ناقش بنجاح طالب الماجستير عمر نصري اليعقوب من قسم الصيدلة السريرية اليوم الخميس الموافق 8/12/2016م أطروحة الماجستير بعنوان:
تقييم التأثير الوقائي للتمبول علی اختلال الإدراك و ضعف الذاكرة
الناتج عن اضطراب ما بعد الصدمة
Evaluating the protective effect of tempol on memory and cognitive
impairment induced by post traumatic stress disorder
وقد
ضمت لجنة المناقشة الأستاذ الدكتور كارم الزعبي رئيساً وعضوية كل من
الدكتورة عبير ربابعة والدكتورة نائلة بولاتوفا كممتحن
خارجي. باسم صفحة أصدقاء كلية الصيدلة_ في جامعة العلوم والتكنولوجيا الأردنية
نبارك للطالب عمر اليعقوب إتمامه درجة الماجستير في الصيدلة السريرية بنجاح وتفوق
متمنين له مزيدا من التقدم.
للإطلاع على ملخص الدراسة
Post-traumatic stress disorder
(PTSD) is a mental health disorder that can be developed after a terrifying or
life threatening event. Many symptoms noticed in patients with PTSD including cognitive and memory impairment. Despite of the different
therapeutic approaches used to treat such disorder; studies showed that the response
rate for these options approximately between 40-50% of cases only. Tempol is highly
efficient membrane-permeable antioxidant, its efficacy in detoxifying reactive
oxygen species is numerously shown in cell and animal studies and it also
improved both behavioral and cognitive functions in animal models of Alzheimer disease, diabetes and sleep deprivation.
In
this study we are investigating the protective effect of tempol on Post-traumatic
stress disorder induced memory and cognitive impairment on rat model of PTSD. To test this hypothesis we used single
prolonged stress (SPS) model (2 h restrain, 20 min forced swimming, 15 min
rest, and 1–2 min diethyl ether exposure) as a model of PTSD. Male Wister rats were randomly assigned into four
groups: control (provided distilled water), Tempol (provided tempol (80 mg/kg)
daily by oral gavage for 4 weeks), PTSD (exposed to SPS and administered
distilled water) and Tempol/PTSD (exposed to SPS and administered tempol). We
used radial arm water maze (RAWM) to test spatial learning and memory functions
and enzyme-linked immunosorbant assay (ELISA) to measure levels of oxidative
stress biomarkers and BDNF in the hippocampus. Our results showed that PTSD
impaired both short and long term memories, and chronic tempol administration
protected against this impairment. Tempol also normalized hippocampal Catalase and SOD activities and increased GSH/GSS
ratio and TBARS
levels
which were all impaired by PTSD. In conclusion, we suggest a protective effect
of tempol administration against PTSD –induced short – and long-term memory
impairment, and we believe that this protective effect of tempol is
accomplished through normalization of oxidative stress in the hippocampus.
ليست هناك تعليقات:
إرسال تعليق