Abstract

A comorbid condition both in diabetes mellitus and in metabolic syndrome is fatty dystrophy of the liver that further progresses to hepatic necrosis. In the article variants of pharmacological correction of ischemia-reperfusion of the liver with agonists of imidazoline receptor are proposed.
 Materials and Methods. The experiment was conducted on 70 rats of both sexes divided into 7 groups (n=10): intact group; pseudo-operated animals (incision of the abdominal wall without ligation of hepatic vessels); animals subject to ischemia/reperfusion without drug correction; animals subject to ischemia/reperfusion of the liver + metformin (50 mg/kg); animals subject to ischemia/reperfusion of the liver + moxonidine (1 μg/kg); animals subject to ischemia/reperfusion of the liver+С7070 (10 mg/kg). For evaluation coefficients were used calculated from the level of hepatic transaminases: alaninaminotranspherase (ALT), aspartataminotranspheras (AST), – and also from morphometric ratios of the areas of necrosis and deep ischemia of the liver on the basis of histological examination.
 Results. Agonist of peripheral imidazoline receptors C7070 reduces ischemic-reperfusion damages to the liver to a significantly larger extent than moxonidine and metformin. Hepatoprotective effect of C7070 was removed by preliminary introduction of peripheral imidazoline receptor blocker. ALT/AST coefficients for C7070, moxonidine and metformin were 72.8/62.13; 44.99/34.20 and 36.88/21.02, respectively. Coefficients of morphological hepatoprotective activity of the drugs were: С7070 – 82.61, moxonidine – 72.33, metformin – 38.96.
 Conclusion. Agonists of imidazoline receptors reliably and significantly reduce functional and morphological manifestations of ischemia/reperfusion of the liver.

Highlights

  • Как при сахарном диабете, так и при метаболическом синдроме в виде коморбидного состояния развивается жировая дистрофия печени, переходящая далее в некроз печени

  • A comorbid condition both in diabetes mellitus and in metabolic syndrome is fatty dystrophy of the liver that further progresses to hepatic necrosis

  • The experiment was conducted on 70 rats of both sexes divided into 7 groups (n=10): intact group; pseudo-operated animals; animals subject to isch emia/reperfusion without drug correction; animals subject to ischemia/reperfusion of the liver + metformin (50 mg/kg); animals subject to ischemia/reperfusion of the liver + moxonidine (1 μg/kg); animals subject to ischemia/reperfusion of the liver+С7070 (10 mg/kg)

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Summary

ОРИГИНАЛЬНОЕ ИССЛЕДОВАНИЕ ORIGINAL STUDY

Коэффициенты морфологической гепатопротекторной активности препаратов составили: РОССИЙСКИЙ МЕДИКО-БИОЛОГИЧЕСКИЙ ВЕСТНИК имени академика И.П. Ключевые слова: ишемия печени, реперфузия печени, сахарный диабет, С7070, моксонидин, метформин, агонисты имидазолиновых рецепторов. Agonist of peripheral imidazoline receptors C7070 reduces ischemic-reperfusion damages to the liver to a significantly larger extent than moxonidine and metformin. Эксперимент проводился на 70 крысах обоего пола, разделённых на 7 групп: интактная группа, ложнооперированные животные (вскрытие брюшной стенки без лигирования печёночных сосудов); животные с моделированной ишемией/реперфузией, не получающие терапию каким-либо препаратом; животные с моделированной ишемией / реперфузией, получающие терапию препаратом метформин (50 мг/кг); животные с моделированной ишемией/реперфузией, получающие терапию препаратом моксонидин (1 мкг/кг); животные с моделированной ишемией / реперфузией, получающие терапию препаратом С7070 (10 мг/кг); животные с моделированной ишемией / реперфузией, получающие терапию препаратом С7070 (10 мг/кг) с одновременным введением антагониста периферических имидазолиновых рецепторов BU224 (BU224 hydrochloridesolid, SigmaAldrich, Switzerland).

ОРИГИНАЛЬНОЕ ИССЛЕДОВАНИЕ
Группы животных

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