Reticuline

Reticuline shows anti-inflammatory effects through JAK2/STAT3 and NF-κB signaling pathways. Reticuline inhibits mRNA expressions of TNF-α, and IL-6 and reduces the phosphorylation levels of JAK2 and STAT3^[1]. Reticuline exhibits cardiovascular effects^[2]. In Vitro: Reticuline (3 μM, 30 μM, 300 μM, 900 μM and 1.5 mM) inhibits in a concentration-dependent manner the contractions induced by Phenylephrine (1 μM), KCl (80 mM) and KCl (30 mM), (IC₅₀=40±10, 240±40 and 300±40 μM, respectively) in isolated rat aortic rings with intact endothelium^[2].
Reticuline (3 μM, 30 μM, 300 μM, 900 μM and 1.5 mM) antagonizes CaCl₂-induced contractions, and also inhibits the intracellular calcium dependent transient contractions induced by Norepinephrine (1μM), but not those induced by Caffeine (20 mM)^[2]. In Vivo: Reticuline (5, 10 and 20 mg/kg, i. v., randomly) injections produced an intense hypotension in normotensive rats. The hypotensive effect of Reticuline is probably due to a peripheral vasodilation in consequence of: 1) muscarinic stimulation and NOS activation in the vascular endothelium, 2) voltage-dependent Ca²⁺ channel blockade and/or 3) inhibition of Ca²⁺ release from norepinephrine-sensitive intracellular stores^[2].