این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
Iranian Journal of Basic Medical Sciences، جلد ۲۵، شماره ۱۱، صفحات ۱۳۷۳-۱۳۸۱
عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله
عنوان انگلیسی JNK and p38 gene and protein expression during liver ischemia-reperfusion in a rat model treated with silibinin
چکیده انگلیسی مقاله Objective(s): Signal transduction of mitogen-activated protein kinases (MAPKs) is activated during ischemia. In this study, c-Jun N-terminal Kinase (JNK) and p38 MAPK (p38) gene and protein expression were evaluated as two members of the MAPK family during liver ischemia-reperfusion in rats.Materials and Methods: Thirty-two male Wistar rats were divided into four groups of eight: Vehicle, ischemia-reperfusion (IR), ischemia-reperfusion+silibinin (IR+SILI), and SILI. The IR and IR+SILI groups differed from the other two groups in that they underwent one hour of ischemia followed by three hr of reperfusion. The Vehicle and IR groups received normal saline while the SILI and IR+SILI groups were treated with silibinin (50 mg/kg). At the end of the reperfusion time, blood and ischemic liver tissue were collected for further experiments.Results: The expression of JNK and p38 gene, the amount of serum hepatic injury indices, and malondialdehyde (MDA) in the IR group increased significantly compared with the vehicle group. The JNK and p38 gene expression decreased significantly in the IR + SILI group compared with the IR group. Glutathione peroxidase (GPx) and total antioxidant capacity (TAC) levels decreased in the IR group while increasing in the IR+SILI group. Histological examination showed that silibinin significantly reduced the severity of hepatocyte degradation. Western blot results were completely consistent with real-time PCR results.Conclusion: The possible pathways of the protective effect of silibinin against hepatic ischemia damages is to reduce the expression of the p38 and JNK gene and protein. 
کلیدواژه‌های انگلیسی مقاله Ischemia, JNK, p38, Reperfusion, Silibinin
نویسندگان مقاله | Nastaran Aamani
Department of Clinical Biochemistry and Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran


| Abouzar Bagheri
Department of Clinical Biochemistry and Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran


| Neda Masoumi Qajari
Genetic Biology, Islamic Azad University of Tonekabon, Tonekabon, Iran


| Majid Malekzadeh Shafaroodi
Department of Anatomy and Biology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran|Faculty of Medicine, Immunogenetic Research Center (IRC), Mazandaran University of Medical Sciences, Sari, Iran


| Abbas Khonakdar-Tarsi
Department of Clinical Biochemistry and Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran|Faculty of Medicine, Immunogenetic Research Center (IRC), Mazandaran University of Medical Sciences, Sari, Iran
نشانی اینترنتی https://ijbms.mums.ac.ir/article_21120.html
فایل مقاله فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده Original Article
برگشت به: صفحه اول پایگاه   |   نسخه مرتبط   |   نشریه مرتبط   |   فهرست نشریات