Study of the influence of various physiologically active substances on changes in the lipid composition and phospholipase activity of damaged somatic nerves

The changes in lipid composition and phospholipase activity in damaged somatic nerves were studied against the background of the action of potassium hyaluronate and insulin-like growth factor-1. It has been shown that nerve cutting is accompanied by an increase in phospholipase A2 activity, resulting in an accumulation of lysophospholipids and free fatty acids, as well as an increase in phosphatidylinositol levels and a decrease in diacylglycerol content, which is most likely due to inactivation of phosphoinositide-specific phospholipase C against the background of injury to the nerve conductor. The introduction of potassium hyaluronate and insulin-like growth factor-1 enhances the recovery processes in the injured nerve conductor, however, the mechanisms of their action remain different. According to the literature data and the results of our own research, the action of potassium hyaluronate and insulin-like growth factor-1 is realized as a result of the launch of signaling pathways associated with the regulation of the activity of enzymes from the phospholipase family. At the same time, our data on a decrease in the activity of phospholipase A2 and the absence of significant changes in the level of phosphatidylinositol and diacylglycerol indicate that potassium hyaluronate most likely exerts its effect through the PL A2-mediated pathway. In addition, it was shown that against the background of the action of IGF-1, an intensification of phosphoinositide metabolism is observed, which is explained by the activation of phosphoinositidespecific phospholipase C. According to the literature, the launch of the phospholipase C-mediated mechanism is accompanied by the formation of components of the phosphatidylinositol 3-kinase signaling pathway involved in stimulation of the expression of various transcription factors necessary for axonal regeneration and restoration of the functioning of injured nerve conductors.