مطالعه اثرات پیشگیرانه نارینژنین از آسیب ایسکمی-خون‌رسانی مجدد روده کوچک در موش صحرایی
الموضوعات :
غفور موسوی
1
(
استادیار گروه علوم درمانگاهی، واحد تبریز، دانشگاه آزاد اسلامی، تبریز، ایران.
)
تاريخ الإرسال : 05 الثلاثاء , جمادى الأولى, 1436
تاريخ التأكيد : 02 الأربعاء , شعبان, 1436
تاريخ الإصدار : 01 الجمعة , جمادى الأولى, 1436
الکلمات المفتاحية:
موش صحرایی,
روده,
ایسکمی-خون‌رسانی مجدد,
نارینژنین,
ملخص المقالة :
مخاط روده به شدت توسط ایسکمی-خون رسانی مجدد (IR) تحت تاثیر قرار می گیرد. نشان داده شده است که نارینژنین در برابر آسیب ایسکمی-خون رسانی مجدد در ارگان های مختلف دارای اثرات محافظتی می باشد. هدف از این مطالعه این است که آیا نارینژنین در آسیب ایسکمی-خون رسانی مجدد روده موش صحرایی نقش محافظتی دارد. بدین منظور، 40 سر موش صحرایی نر ویستار به طور تصادفی به چهار گروه شاهد (گروه 1)، شاهد جراحی (گروه 2)، ایسکمی-خون رسانی مجدد (گروه 3) و ایسکمی-خون رسانی مجدد به علاوه تیمار با نارینژنین (گروه 4) تقسیم شدند. آسیب ایسکمی-خون رسانی مجدد با 30 دقیقه ایسکمی روده و 60 دقیقه خون رسانی مجدد ایجاد شد. موش های گروه 4 نارینژنین (mg/kg 20) را 120 دقیقه قبل از القاء ایسکمی از طریق تزریق داخل صفاقی دریافت کردند. پس از انجام آزمایشات، ژوژنوم خارج و جهت آسیب شناسی بافتی آماده گردید. فعالیت تام آنتی اکسیدانی سرم و مقادیر مالون دی آلدئید، سوپراکسید دیسموتاز، کاتالاز، گلوتاتیون پراکسیداز و گلوتاتیون ردوکتاز در بافت ژوژنوم اندازه گیری شد. آسیب‌شناسی بافتی، ارتشاح شدید سلول های آماسی، کوتاه و کُند شدگی پرزها، خونریزی لامینا پروپریا و نکروز سلول های بافت پوششی ژوژنوم را در گروه ایسکمی-خون رسانی مجدد نشان داد. مصرف نارینژنین آسیب ژوژنوم را موش های گروه 4 کاهش داد. فعالیت تام آنتی اکسیدانی سرم و مقادیر سوپراکسید دیسموتاز، کاتالاز، گلوتاتیون پراکسیداز و گلوتاتیون ردوکتاز در گروه ایسکمی-خون رسانی مجدد کاهش یافت ولی به طور معنی داری (05/0>p) در گروه ایسکمی-خون رسانی مجدد به علاوه تیمار با نارینژنین افزایش یافت. نارینژنین مقدار مالون دی آلدئید را که در اثر ایسکمی-خون رسانی مجدد افزایش یافته بود به طور معنی داری (05/0>p) کاهش داد. نتایج ما نشان داد نارینژنین روده باریک موش های صحرایی را از آسیب ایسکمی-خون رسانی مجدد محافظت کرد.
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