Deneysel olarak renal iskemi-reperfüzyon oluşturulan sıçanlarda diosmin+hesperidinin etkisi
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Tarih
2011
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Yayıncı
Trakya Üniversitesi Tıp Fakültesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
İskemi, hücrede enerji düzeyinin düşmesine ve toksik metabolitlerin dokuda birikmesine yol açarak, hücre disfonksiyonu ve hücre ölümüne kadar gidebilen bir dizi biyokimyasal reaksiyonu başlatır. Reperfüzyon sonrası, ortama gelen nötrofiller ve bunlardan açığa çıkan mediatörlerin zararlı etkileri de eklenince, organ hasarı ve hatta ölümü kaçınılmaz olmaktadır. Böbrekte, sistemik hipotansiyon, hipovolemik şok, kardiak arrest, renovasküler cerrahi, aortun klempajı gibi klinik durumlarda sıcak iskemi- reperfüzyon hasarı oluşabilmektedir. Bu hasarın derecesi, iskeminin süresine bağlı olarak artmakta ve sonuçta, belirgin doku hasarı olmaksızın gelişen prerenal azotemiden, tübüler veya kortikal nekroza bağlı gelişen ciddi akut böbrek yetmezliğine kadar değişebilen, farklı klinik tablolar karşımıza çıkabilmektedir. Çalışmamızda iskemi-reperfüzyon oluşturulan ratlarda Diosmin+ Hesperidinin, renal dokuda malondialdehit ve glutatyon, serumda üre ve kreatinin ile renal histopatoloji bakılarak, iskemi-reperfüzyon hasarına etkili olup olmadığını araştırdık. Çalışmada 190-250 gr ağırlığında, 40 adet dişi Sprague-Dawley rat kullanıldı ve hayvanlar her biri 10'arlı rastgele 4 gruba ayrıldı. Kontrol grubu (grup 1, n=10): Sadece standart su ve yem verildi ve 7. gün sonunda laparatomi yapılarak intrakardiak kan ve renal doku örnekleri alındı. Diosmin+Hesperidin grubu (grup 2, n=10 ): 7 gün boyunca hergün aynı saatte 50mg/kg Diosmin + Hesperidin orogastrik gavaj yoluyla verildi ve 7. Gün sonunda laparatomi yapılarak intrakardiak kan ve renal doku örnekleri alındı. İskemi-reperfüzyon grubu (grup 3, n=10):7 gün sadece standart su ve yem verilen bu gruba 7. gün sonunda laparatomi yapıldı ve bilateral renal pedikülün 45 dakika oklüzyonunu takiben, 24 saat reperfüzyon yapıldı. İskemi reperfüzyon uygulanıp Diosmin+Hesperidin verilen grup (grup 4, n=10): 7 gün boyunca hergün aynı saatte 50mg/kg Diosmin+Hesperidin orogastrik gavaj yoluyla verilen bu gruba 7. gün sonunda laparatomi yapıldı ve bilateral renal pedikülün 45 dk. klemplenmesini takiben, 24 saat reperfüzyon yapıldı. Grup 3 ve 4' teki ratlara 24 saatlik reperfüzyonu takiben relaparatomi yapılarak intrakardiak kan ve renal doku örnekleri alındı. Kontrol, Diosmin+Hesperidin, İskemi-reperfüzyon, İskemi-reperfüzyon uygulanıp Diosmin+Hesperidin verilen grup mukayese edildiğinde; İskemi-reperfüzyon grubunda renal doku glutatyon düşüklüğünü, serum üre ve kreatinin yüksekliğini istatistik olarak anlamlı bulmamız bize, uyguladığımız iskeminin, böbrekte hasar oluşturduğunu gösterdi. Kullandığımız Diosmin+Hesperidin ile böbrekte, bu hasarlanmada hasarı azaltıcı etkilerini, istatiksel olarak anlamlı olmasa da tespit ettik. Zira İskemi-reperfüzyon uygulanıp Diosmin+Hesperidin verilen grup, İskemi-reperfüzyon grubuna göre; istatistiksel olarak anlamlı olmasa da serum üre ve kreatinin düzeyleri bakımından daha düşük, renal doku glutatyon seviyeleri bakımından daha yüksek değerlere sahipti. Kontrol grubu ile Diosmin+Hesperidin grubu arasında; renal doku glutatyon seviyeleri, serum üre ve serum kreatinin düzeyleri bakımından anlamlı farklılık olmaması, Diosmin +Hesperidinin renal dokuya, uyguladığımız dozlarda toksik etki göstermediği düşüncesini destekledi. Sonuç olarak; Renal iskemi-reperfüzyon oluşturulan ratlarda kullandığımız Diosmin +Hesperidinin, iskemi-reperfüzyon hasarını bir ölçüye kadar azaltabileceği ancak, iskemi-reperfüzyon hasarında istatistiksel olarak anlamlı bir iyileşme sağlayamayacağı kanaatindeyiz. Anahtar kelimeler: İskemi-reperfüzyon hasarı, böbrek, Diosmin +Hesperidin.
Abstract
By reducing cellular energy levels and causing an accumulation of toxic metabolites in tissue, ischemia triggers a chain of biochemical reactions that cause cell dysfunction and even cell death. After reperfusion, when the harmful effects of neutrophils and the mediators they produce are added to the setting, organ injury or even death become inevitable. In clinical conditions like hypotension, hypovolemic shock, cardiac arrest, renalvascular surgery or clamping of the aorta, hot ischemia reperfusion injuries may occur in the kidney. The degree of injury increases with the duration of ischemia and as a result different clinical conditions ranging from prerenal azotemia without distinctive tissue damage to acute kidney failure resulting from tubular or cortical necrosis come about. In our trial we investigated whether Diosmin+Hesperidine were effective in ischemia-reperfusion injury (renal ischemia-reperfusion) by looking at malondialdehyde and glutation in the renal tissue, and serum urea and creatinine together with renal histopathology in rats with induced ischemia-reperfusion. In our trial, 40 female Sprague-Dawley rats weighing 190-250 gr were used. The rats were assigned to 4 groups consisting of 10 rats each. In the control group (group 1, n=10 ) only standard water and food were given and after seven days laparotomy was performed and intracardiac blood and renal tissue samples were taken. In the Diosmin+Hesperidine group (group 2, n=10 ) 50 mg/kg Diosmin+Hesperidine were given through orogastric gavage at the same time everyday for seven days and after seven days laparotomy was performed and intracardiac blood and renal tissue samples were taken. In the ischemia-reperfusion group (group 3,n=10) only standard water and food were given for seven days and after seven days laparotomy was performed. Bilateral renal pedicules were occluded for 45 minutes then reperfusion was performed over 24 hours. In the Ischemia-reperfusion+Diosmin+Hesperidine group (group 4, n=10) 50 mg/kg Diosmin+Hesperidine were given through orogastric gavage at the same time everyday for seven days. After seven days laparotomy was performed and bilateral renal pedicules were occluded for 45 minutes then over 24 hours reperfusion was performed.In groups 3 and 4, after 24 hours of reperfusion relaparotomy was performed on the rats and intracardiac blood and renal tissue samples were taken. When the control, Diosmin+Hesperidine, Ischemia-reperfusion and Ischemia-reperfusion+Diosmin+Hesperidine groups were compared it was discovered that in the Ischemia-reperfusion group statistically significant low glutation in renal tissue, and high serum urea and creatinine showed that the ischemia we induced caused kidney injury. Although statistically insignificant we discovered that in the kidneys, the Diosmin+ Hesperidine we used reduced harmful effects in such injuries. Compared to the İschemia-reperfusion group, in the Ischemia-reperfusion+Diosmin+Hesperidine group the serum urea and creatinine levels were lower, and the renal tissue glutation levels were higher; although the difference was statistically insignificant. The fact that no significant difference was seen in terms of renal tissue glutation levels or serum urea and creatinine levels between the control and Diosmin+Hesperidine groups supports the fact that the dose of diomin + hesperidine used did not cause toxic effects on the renal tissue. In conclusion, we are of the opinion that Diosmin+Hesperidine given to rats with induced renal ischemia-reperfusion reduces the ischemia-reperfusion injury upto a certain extent but do not bring about a statistically significant recovery of the ischemia-reperfusion injury. Key Words: Ischemia reperfusion injury, kidney, Diosmin+Hesperidine.
Abstract
By reducing cellular energy levels and causing an accumulation of toxic metabolites in tissue, ischemia triggers a chain of biochemical reactions that cause cell dysfunction and even cell death. After reperfusion, when the harmful effects of neutrophils and the mediators they produce are added to the setting, organ injury or even death become inevitable. In clinical conditions like hypotension, hypovolemic shock, cardiac arrest, renalvascular surgery or clamping of the aorta, hot ischemia reperfusion injuries may occur in the kidney. The degree of injury increases with the duration of ischemia and as a result different clinical conditions ranging from prerenal azotemia without distinctive tissue damage to acute kidney failure resulting from tubular or cortical necrosis come about. In our trial we investigated whether Diosmin+Hesperidine were effective in ischemia-reperfusion injury (renal ischemia-reperfusion) by looking at malondialdehyde and glutation in the renal tissue, and serum urea and creatinine together with renal histopathology in rats with induced ischemia-reperfusion. In our trial, 40 female Sprague-Dawley rats weighing 190-250 gr were used. The rats were assigned to 4 groups consisting of 10 rats each. In the control group (group 1, n=10 ) only standard water and food were given and after seven days laparotomy was performed and intracardiac blood and renal tissue samples were taken. In the Diosmin+Hesperidine group (group 2, n=10 ) 50 mg/kg Diosmin+Hesperidine were given through orogastric gavage at the same time everyday for seven days and after seven days laparotomy was performed and intracardiac blood and renal tissue samples were taken. In the ischemia-reperfusion group (group 3,n=10) only standard water and food were given for seven days and after seven days laparotomy was performed. Bilateral renal pedicules were occluded for 45 minutes then reperfusion was performed over 24 hours. In the Ischemia-reperfusion+Diosmin+Hesperidine group (group 4, n=10) 50 mg/kg Diosmin+Hesperidine were given through orogastric gavage at the same time everyday for seven days. After seven days laparotomy was performed and bilateral renal pedicules were occluded for 45 minutes then over 24 hours reperfusion was performed.In groups 3 and 4, after 24 hours of reperfusion relaparotomy was performed on the rats and intracardiac blood and renal tissue samples were taken. When the control, Diosmin+Hesperidine, Ischemia-reperfusion and Ischemia-reperfusion+Diosmin+Hesperidine groups were compared it was discovered that in the Ischemia-reperfusion group statistically significant low glutation in renal tissue, and high serum urea and creatinine showed that the ischemia we induced caused kidney injury. Although statistically insignificant we discovered that in the kidneys, the Diosmin+ Hesperidine we used reduced harmful effects in such injuries. Compared to the İschemia-reperfusion group, in the Ischemia-reperfusion+Diosmin+Hesperidine group the serum urea and creatinine levels were lower, and the renal tissue glutation levels were higher; although the difference was statistically insignificant. The fact that no significant difference was seen in terms of renal tissue glutation levels or serum urea and creatinine levels between the control and Diosmin+Hesperidine groups supports the fact that the dose of diomin + hesperidine used did not cause toxic effects on the renal tissue. In conclusion, we are of the opinion that Diosmin+Hesperidine given to rats with induced renal ischemia-reperfusion reduces the ischemia-reperfusion injury upto a certain extent but do not bring about a statistically significant recovery of the ischemia-reperfusion injury. Key Words: Ischemia reperfusion injury, kidney, Diosmin+Hesperidine.
Açıklama
Tıpta Uzmanlık Tezi
Anahtar Kelimeler
İskemi-Reperfüzyon Hasarı, Böbrek, Diosmin +Hesperidin, Ischemia Reperfusion Injury, Kidney, Diosmin+Hesperidine
