Acute kidney injury provokes liver dysfunction, which is an aggravating factor for effective treatment. In this study, ischemic-reperfusion kidney injury was used as a model. Since the main damaging factor in this case is the hyperproduction of reactive oxygen species, to prevent liver injury under kidney injury, an exogenous antioxidant enzyme peroxyredoxin 6 was used, which is able to neutralize the hyperproduction of a wide range of reactive oxygen species. Kidney injury was initiated by 45 min ischemia with simultaneous left-sided nephrectomy. The liver was not manipulated. Peroxiredoxin 6 was administered intravenously 15 min before ischemia. Liver condition was assessed 2, 5 and 24 h after kidney reperfusion by histological and biochemical methods. The maximum signs of liver injury were detected after 5 h of kidney reperfusion. The use of peroxiredoxin 6 led to a decrease in the severity of vascular reaction and leukocyte infiltration in the liver, a decrease in the degree of dystrophy and apoptosis of hepatocytes, the absence of an increase in the concentration of TBA-reactive products and stabilization of the level of cytokines IL-6, IL-10 in liver tissue, as well as normalization of the activity of intracellular transferases in the blood with the onset of reperfusion. The protective effect of peroxiredoxin 6 was primarily associated with its antioxidant properties, which make it possible to neutralize the hyperproduction of reactive oxygen species at the initial period of kidney reperfusion; however, the contribution of the signal-regulatory function of the protein to its protective effect should not be excluded.

Oxidative stress caused by ischemia–reperfusion kidney injury may play a key role in liver dysfunction. To reduce liver and kidney damage in ischemia–reperfusion kidney injury, an exogenous enzyme antioxidant peroxiredoxin 6 was used, which is able to restore a wide range of hydroperoxides and is a participant in intracellular and intercellular signal transmission. Rats were subjected to ischemic kidney injury for 45 min with simultaneous left-sided nephroectomy and examined after 24 and 48 h of reperfusion. Peroxiredoxin 6 was administered intravenously 15 min before ischemia. Injury to the renal and hepatic tissues was determined by histological methods; in addition, the concentrations of creatinine, urea, alanine aminotransferase and aspartate aminotransferase in the blood were measured to assess the functionality of the organs. Reperfusion led to an increase in the concentrations of creatinine, urea, alanine aminotransferase and aspartate aminotransferase in blood plasma; there was also violation of the architecture of renal nephrons and the development of a pronounced vascular reaction in the liver with foci of degenerative changes. The use of exogenous peroxiredoxin 6 led to a decrease in the damage to the renal and hepatic tissues and normalization of the level of renal and hepatic metabolites. Thus, peroxiredoxin 6 showed both a nephroprotective effect in renal ischemia–reperfusion and reduced morphofunctional damage to distant organs, in particular, the liver.

Окислительный стресс, вызванный ишемически-реперфузионным поражением почек, может играть ключевую роль в дисфункции печени. Для снижения поражения печени и почек при ренальном ишемически-реперфузионном поражении в работе использовали экзогенный фермент-антиоксидант пероксиредоксин 6, который способен восстанавливать широкий спектр гидропероксидов и является участником во внутриклеточной и межклеточной передаче сигналов. Крыс подвергали ишемическому поражению почек в течение 45 мин с одновременной левосторонней нефроэктомией и обследовали через 24 и 48 ч реперфузии. Пероксиредоксин 6 вводили внутривенно за 15 мин до ишемии. Повреждение почечной и печеночной тканей определяли гистологическими методами, для оценки функциональности органов измеряли концентрации креатинина, мочевины, аланинаминотрансферазы и аспартатаминотрасферазы в крови. Реперфузия привела к увеличению концентраций креатинина, мочевины, аланинаминотрансферазы и аспартатаминотрасферазы в плазме; нарушению архитектуры почечных нефронов и развитию выраженной сосудистой реакции в печени с очагами дегенеративных изменений. Использование экзогенного пероксиредоксина 6 привело к снижению поражения ренальной и печеночной тканей и нормализации уровня почечных и печеночных метаболитов. Таким образом, пероксиредоксин 6 проявляет как нефро-протекторный эффект при ренальной ишемии-реперфузии, так и уменьшает морфофункциональное повреждение отдаленных органов, в частности печени.