In vitro: |
Korean Journal of Pharmacognosy, 2007, 38(2):176-180. | Hepatoprotective constituents of Saururus chinensis roots against tacrine-induced cytotoxicity in human liver-derived Hep G2 cells.[Reference: WebLink] | METHODS AND RESULTS:
Five lignans, sauchinone (1), di-O-methyltetrahydrofuriguaiacin B (2), manassantin A (3), manassantin B (4) and saucerneol B (5), have been isolated from the MeOH extract of Saurunis chinensis roots. The evaluation for protective effect of compounds 1-5 against tacrine-induced cytotoxicity in human liver-derived Hep G2 cells was conducted.
CONCLUSIONS:
Compounds 1, 2, and 5 showed significant protective effects with the EC 50 values of 74.2±0.9, 111.3±0.8, 64.3±0.8 μM, respectively. Silybin, one of the well-known hepatoprotective agents, used as a positive control, and also showed protective effect with an EC 50 value of 86.2±0.5 μM. | Experimental dermatology, 2011, 20(9):761-763. | Manassantin A inhibits cAMP-induced melanin production by down-regulating the gene expressions of MITF and tyrosinase in melanocytes.[Reference: WebLink] | Microphthalmia-associated transcription factor (MITF) is inducible in response to cAMP through the cAMP-responsive element-binding protein (CREB) and plays a pivotal role in the melanocyte-specific expression of tyrosinase or tyrosinase-related proteins (TRPs) for melanin biosynthesis. Manassantin A from Saururus chinensis inhibits cAMP-induced melanin production in B16 melanoma cells. METHODS AND RESULTS: Here, we focused on molecular basis of the antimelanogenic activity. Manassantin A consistently inhibited the cAMP elevator 3-isobutyl-1-methylxanthine (IBMX)- or dibutyryl cAMP-induced melanin production in B16 cells or in melan-a melanocytes by down-regulating the expression of tyrosinase or TRP1 gene. Moreover, manassantin A suppressed MITF induction through IBMX-activated CREB pathway, directly inhibiting the Ser-133 phosphorylation of CREB. However, manassantin A did not affect IBMX-increased cAMP levels in these cells but also other cAMP-dependent melanogenic pathways through post-translational modifications of MITF.
CONCLUSIONS:
This putative molecular mechanism of manassantin A in the inhibition of melanin production suggests its pharmacological potential in skin hyperpigmentation. |
|