The effect of dexmedetomidine nanocrystals on the proliferation and metabolism of lymphocytes behind the ears through the JAK2/STAT3 signaling pathway

Dexmedetomidine affects the activity of lymphocytes behind the head, but the molecular mechanism is unclear. 40 SPF SD rats were separated into control group, dexmedetomidine group, pathway inhibitor group, and positive control group, followed by analysis of CD4+, CD4+/CD8+, CD8+ T cell ratios, T lymphocyte proliferation inhibition rate, expression of T lymphocyte metabolism-related genes such as beta-ACTIN, HIF1A, GLUT1, HK2 and JAK2/STAT3 signaling pathway factors such as p-JAK2, p-STAT3, JAK2, STAT3. The ratios of CD4+ and CD4+/CD8+ T cells in dexmedetomidine group and positive control group were higher and that of CD8+ T cells was lower, which all showed opposite changes in pathway inhibitor group. Cell proliferation inhibition rates in dexmedetomidine and positive control group were markedly lower and those of control group and pathway inhibitor group were both higher. The expression of beta-ACTIN, HIF1A, GLUT1 and HK2 related to T lymphocyte metabolism were the lowest in dexmedetomidine group and positive control group (P < 0.05), while control group and the pathway inhibitor group were higher (P < 0.05). The expression of p-JAK2 and p-STAT3 were the highest in dexmedetomidine group (P < 0.05). Dexmedetomidine nanocrystals can inhibit the expression of T lymphocyte metabolism-related genes such as beta-ACTIN, HIF1A, GLUT1, and HK2, thereby down-regulating CD4+/CD8+ cells, inhibiting proliferation and metabolism of lymphocytes behind the head and ears, and maintaining the number and function of T lymphocytes. The molecular mechanism of dexmedetomidine is related to the JAK2/STAT3 pathway, which can be used as a target for dexmedetomidine nanocrystals to improve the proliferation and metabolism of lymphocytes.