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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. [ABSTRACT FROM AUTHOR]

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-specifi c 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 diff erent. 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 signifi cant changes in the level of phosphatidylinositol and diacylglycerol indicate that potassium hyaluronate most likely exerts its eff ect through the PL A2 -mediated pathway. In addition, it was shown that against the background of the action of IGF-1, an intensifi cation of phosphoinositide metabolism is observed, which is explained by the activation of phosphoinositidespecifi c 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.

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 levels of neurotrophic factors and the protein composition of somatic nerve membranes were studied during injury and survival of nerves in rats exposed to the action of clobetasol. It was shown that the drug administered intramuscularly induced a more pronounced increase in the level of neurotrophic growth factors and structural proteins responsible for recovery processes than the drug released from a hydrogel derived from microbial polysaccharides; it also stabilized the content of the total protein fraction in the damaged somatic nerves. Proteins of the injured neural conductor degraded less in animals receiving intramuscular injections of clobetasol, probably because the drug administered by injection had better availability than the drug administered from hydrogel composite (slow drug release). In addition, an increase in the amounts of DNA and some protein fractions indicated that clobetasol contributed the activation of genes associated with remyelination. We suppose that clobetasol can stimulate synthesis of neurotrophic growth factors, thereby triggering the phosphatidylinositol-3-kinase and mitogen-activated protein kinase signaling pathways that regulate the processes of cytoskeletal reorganization and axonal growth, as well as enhance the synthesis of structural and axonal proteins necessary to restore the functional activity of the injured nerve fibers. [ABSTRACT FROM AUTHOR]