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Volume 12, Issue 4 (July-August 2018)
IJT 2018, 12(4): 5-9 |
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Kor A, Shahroozian E, Ahmadi-Hamedani M, Naeimi S. The Modulatory Effects of Pentoxifylline in Biochemical Changes Induced By 17α-Ethinyl Estradiol in the Rat Model. IJT 2018; 12 (4) :5-9
URL: http://ijt.arakmu.ac.ir/article-1-682-en.html
URL: http://ijt.arakmu.ac.ir/article-1-682-en.html
1- DVM, Faculty of Veterinary Medicine, Semnan University, Semnan, Iran.
2- Department of Basic Science, Faculty of Veterinary Medicine, Semnan University, Semnan, Iran. ,shahroozian@semnan.ac.ir
3- Department of Clinical Science, Faculty of Veterinary Medicine, Semnan University, Semnan, Iran.
4- Department of Basic Science, Faculty of Veterinary Medicine, Semnan University, Semnan, Iran.
2- Department of Basic Science, Faculty of Veterinary Medicine, Semnan University, Semnan, Iran. ,
3- Department of Clinical Science, Faculty of Veterinary Medicine, Semnan University, Semnan, Iran.
4- Department of Basic Science, Faculty of Veterinary Medicine, Semnan University, Semnan, Iran.
Abstract: (3944 Views)
Background: Ethinylestradiol (EE) has induced cholestasis and hepatotoxicity in animal studies through reducing bile acid uptake by hepatocytes and induce of oxidative stress. Pentoxifylline (PTX) is a drug that by inhibition of release or transcription of proinflammatory cytokine cause prevents oxidative stress of liver cell and reduction of damage. We aimed to evaluate the effects of pentoxifylline on liver injury induced by Ethinylestradiol in rats.
Methods: Twenty-four female Wistar rats (300±20 gr) were divided into four groups, equally. Duration of treatment was 5 consecutive days for each group. The control group Simultaneously received orally and subcutaneously normal saline. PTX group Simultaneously received Pentoxifylline orally and normal saline subcutaneously, EE Group Simultaneously received EE subcutaneously and normal saline orally. In the EE+PTX group, rats Simultaneously received EE subcutaneously and PTX orally. Rats were anesthetized and blood and tissue samples were collected for measurement of hematological and biochemical parameters.
Results: The EE administration increased the serum levels of ALP and MDA significantly. The EE administration also decreased albumin and GPX levels were significant. These aberrations were improved by PTX treatment in EE + PTX group. Most of hematological parameters were not significant by the EE. The plasma level of TNF- in the PTX+ES treated group showed a significant decrease in comparison to that in the ethinyl estradiol group.
Conclusion: PTX has partial capacity to protect against liver changes induced by Ethinyl Estradiol.
Methods: Twenty-four female Wistar rats (300±20 gr) were divided into four groups, equally. Duration of treatment was 5 consecutive days for each group. The control group Simultaneously received orally and subcutaneously normal saline. PTX group Simultaneously received Pentoxifylline orally and normal saline subcutaneously, EE Group Simultaneously received EE subcutaneously and normal saline orally. In the EE+PTX group, rats Simultaneously received EE subcutaneously and PTX orally. Rats were anesthetized and blood and tissue samples were collected for measurement of hematological and biochemical parameters.
Results: The EE administration increased the serum levels of ALP and MDA significantly. The EE administration also decreased albumin and GPX levels were significant. These aberrations were improved by PTX treatment in EE + PTX group. Most of hematological parameters were not significant by the EE. The plasma level of TNF- in the PTX+ES treated group showed a significant decrease in comparison to that in the ethinyl estradiol group.
Conclusion: PTX has partial capacity to protect against liver changes induced by Ethinyl Estradiol.
Keywords: Biochemical Parameters, Hepatotoxicity, Oxidative Stress, Pentoxifylline, 17α-Ethinylestradiol
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The Iranian Journal of Toxicology
Arak University of Medical Sciences in collaboration with the Iranian Society of Toxicology
Website: http://ijt.arakmu.ac.ir
Email: tox.journal@gmail.com
