Safranal protects against beta-amyloid peptide-induced cell toxicity in PC12 cells via MAPK and PI3 K pathways
محل انتشار: پانزدهمین همایش سراسری سم شناسی ایران
سال انتشار: 1398
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 422
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شناسه ملی سند علمی:
TOXICOLOGY15_246
تاریخ نمایه سازی: 15 بهمن 1398
چکیده مقاله:
Alzheimer s disease is a type of cerebrovascular problem with progressive mental disabilities for the patient. This study aimed to investigate the protective effect of safranal on toxicity and oxidative damage induced by beta-amyloid (Aβ) and hydrogen peroxide (H2O2) in PC12 cells as an appropriate model of Alzheimer s cell damage. PC12 cells pretreated with saffron extract (2.5-40 μg/ml), essential oil (2.5-40 μg/ml), safranal (2.5-5-40 μM) and donepezil (5, 10 and 20 μM) for 120 min. Then exposed to either Aβ (25 μM) for 48 h or H2O2 (150 μM) for 24 h. In the end, the cell survival and intracellular reactive oxygen species (ROS) production analyzed. The anti-apoptotic effects of safranal in PC12 cells were studied using flow cytometry after PI staining. Also, western blot analysis of Cyt c, survivin, p44/42 MAPK (ERK1/2), Phospho-p44/42 MAPK (ERK1/2), PI3 Kinase P85, Phospho-PI3 Kinase P85, phospho SAPK/JNK, SAPK/JNK and caspase 3 for detection of apoptosis was done. Safranal (2.5 and 5 μM) and donepezil (10 and 20 μM) significantly decreased the Aβ toxicity. The ROS significantly attenuated when cells were pretreated with essential oil, saffron extract, safranal, and donepezil. Cell apoptosis significantly increased after treatment with Aβ (25-35) (25 μM) compared to control. However, after pretreatment with safranal (2.5 μM) apoptosis was significantly reduced. Western blot analysis of PC12 cells showed that 25 μM Aβ (25-35) could increase proteins involved in apoptosis signaling and pretreatment with safranal (2.5 μM) could decrease the apoptosis. According to the results, safranal showed anti-apoptotic and antioxidant effects and may exert promising potential for the prevention of Alzheimer s disease.
کلیدواژه ها:
نویسندگان
Faezeh Rafieipour
Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
Elham Hadipour
Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran
Seyed Ahmad Emami
Department of Pharmacognosy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
Javad Asili
Department of Pharmacognosy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
Zahra Tayarani-Najaran
Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran- Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran