Scutellarin 是从黄芩中分离的黄酮，可抑制破骨细胞中 RANKL 介导的 MAPK 和 NF-Κb 信号通路，并下调 HCC 细胞中的 STAT3/Girdin/Akt 信号通路。

Scutellarin, an active flavone isolated from Scutellaria baicalensis, can inhibit RANKL-mediated MAPK and NF-κB signaling pathway in osteoclasts, and down-regulate the STAT3/Girdin/Akt signaling in HCC cells.

Scutellarin treatment significantly reduces HepG2 cell viability in a dose-dependent manner. It also inhibits migration and invasion of HCC cells in vitro. Scutellarin treatment significantly reduces STAT3 and Girders of actin filaments (Girdin) expression, STAT3 and Akt phosphorylation in HCC cells. The introduction of STAT3 overexpression restores the scutellarin-downregulated Girdin expression, Akt activation, migration and invasion of HCC cells. Moreover, induction of Girdin overexpression completely abrogates the inhibition of scutellarin on the Akt phosphorylation, migration and invasion of HCC cells. Scutellarin can inhibit HCC cell metastasis in vivo, and migration and invasion in vitro by down-regulating the STAT3/Girdin/Akt signaling[1]. Scutellarin selectively enhances Akt phosphorylation[2]. Scutellarin is a putative therapeutic agent as it has been found to not only suppress microglial activation thus ameliorating neuroinflammation, but also enhance astrocytic reaction. Acutellarin amplifies the astrocytic reaction by upregulating the expression of neurotrophic factors among others thus indicating its neuroprotective role. Remarkably, the effects of scutellarin on reactive astrocytes are mediated by activated microglia supporting a functional "cross-talk" between the two glial types[3]. Scutellarin can suppress RANKL-mediated osteoclastogenesis, the function of osteoclast bone resorption, and the expression levels of osteoclast-specific genes (tartrate-resistant acid phosphatase (TRAP), cathepsin K, c-Fos, NFATc1). Further investigation indicates that Scutellarin can inhibit RANKL-mediated MAPK and NF-κB signaling pathway, including JNK1/2, p38, ERK1/2, and IκBα phosphorylation[5].

Scutellarin (50 mg/kg/day) significantly mitigates the lung and intrahepatic metastasis of HCC tumors in vivo. The numbers of lung and intrahepatic metastatic tumors in the scutellarin-treated group are significantly less compared to the controls[1]. The rats treated with Scutellarin display a significant alleviation in neurobehavioral deficits compared to the SAH group. Scutellarin enhanced eNOS expression compared with SAH rats[4].

HepG2 cells (1×105/well) are cultured in 96-well plates and treated in triplicate with scutellarin at concentrations of 5, 10, 20, 30, and 100 μM or vehicle alone for 24 h. The cellular viability is tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and is expressed as a percentage of proliferation versus controls.

27740-01-8

C21H18O12

462.37

Scutellarein-7-glucuronide;Breviscapine;黄岑素;野黄芩苷;Breviscapinun;Breviscapin

DMSO:50mg/mL(108.14 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years