Magnolol

Magnolol, a natural lignan isolated from the stem bark of Magnolia officinalis, is a dual agonist of both RXRα and PPARγ, with EC₅₀ values of 10.4 µM and 17.7 µM, respectively. IC50 & Target:EC50: 10.4 µM (RXRα), 17.7 µM (PPARγ)^[1] In Vitro:Magnolol is a dual agonist of both RXRα and PPARγ, with EC₅₀ values of 10.4 μM and 17.7 μM, respectively. Magnolol (26.2-80 μM) binds to RXRαLBD and PPARγLBD in a dose dependent manner, with K_d values of 45.7 μM and 1.67 μM, respectively. Magnolol (1-20 μM) induces the transcription of PPRE in a dose-dependent manner, but shows no activity on RXRE transcription^[1]. Magnolol (1, 3, 10 μM) enhances adipocyte differentiation of both 3T3-L1 pre-adipocystes and C3H10T1/2 pluripotent stem cells in the presence of insulin. Magnolol (10 μM) upregulates mRNA expression of marker genes for adipocyte differentiation. Magnolol (1, 10 μM) shows an increase in basal and insulin-stimulated glucose uptake in differentiated 3T3-L1 adipocytes^[2]. In Vivo:Magnolol (5-15 mg/kg, p.o.) significantly attenuates the phenotypic severity of dextran sulfate sodium (DSS)-induced colitis in mice. Magnolol (10, 15 mg/kg, p.o.) attenuates histopathological changes and myeloperoxidase activity in the colon of DSS-treated mice, decreases DSS-induced high levels of proinflammatory cytokines TNF-α, IL-1β and IL-6 in the colonic tissues. Magnolol (10 mg/kg, p.o.) also reverses abnormality of serum metabolome, and regulates tryptophan metabolic pathway in mice^[3].