The Effects of Apigenin on the Expression of Fas/FasL Apoptotic Pathway in Warm Liver Ischemia-Reperfusion Injury in Rats

Abstract

Background. The aim of this experimental study was to investigate the role of apigenin in liver apoptosis, in an experimental model of hepatic ischemia-reperfusion in rats. Materials and Methods. Forty-eight Wistar rats (apigenin and control groups), 14 to 16 weeks old and weighing 220 to 350 g, were used. They were all subjected to hepatic ischemia by occlusion of the hepatic artery and portal vein for 45 minutes and reperfusion was followed for 60, 120, and 240 minutes. Apigenin was administrated intraperitoneally. Liver tissues were used for the detection of apoptosis by TUNEL assay and caspase 3 antibodies. Expression analysis of Fas/FasL genes was evaluated by real time PCR. Results. The expression analysis of Fas and FasL genes was increasing during reperfusion (significantly in the group of 240 minutes of reperfusion). It was in the same group that apigenin decreased Fas receptor levels and inhibited apoptosis as confirmed by TUNEL assay and caspase 3 antibodies. Conclusions. The effects of apigenin in the Fas/FasL mediated pathway of apoptosis, in the hepatic ischemia-reperfusion, seem to have a protective result on the hepatic cell.

MiR‐27a‐5p regulates apoptosis of liver ischemia‐reperfusion injury in mice by targeting Bach1

“…15 One of the typical features of liver diseases, such as I/R injury, is cell death, and apoptosis is the mainly pattern of it. 10 Bach1 plays an important role in targeting the Hmox1 (HO-1) gene; 17 by binding to the Maf recognition elements of the HO-1 gene, it inhibits transcription. Apoptosis repression represents a way to improve hepatocyte survival and minimize reperfusion injury.…”

“…6 The HO-1 enzyme can degrade the heme into carbon monoxide (CO), free iron, and biliverdin; 7 these products serve antiapoptotic and anti-inflammatory functions. 9 I/R injury is a continuous process; in the ischemic phase, the main injury is caused by oxygen-dependent cells 10 and in the reperfusion phase, the injury is enhanced by the accumulation of metabolic products, which leads to the generation of some toxic substances, such as free radicals, that eventually induce apoptosis. 9 I/R injury is a continuous process; in the ischemic phase, the main injury is caused by oxygen-dependent cells 10 and in the reperfusion phase, the injury is enhanced by the accumulation of metabolic products, which leads to the generation of some toxic substances, such as free radicals, that eventually induce apoptosis.…”

“…9 I/R injury is a continuous process; in the ischemic phase, the main injury is caused by oxygen-dependent cells 10 and in the reperfusion phase, the injury is enhanced by the accumulation of metabolic products, which leads to the generation of some toxic substances, such as free radicals, that eventually induce apoptosis. 12 Meanwhile, the caspase family is one of the basic molecules in apoptosis 10 and the extent of injury is reflected by its activity. 12 Meanwhile, the caspase family is one of the basic molecules in apoptosis 10 and the extent of injury is reflected by its activity.…”

“…11 The Bcl-2 family is the fundamental regulator of the intrinsic apoptosis pathway. 12 Meanwhile, the caspase family is one of the basic molecules in apoptosis 10 and the extent of injury is reflected by its activity. 11 MicroRNAs (miRNAs) are small noncoding RNAs (~18 to 24 nucleotides) that negatively regulate gene expression by binding to the 3′-untranslated region (UTR) of target messenger RNAs (mRNAs).…”

Intraperitoneal administration of apigenin in liver ischemia/reperfusion injury protective effects

“…[30] Even more specifically in hepatic ischemia-reperfusion injury, Tsalkidou et al ., in 2014, have demonstrated that apigenin seems to affect the Fas/FasL mediated pathway of apoptosis, resulting in apoptosis inhibition. [31]…”