A wound healing agent was found in the skin
Oleg Lischuk, N+1.
Italian and American scientists have discovered substances in the skin that regulate wound healing. They can become the basis for effective wound healing drugs. The report on the work is published in the journal Proceedings of the National Academy of Sciences.
Employees of the Italian Institute of Technology in Genoa, the Dermatological Institute of San Gallicano in Rome and the University of California at Irvine discovered fatty acid amide hydrolase (HFA) in the skin of mice, an enzyme that inactivates several classes of biologically active substances. These substances include ethanolamides of polyunsaturated fatty acids that activate cannabinoid receptors; ethanolamides of saturated and monounsaturated fatty acids acting on the transcription factor PPAR-α (alpha receptor activated by the proliferator peroxisom), and amides of long-chain fatty acids with taurine (N-acyltaurines, NAT), the physiological role of which is not sufficiently clear.
The localization of GHK in the skin has led scientists to believe that this enzyme can take part in wound healing processes. The genetic and pharmacological blocking of the HCA confirmed this guess – surgical skin incisions in mice healed significantly faster than under normal conditions. In an experiment with human cell cultures, it stimulated the proliferation of keratinocytes and fibroblasts, a process responsible for skin repair.
Since the enzyme acts by inactivating biologically active compounds, the researchers searched for its target, which is responsible for wound healing. Chromatographic mass spectrometry of lipid extracts of the skin with subsequent statistical modeling showed that the desired substances are N-teracosanoyltaurine, or NAT (24:0), and N-eicosanoyltaurine, or NAT (20:0).
Further experiments have shown that the content of these substances in the edges of a fresh wound is sharply reduced compared to intact skin and is restored during the healing process. Treatment of wound edges with synthetic NAT(24:0) and NAT(20:0) caused a dose-dependent acceleration of healing in mice. The same substances added to the culture of human keratinocytes and fibroblasts stimulated the processes corresponding to wound healing.
Screening of the effect of NAT on various molecular signaling pathways of the skin showed that its effect is associated with phosphorylation of receptors for epithelial growth factor and an increase in intracellular calcium concentration – processes key to healing.
According to the researchers, the drugs that block GHA and synthetic analogues of NAT(24:0) and NAT(20:0) may become promising agents for the treatment of chronic non-healing skin lesions, such as bedsores, diabetic ulcers and wounds in patients with immunosuppression.
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13.07.2016