Kadmiyumun hepatoksik etkilerine yönelik ursodeoksikolik asitin koruyucu etkisinin araştırılması
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Dosyalar
Tarih
2024
Yazarlar
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Yayıncı
Selçuk Üniversitesi, Sağlık Bilimleri Enstitüsü
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Teratojenik ve karsinojenik etkileri olan toksik çevresel kirleticilerden Kadmiyum (Cd), vücuda alındıktan sonra çeşitli sistem ve dokulardaki hücreleri ve kemikleri etkileyerek toksisiteye sebep olur. Ursodeoksikolik asit (UDCA), genellikle karaciğer hastalıklarının tedavisinde kullanılan bir safra asitidir ve sistemik sirkülasyonda ve karaciğerde biriken güçlü toksik bileşenlerin mobilizasyonunu sağlar. Çalışmamızda 28 erkek Wistar Albino rat (180-220 gr) dört gruba ayrıldı: (1. Kontrol (K, n:6) grubu; 2.Kadmiyum (Cd, n:8) grubu; 3.Ursodeoksikolik asit (UDCA, n:6) grubu; 4. Kadmiyum ve ursodeoksikolik asit grubu (Cd+UDCA, n:8). 16 gün süren çalışmada tüm ratlara ad-libitum standart yem ve içme suyu; Cd grubuna denemenin 8-15. günlerinde 3 mg/kg CdCl2 intraperitonel (IP); UDCA grubuna 1- 15.günlerinde 60mg/kg UDCA intragastrik (IG); Cd+UDCA grubuna ise 3mg/kg CdCl2 ve 60 mg UDCA uygulandı. Deneme süresi sonunda, alınan kan örneklerinde ALT, AST, ALP ve GGT düzeylerinin Cd grubunda artış sergilediği gözlenirken, Cd+UDCA grubunda tüm parametrelerde rakamsal olarak azalma gözlenmesine karşın bu durum ALT ve GGT'de istatistiksel olarak anlamlı bulundu (p<0.05). Cd grubunda canlı ağırlık ve relatif karaciğer ağırlığı önemli oranda azalırken (p<0.001), Cd+UDCA grubunda bu durumun önüne geçildiği saptandı (p>0.05). Histopatolojik olarak Cd grubunda, kontrol gruplarına kıyasla dejenerasyon, nekroz, safra kanalı proliferasyonu, disintegrasyon, konjesyon, Kupffer aktivasyonu ve mononükleer hücre infiltrasyonu artışıyla karakterize hepatoselüler hasar belirlendi. Ayrıca, karaciğer dokusunda Nrf2 ve Kaspaz-3 mRNA ekspresyonunun CdCl2 ile önemli oranda arttığı ortaya konuldu (p<0.001). Sonuç olarak, CdCl2 tarafından oluşturulan karaciğer toksisitesine karşı UDCA'nın belirgin bir hepatoprotektif etki sergilediği sonucuna ulaşıldı.
Cadmium (Cd), a toxic environmental pollutant with teratogenic and carcinogenic effects, causes toxicity by affecting cells and bones in various systems and tissues after ingestion. Ursodeoxycholic acid (UDCA) is a bile acid generally used in the treatment of liver diseases and provides mobilisation of strong toxic components accumulated in the systemic circulation and liver. In our study, 28 male Wistar Albino rats (180-220 g) were divided into four groups (1. Control (C, n:6) group; Cadmium (Cd, n:8) group; 3. Ursodeoxycholic acid (UDCA, n:6) group; 4. Cadmium and ursodeoxycholic acid group (Cd+UDCA, n:8). In the 16-day study, ad-libitum standard feed and drinking water were administered to the control group; 3 mg/kg CdCl2 intraperitoneally (IP) to the Cd group on the 8th-15th days of the experiment; 60 mg/kg UDCA intragastric (IG) to the UDCA group on the 1st-15th days; 3 mg/kg CdCl2 and 60 mg UDCA to the Cd+UDCA group. At the end of the experimental period, ALT, AST, ALP and GGT levels in the blood samples were found to increase in the Cd group, whereas a numerical decrease was observed in the Cd+UDCA group, but this was statistically significant in ALT and GGT (p<0.05). Relative liver weight decreased significantly in the Cd group (p<0.001), whereas this was prevented in the Cd+UDCA group (p>0.05). A histopathological examination revealed that the Cd group exhibited hepatocellular damage, characterised by degeneration, necrosis, bile duct proliferation, disintegration, congestion, Kupffer cell activation, and increased mononuclear cell infiltration, in comparison to the control groups. Furthermore, the Nrf2 and Caspase-3 mRNA expression levels in the liver tissue were found to be significantly elevated in the CdCl2 group (p < 0.001). The results indicated that UDCA exhibited a significant hepatoprotective effect against CdCl2-induced liver toxicity.
Cadmium (Cd), a toxic environmental pollutant with teratogenic and carcinogenic effects, causes toxicity by affecting cells and bones in various systems and tissues after ingestion. Ursodeoxycholic acid (UDCA) is a bile acid generally used in the treatment of liver diseases and provides mobilisation of strong toxic components accumulated in the systemic circulation and liver. In our study, 28 male Wistar Albino rats (180-220 g) were divided into four groups (1. Control (C, n:6) group; Cadmium (Cd, n:8) group; 3. Ursodeoxycholic acid (UDCA, n:6) group; 4. Cadmium and ursodeoxycholic acid group (Cd+UDCA, n:8). In the 16-day study, ad-libitum standard feed and drinking water were administered to the control group; 3 mg/kg CdCl2 intraperitoneally (IP) to the Cd group on the 8th-15th days of the experiment; 60 mg/kg UDCA intragastric (IG) to the UDCA group on the 1st-15th days; 3 mg/kg CdCl2 and 60 mg UDCA to the Cd+UDCA group. At the end of the experimental period, ALT, AST, ALP and GGT levels in the blood samples were found to increase in the Cd group, whereas a numerical decrease was observed in the Cd+UDCA group, but this was statistically significant in ALT and GGT (p<0.05). Relative liver weight decreased significantly in the Cd group (p<0.001), whereas this was prevented in the Cd+UDCA group (p>0.05). A histopathological examination revealed that the Cd group exhibited hepatocellular damage, characterised by degeneration, necrosis, bile duct proliferation, disintegration, congestion, Kupffer cell activation, and increased mononuclear cell infiltration, in comparison to the control groups. Furthermore, the Nrf2 and Caspase-3 mRNA expression levels in the liver tissue were found to be significantly elevated in the CdCl2 group (p < 0.001). The results indicated that UDCA exhibited a significant hepatoprotective effect against CdCl2-induced liver toxicity.
Açıklama
Anahtar Kelimeler
Toksik, Histopatoloji, Kadmiyum, Karaciğer, Ursodeoksikolik Asit, Cadmium, Toxic, Histopathology, Liver, Ursodeoxycholic Acid
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Künye
Sarıhan, Ö. (2024). Kadmiyumun hepatoksik etkilerine yönelik ursodeoksikolik asitin koruyucu etkisinin araştırılması. (Yüksek Lisans Tezi). Selçuk Üniversitesi, Sağlık Bilimleri Enstitüsü, Konya.
