| Autor: |
Kryl'skii ED; Department of Medical Biochemistry and Microbiology, Voronezh State University, Voronezh, Voronezh region 394018, Russia., Sinitsyna DA; Department of Medical Biochemistry and Microbiology, Voronezh State University, Voronezh, Voronezh region 394018, Russia., Popova TN; Department of Medical Biochemistry and Microbiology, Voronezh State University, Voronezh, Voronezh region 394018, Russia., Shikhaliev KS; Department of Organic Chemistry, Voronezh State University, Voronezh, Voronezh region 394018, Russia., Medvedeva SM; Department of Organic Chemistry, Voronezh State University, Voronezh, Voronezh region 394018, Russia., Matasova LV; Department of Medical Biochemistry and Microbiology, Voronezh State University, Voronezh, Voronezh region 394018, Russia., Mittova VO; Department of Clinical Laboratory Diagnostics, Voronezh State Medical University named after N.N. Burdenko, Voronezh, Voronezh region 394036, Russia. |
| Abstrakt: |
Liver diseases with the central pathogenetic mechanism of oxidative stress are one of the main causes of mortality worldwide. Therefore, dihydroquinoline derivatives, which are precursors of hepatoprotectors and have antioxidant activity, are of interest. We have previously found that some compounds in this class have the ability to normalize redox homeostasis under experimental conditions. Here, we initially analyzed the hepatoprotective potential of the dihydroquinoline derivative 1-benzoyl-6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline (BHDQ) for carbon tetrachloride (CCl 4 )-induced liver injury in rats. Results suggested that BHDQ normalized the alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transpeptidase in serum. We also observed an improvement in liver tissue morphology related to BHDQ. Animals with CCl 4 -induced liver injuries treated with BHDQ had less oxidative stress compared to animals with CCl 4 -induced liver injury. BHDQ promoted activation changes in superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione transferase on control values in animals with CCl 4 -induced liver injury. BHDQ also activated gene transcription in Sod1 and Gpx1 via nuclear factor erythroid 2-related factor 2 and forkhead box protein O1 factors. Therefore, the compound of concern has a hepatoprotective effect by inhibiting the development of necrotic processes in the liver tissue, through antioxidation. |
