Soluble Pearl Extract provides effective skin lightening by antagonizing endothelin.

BACKGROUND: Incidence of skin pigmentation disorders has been on the rise globally. This calls for safer and more effective topical skin lightening and freckle-removing products. In this study, we hypothesized that Soluble Pearl Extract (SPE) may possess endothelin antagonizing compounds with good skin whitening effects. OBJECTIVES: (a) To determine the effect and mechanisms of SPE on ET-1-treated B16 melanoma cells. (b) To explore the cytotoxic effects of SPE on B16 melanoma cells. METHODS: CCK-8 assay was performed to determine how SPE and ET-1 affect the proliferation rate of B16 melanoma cells, the NaOH lysis assay was conducted to quantify the content of melanin while the tyrosinase activity was determined by DOPA oxidation test. The mRNA and protein expression levels of TYR and TRP-1 were determined by qRT-PCR assay and Western blot assay, respectively. RESULTS: We found that SPE at 0.1 and 1 µg/mL concentrations has no effect on the proliferation of the cells and 10 nmol/L ET-1 promoted B16 melanoma cells proliferation. Notably, B16 melanoma cells treated with 10 nmol/L ET-1 exhibited significantly higher melanin synthesis, tyrosinase activity, TYR, and TRP-1 mRNA expression levels compared with untreated cells. Of note, the effects of 10 nmol/L ET-1 treatment were abolished with SPE in a dose-dependent manner. CONCLUSIONS: SPE inhibits endothelin thereby safely and effectively lightening lightens the skin by antagonizing endothelin. Moreover, SPE is safe and effective.

Cardiac toxicity of Triptergium wilfordii Hook F. may correlate with its inhibition to hERG channel.

Tripterygium wilfordii Hook F. (TWHF) is a Chinese traditional medicine with cardiac toxicities. However, the mechanism of acute cardiac toxicity is not very clear. By using patch clamp techniques, we found that 0.05 mg/ml and 0.1 mg/ml of the aqueous crude extract of TWHF inhibit 21.4 ± 1.6% and 86.7 ± 5.7% (n = 5) of hERG current Amplitudes (IhERG) respectively. We further found that Celastrol, one of main components of TWHF, inhibits hERG with an IC50 of 0.83 µM. Additional mutagenesis studies show that mutations of T623A, S624A and F656A significantly alter the inhibition and S624A has the strongest effect, supported by our docking model. Our data suggest that inhibition of hERG channel activity by Celastrol contributed to TWHF cardiotoxicity.