مطالعه اثرات پیشگیرانه نارینژنین از آسیب ایسکمی-خونرسانی مجدد روده کوچک در موش صحرایی
محورهای موضوعی :
آسیب شناسی درمانگاهی دامپزشکی
غفور موسوی
1
1 - استادیار گروه علوم درمانگاهی، واحد تبریز، دانشگاه آزاد اسلامی، تبریز، ایران.
تاریخ دریافت : 1393/12/05
تاریخ پذیرش : 1394/02/30
تاریخ انتشار : 1393/12/01
کلید واژه:
موش صحرایی,
روده,
ایسکمی-خونرسانی مجدد,
نارینژنین,
چکیده مقاله :
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.
چکیده انگلیسی:
The intestinal mucosa is known to be adversely affected by ischemia-reperfusion (I/R). It has been demonstrated that Naringenin has protective effects against ischemia-reperfusion injury in various organs. The aim of this study is to determine whether Naringenin has any protective role in I/R injury of the intestine in rats. For this purpose, forty male Wistar rats were randomly divided into four groups as control (group 1), sham IR (group 2), intestinal IR group (group 3) and Naringenin plus intestinal IR (group 4). Intestinal IR was produced by 30 minutes of intestinal ischemia followed by a 60 minutes of reperfusion. Rats in group 4 received Naringenin (20 mg/kg) intraperitoneally, 120 minutes before ischemia. After the experiments, the jejunum was removed and the tissues were processed for histopathological examination. Serum total antioxidant activity (TAA), and levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) were measured in jejunal tissue. Histopathologically, jejunal tissues of the intestinal IR group showed severe inflammatory cell infiltration, villus shortening and blunting and hemorrhage in lamina propria, as well as epithelial cell necrosis. Administration of Naringenin alleviated the jejunal damage in group 4. Levels of TAA, SOD, CAT, GPx and GR decreased in the intestinal IR group, but increased significantly (p<0.05) in the IR+Naringenin group. Naringenin significantly (p<0.05) decreased MDA levels which was increased by IR. Our results showed that Naringenin treatment protected the rat's intestinal tissue against intestinal ischemia-reperfusion injury.
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