اثر دگزامتازون بر آسیب گلیکوکالیکس بافت کبد و بیان ژن گیرنده نوع B اندوتلین طی ایسکمی- ریپرفیوژن کبدی در رت

Background and purpose: Damage caused by ischemia/reperfusion (I/R) is one of the major causes of liver failure during surgeries. Endothelin as the main vasoconstrictor has two receptors; ETA and ETB. Increased number of ETB during ischemia-reperfusion, reduces tissue damages by sinusoidal dilation. This study investigated the effects of dexamethasone against liver endothelial glycocalyx injury and ETB receptor gene expression during hepatic ischemia/reperfusion in rats. Materials and methods: Thirty two male Wistar rats were divided into four groups; a SHAM-operated group that received normal saline, DEX; which had dexamethasone injection (10 mg/kg), the I/R; received normal saline during ischemia/reperfusion, and the DEX + IR with I/R that received dexamethasone (10 mg/kg, 60 minutes before ischemia and immediately after reperfusion). After 1 hour of ischemia and 3 hours of reperfusion the blood samples and liver tissues were collected. The relative gene expression of ETB was assessed by real time PCR. Serum samples were used to measure the level of ALT and AST and hyaluronic acid (HA). Results: The level of ALT, AST and HA significantly increased in I/R compared with those of the SHAM-operated group (P<0.001). Injection of dexamethasone in the DEX+IR caused a significant reduction in serum indicators compared to those of the I/R group (P<0.001). Elevated ETB receptor gene expression reduced by dexamethasone injection (P> 0.05). Conclusion: Dexamethasone decreased ETB receptor gene expression during liver I/R. In addition, it significantly protected the parenchymal cells and sinusoidal endothelial glycocalyx. Therefore, dexamethasone could play an important role in reducing liver injury during I/R.