM
    Objective: Cadmium (CD), which is used for many industrial purposes, is a toxic agent. CD accumulates in the liver; therefore, exposure to toxic doses of Cd results in hepatic damage. Studies in rats have shown that CD induces apoptosis in hepatocytes. Curcumin is a natural compound isolated from Curcuma longa. It has a powerful anti-inflammatory affect and scavenges reactive oxygen radicals. Additionally, it has been shown to have an anti-apoptotic effect in a dose-dependent manner. The aim of the present study was to evaluate the effects of therapeutic doses of curcumin on Cd-induced hepatic apoptosis as well as hepatic biochemical and inflammatory changes in Sprague-Dawley rats. Methods: In this study, 24 female Sprague-Dawley rats (6 months old) were randomly assigned to four main groups (n=6): control, CD, CD+curcumin, and curcumin. At the end of the experiment, after collecting blood samples from the heart, the rats were sacrificed and their livers were removed for histopathological and biochemical examinations. The number of apoptotic cells, total anti-oxidant status, total oxidant status, and thiol and MPO levels were measured in liver tissue; interleukin-6 and procalcitonin levels were measured in sera. Results: Chronic CD administration induced apoptosis. The number of apoptotic cells was significantly increased in the Cd group (almost 2 fold) compared to that in the control group. However, in the CD+curcumin group, the number of apoptotic cells was significantly decreased (almost 2 fold) compared to that in the Cd group. However, there were no statistically significant differences. Conclusion: We suggest that curcumin protects the liver against toxin-induced apoptosis.