One of the pressing issues in regenerative medicine is the restoration of somatic nerve function after injury. In this study, extraction methods were used to obtain lipids from nervous tissue, followed by chromatographic separation, quantitative analysis via densitometry, and qualitative and quantitative analyses of the fatty acid composition through gas chromatography. The results showed that nerve cutting results in the accumulation of all forms of phosphoinositides and a decrease in diacylglycerol (DAG) levels in both the proximal and distal segments of the nerve conductor. This phenomenon is likely attributable to the inactivation of phosphoinositide-specific phospholipase C and the activation of lipolytic enzymes, particularly phospholipases A₁ and A₂, resulting in an increase in the amount of free fatty acids (FFAs). The intramuscular administration of insulin-like growth factor-1 (IGF-1) was associated with enhanced phosphoinositide metabolism, increased DAG levels, reduced FFA levels, and a redistribution of fatty acids within the studied lipid fractions. The registration method of action potentials demonstrated the restoration of nerve conduction in the proximal segment of somatic nerves following the introduction of IGF-1. This correlates with our findings regarding alterations in the lipid fraction composition of damaged nerve conductors in response to the drug’s effects. Most likely, IGF-1 exerts its effects through activation of the phosphoinositide-specific phospholipase C and phosphatidylinositol-3 kinase signaling pathways, which are necessary for axonal regeneration and the restoration of functioning damaged nerve conductors.

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.