Dietary curcumin and capsaicin: Relationship with hepatic oxidative stress and apoptosis in rats fed a high fat diet
Erişim
info:eu-repo/semantics/openAccessTarih
2019Yazar
Tannkulu-Kucuk, SevdaBasaran-Kucukgergin, Canan
Sogut, Ibrahim
Tuncdemir, Matem
Dogru-Abbasoglu, Semra
Seyithanoglu, Muhammed
Oner-Iyidogan, Yidiz
Üst veri
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Background. Apoptosis plays a major role in fatty liver disease. High-fat diets are related to the onset of fatty liver disease and hepatic oxidant-antioxidant imbalance. Curcumin and capsaicin are somewhat beneficial in reducing hepatic triglycerides; this is most likely because they are known to downregulate reactive oxygen species (ROS) and apoptosis. Objectives. the aim of this study was to investigate the effects of curcumin and capsaicin on apoptosis through the oxidative effect in an animal model of fatty liver disease. Material and methods. Male Sprague-Dawley rats were fed a normal control diet, a high-fat diet (HFD; 60% of total calories from fat), a HFD+curcumin (1.5 g curcumin/kg HFD), a HFD+capsaicin (0.15 g capsaicin/kg HFD), or a HFD+curcumin+capsaicin (1.5 g curcumin and 0.15 g capsaicin/kg HFD). Liver lysate levels of BAX, Bcl-2 and caspase-3 were determined via immunoblotting. Caspase-3 activity was measured with a colorimetric caspase-3 measurement kit. Total antioxidant status (TAS) and total oxidant status (TOS) were assayed using commercial kits. the generation of hepatic ROS was measured with fluorimetry. Fragmentation of DNA was detected using the TUNEL method. Results. High-fat diet caused increased expression of BAX and caspase-3, as well as increased TOS and caspase-3 activity, but decreased expression of Bcl-2. HFD+curcumin+capsaicin caused decreased BAX, caspase-3, TOS, and ROS levels as compared to HFD, but increased TAS and Bcl-2. A HFD +curcumin+capsaicin also decreased the number of TUNEL-positive cells. Conclusions. These results suggest that supplementation with curcumin and capsaicin balances the hepatic oxidant-antioxidant status and may have a protective role in the apoptotic process in an HFD-induced fatty liver model.