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Triamcinolone is a synthetic glucocorticoid.1,2 It increases expression of the calcitonin receptor in murine osteoclast-like cells when used at a concentration of 1 μM.3 Triamcinolone (3 mg/kg, s.c.) reduces heat hyperalgesia and mechano-allodynia and decreases the number of TNF-α-positive mast cells in injured sciatic nerve in a rat model of chronic constriction injury-induced neuropathic pain.1 It also reduces levels of the glycosaminoglycans (GAGs) hyaluronic acid and chondroitin-4-sulfate in human keloid implants in athymic nude mice.4 Triamcinolone has been used in the formation of lipid nanoparticles (LNPs) for the delivery of mRNA in vitro and in vivo.5 LNPs containing triamcinolone and encapsulating reporter mRNA reduce LNP-induced increases in the serum levels of inflammatory cytokines in mice to a greater extent than LNPs that do not contain triamcinolone. LNPs containing triamcinolone and encapsulating MOG35-55 mRNA reduce spinal cord CD3+ T cell infiltration and disease severity in a mouse model of experimental autoimmune encephalomyelitis (EAE).
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1. Systemic glucocorticoid therapy reduces pain and the number of endoneurial tumor necrosis factor-
2. Effects of triamcinolone on carbohydrate synthesis by rat liver slices. The Journal of Biological Chemisty 238(9), 2906-2911 (1963).
3. Regulation by calcitonin and glucocorticoids of calcitonin receptor gene expression in mouse osteoclasts. Endocrinology 138(2), 521-529 (1997).
4. Involution of keloid implants in athymic mice treated with pirfenidone or with triamcinolone. J. Lab Clin. Med. 132(6), 491-496 (1998).
5. Ionizable lipid-