بررسی آپوپتوزیس و هیستوپاتولوژی قلب متعاقب ایسکمی – بازخونرسانی وابسته به زمان کلیوی در موش صحرایی نر
مهبد باژبان
1
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فارغ التحصیل دکترای حرفه ای دامپزشکی، دانشکده دامپزشکی، علوم پزشکی تبریز، دانشگاه آزاد اسلامی، تبریز، ایران
)
یوسف دوستار
2
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دانشیار گروه پاتوبیولوژی، دانشکده دامپزشکی، علوم پزشکی تبریز، دانشگاه آزاد اسلامی، تبریز، ایران
)
میرعلیرضا نورآذر
3
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استادیار گروه علوم پایه، دانشکده دامپزشکی، علوم پزشکی تبریز، دانشگاه آزاد اسلامی، تبریز، ایران
)
کلید واژه: ایسکمی-بازخونرسانی, کلیه, قلب, موش¬صحرایی, آپوپتوزیس.,
چکیده مقاله :
آسیب ایسکمی-بازخونرسانی (I/R) کلیه یکی از مهمترین عوامل نارسایی حاد کلیوی و متعاقب آن آسیب به اندامهای دیگر همچون قلب به شمار میرود. هدف از مطالعه حاضر، بررسی وقوع آسیب و آپوپتوزیس در قلب متعاقب آسیب ایسکمی–بازخونرسانی وابسته به زمان کلیوی در موش صحرایی بود. بدین منظور 32 سر موش صحرایی نر ویستار به طور تصادفی به 4 گروه مساوی تقسیم شدند. در گروه اول (Sham) فقط محل جراحی باز و بسته شد. در گروه دوم (30-I/R) پس از القاء ایسکمی کلیوی 30 دقیقه بعد، در گروه سوم (45-I/R) 45 دقیقه بعد و در گروه چهارم (60-I/R) 60 دقیقه بعد بازخونرسانی انجام شدند. پس از 24 ساعت همهحیوانات آسان¬کشی شده و از بافت کلیه و قلب آن¬ها جهت مطالعه ریزبینی نمونهبرداری شد. واکاوی آماري دادهها توسط آزمون تحلیل واریانس یک¬طرفه (ANOVA) و پس¬آزمون توكي (tukey) انجام و مقادیر 05/0p< معنيدار تلقی شد. یافتههایهیستوپاتولوژی، آسیب کلیوی متعاقب I/R را به¬شکل تغییرات دژنراتیو و نکروز توبول¬های پروگزیمال و دیستال، آسیب¬های گلومرولی و بافت بینابینی به صورت وابسته به زمان نشان داد. همچنین I/R کلیه منجر به آسیب بافت قلب شامل تغییرات دژنراتیو و نکروز و آپوپتوز کادیومیوسیتها در تمامی گروه¬ها شد، اما شدت آسیب بافتی و آپوپتوز کادیومیوسیت¬ها در گروه 60-I/R به طور معنیداری بیشتر از سایر گروهها بود (05/0p<). نتایج مطالعه نشان داد با کاهش مدت زمان ایسکمی در کلیه، آسیب خود بافت کلیه، بافت قلب و آپوپتوزیس کاردیومیوسیت¬ها¬ کمتر خواهد بود.
چکیده انگلیسی :
Kidney ischemia-reperfusion injury (I/R) is one of the most important causes of acute renal failure and subsequent damage to other organs such as the heart. was to investigate the occurrence of damage and apoptosis in the heart following renal ischemia-reperfusion time-dependent injury in rats. For this purpose, 32 male Wistar rats were randomly divided into 4 equal groups. In the first group (Sham), only the surgical site was opened and closed. In the second group (30-I/R) after the induction of renal ischemia, reperfusion was performed 30 minutes later, in the third group (45-I/R) 45 minutes later, and in the fourth group (60-I/R) 60 minutes later. After 24 hours, all animals were euthanized and their kidney and heart tissues were sampled for microscopic study. Statistical analysis of the data was done by one-way analysis of variance (ANOVA) and Tukey's post-test, and values of p<0.05 were considered significant.Histopathological findings showed renal damage following I/R in the form of degenerative changes and necrosis of proximal and distal tubules, glomerular and interstitial tissue damage in a time-dependent manner. Also, renal I/R resulted in heart tissue damage including degenerative changes and necrosis along with apoptosis of cardiomyocytes in all groups, but the severity of tissue damage and apoptosis of cardiomyocytes in the 60-I/R group was significantly higher than other groups (p<0.05). The results of the study showed that by reducing the duration of renal ischemia, the damages to the kidney tissue and subsequently heart tissue as well as apoptosis of cardiomyocytes will be less.
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