Mollugin is a major bioactive component isolated from Rubia cordifolia L. Mollugin attenuated the LPS-induced expression of nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin (IL)-1β and IL-6 but augmented the expression of tumor necrosis factor (TNF)-α[3]. Mollugin induces cell death in a dose-dependent manner in primary and metastatic OSCCs (human oral squamous cell carcinoma cells). Mollugin-induced cell death involved apoptosis, characterized by the appearance of nuclear shrinkage, flow cytometric analysis of sub-G1 phase arrest, and annexin V-FITC and propidium iodide staining[4]. Mollugin significantly inhibited the expression of an NF-κB reporter gene induced by tumor necrosis factor (TNF)-α in a dose-dependent manner. Moreover, mollugin inhibited TNF-α-induced phosphorylation and nuclear translocation of p65, phosphorylation and degradation of inhibitor of κB (IκBα), and IκB kinase (IKK) phosphorylation[5].
Mollugin/大叶茜草素 细胞实验
Cell Line
Concentration
Treated Time
Description
References
HeLa cells
20 μM, 40 μM, 80 μM
12 hours
Mollugin significantly inhibited TNF-α-induced NF-κB reporter gene expression in a dose-dependent manner.
Int J Mol Sci. 2017 Jul 26;18(8):1619
Mollugin/大叶茜草素 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Rats
Oral administration model
Oral
0.82 g/kg
Single dose
Pharmacokinetic study to determine the concentration of Mollugin in plasma
Molecules. 2016 Jun 1;21(6):717
Nude mice
HeLa cell xenograft model
Oral
25 mg/kg, 75 mg/kg
Three times a week until the end of the study
Mollugin significantly suppressed the growth of HeLa cell xenografts without affecting body weight.
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