Breast Colon Prostate cancer anti tumoural anti inflammatory Inhibits angiogenesis


† Daily Value not established.


Experimental study on Baicalein inhibiting the invasion and migration of human breast cancer cells

Wang X-f, Zhou Q-m, Su S-b. Experimental study on Baicalein inhibiting the invasion and migration of human breast cancer cells. Zhong Guo Yao Li Xue Tong Bao. 2010; 26(6): 745-750.

The effect of Baicalein on cell viability of the human breast cancer MDA-MB-231 cell line was tested by MTT. The cell invasion and migration were determined by transwell chamber model. The cell movement capability was determined by cell scratch assay. The expressions of matrix metalloproteinase (MMP) 2 and 9, urokinase-type plasminogen activator(uPA)were detected by Western blot. Results 50, 100 ?mol·L-1 of Baicalein inhibited significantly cell invasion(P0.01) and migration(P0.01) compared with control groups. The inhibitory rates were 50% and 77% in cell migration and 15% and 44% in cell invasion, respectively. 50 ?mol·L-1 of Baicalein significantly inhibited the level of MMP 2 expression. 100 ?mol·L-1 of Baica-lein significantly inhibited the level of MMP 9 and uPA expressions. Baicalein inhibits invasion and migration of MDA-MB-231 cells. The mechanisms may be involved in the direct inhibition of cell invasion and migration abilities, and the inhibition of MMP 2, MMP 9, and uPA expressions.

Study on Baicalin Induced Apoptosis of Human Breast Cancer Cell Line MDA-MB-231

Zhu G-q, Tang L-j, Wang L, Su J-j, et al. Study on Baicalin Induced Apoptosis of Human Breast Cancer Cell Line MDA-MB-231. An Hui Zhong Yi Xue Yuan Xue Bao. 2008 ; 27(2) : 20-23

The inhibitory effect of different concentrations of baicalin on the MDA-MB-231 cells was measured by MTT method. Transmission electron microscope was employed to observe the apoptosis of the cells. Cell cycle was analyzed by flow cytometry. The mRNA level of expression of bcl-2 and bax was determined by RT-PCR. The proliferation of MDA-MB-231 cells was inhibited by baicalin in a dose-and time-dependent manner and the IC50 was 151 ?mol/L. The apoptotic rate of the baicalin-treated MDA-MB-231 cells increased significantly at 48 h. Flow cytometer analysis also revealed that most of the baicalin-treated MDA-MB-231 cells were arrested in the G2/M phase. Typically apoptotic characteristics such as condensed chromatin and apoptotic bodies were observed after being treated with baicalin for 48 h. The results of RT-PCR showed that the expression of bax was up-regulated; meanwhile, the expression of bcl-2 was down-regulated. Baicalin could inhibit the proliferation of MDA-MB-231 cells through apoptosis by regulating the expression of bcl-2, bax and intervening the process of the cell cycle.

The Anti-inflammatory and Analgesic Effects of Baicalin in Carrageenan-Evoked Thermal Hyperalgesia

Tz-Chong Chou, PhD, Li-Ping Chang, MD PhD, Chi-Yuan Li, MD, Chih-Shung Wong, MD PhD, Shih-Ping Yang, MD PhD. A & A December 2003 vol. 97 no. 6 1724-1729

Scutellaria baicalensis Georgi (Huang Qin), a Chinese traditional medicinal herb, is widely used as an antiinflammatory, antibacterial, and hepatoprotective drug (1,2). Baicalin (7-glucuronic acid,5,6-dihydroxy-flavone), a flavonoid compound isolated from Huang Qin, possesses antioxidant properties (3) and has an inhibitory effect on carrageenan-induced rat paw oedema (1), suggesting that it may be a potential antiinflammatory drug.

The carrageenan-evoked thermal hyperalgesia resulting from the combined effect of the release of proinflammatory cytokines, cyclooxygenase (COX) products, and sympathomimetic amines (4) is a common model used to study inflammatory pain. Tumour necrosis factor Alpha has an early and crucial role in the cascade of proinflammatory cytokine production and subsequent inflammatory processes (5). COX catalyses the conversion of arachidonic acid to many biologically active mediators, such as prostaglandin E2 (PGE2). It has been reported that overproduction of inflammatory prostaglandins by an inducible form of COX (COX-2) plays an important pathophysiological role in the development of inflammatory pain (6,7).

Nitric oxide (NO), synthesized by the enzyme NO synthase (NOS), is an important mediator in the regulation of cell functions (8). However, overproduction of NO derived from inducible NOS (iNOS) activated by proinflammatory cytokines, free radicals, and lipopolysaccharide (LPS) may cause the pathogenesis of inflammatory diseases, including carrageenan-evoked inflammatory pain (6,9). Inhibition of COX-2 activity in a castor-oil-induced diarrhoea model, as well as NO formation and iNOS expression in LPS-treated RAW 264.7 macrophages by baicalin (10,11), suggests that baicalin may suppress the COX-2 and iNOS pathways, a critical mediator accounting for the carrageenan-induced inflammatory pain.

Studies showed that baicalin exhibits an analgesic effect in a rat model of carrageenan-evoked thermal hyperalgesia. The effect of baicalin on the formation of important inflammatory mediators, including cytokine, NO, and PGE2 formation, as well as neutrophil infiltration at inflammatory sites, was also studied.

Baicalin induces apoptosis via mitochondrial pathway as pro-oxidant

Ueda S, Nakamura H, Masutani H, Sasada T, Takabayashi A, Yamaoka Y, Yodoi J. Mol Immunol. 2002 Feb;38(10):781-91.

Baicalin is a flavonoid and a major component of a herbal medicine. Flavonoids including baicalin have been reported to not only function as anti-oxidants but also cause cytotoxic effect. We investigated the mechanism of baicalin-induced cytotoxicity in leukemia-derived T cell line, Jurkat cells. When cells were cultured with 50-200 microg/ml baicalin for 6h, caspase-3 was activated and then cells fell into apoptosis. Induction of apoptosis by baicalin was accompanied with the marginal generation of intracellular reactive oxygen species (ROS), the increase of the cytosolic fractions of cytochrome c, and the disruption of mitochondrial transmembrane potential (DeltaPsi (m)) prior to the activation of caspase-3. The pre-culture with 5 mM of buthionine sulfoximine (BSO), an inhibitor of glutathione (GSH) synthesis, facilitated baicalin-induced disruption of DeltaPsi (m) and induction of apoptosis. The pre-culture with N-benzyloxycarbonyl-valyl-alanyl-aspartyl fluoromethylketone (Z-VAD-fmk), a pan-caspase inhibitor, partially suppressed the induction of apoptosis. On the other hand, baicalin showed little toxic effect on peripheral blood mononuclear cells (PBMCs) from healthy volunteers. These results indicate that baicalin acts as a prooxidant and induces caspase-3 activation and apoptosis via mitochondrial pathway.

Baicalein and baicalin are potent inhibitors of angiogenesis: Inhibition of endothelial cell proliferation, migration and differentiation.

Liu JJ, Huang TS, Cheng WF, Lu FJ. Int J Cancer. 2003 Sep 10;106(4):559-65.

When CAMs were treated with either baicalein or baicalin for 48 hr, the angiogenic response induced by basic fibroblast growth factor (bFGF) was markedly reduced in a dose-dependent manner. Further characterization showed that both flavonoids exhibited dual antiproliferative (at low dose) and apoptogenic (at high dose) effects on HUVECs. In biochemical analysis, treatment of HUVECs with baicalein and baicalin for 24 hr resulted in a dose-dependent decrease in the matrix metalloproteinase (MMP)-2 activity. Moreover, the migration of endothelial cells and the differentiation of endothelial cells into branching networks of tubular structures in vitro were also inhibited by these 2 flavonoids in a dose-dependent manner. Baicalein is more potent than baicalin in anti-angiogenesis in vivo as well as in vitro. Taken together, the results of our study provide evidence that baicalein and baicalin possess an anti-angiogenesis potential that is a previously unrecognized biologic activity.

Baicalein, a component of Scutellaria radix from Huang-Lian-Jie-Du-Tang (HLJDT), leads to suppression of proliferation and induction of apoptosis in human myeloma cells.

Ma Z, Otsuyama K, Liu S, Abroun S, Ishikawa H, Tsuyama N, Obata M, Li FJ, Zheng X, Maki Y, Miyamoto K, Kawano MM. Blood. 2005 Apr 15;105(8):3312-8. Epub 2004 Dec 30.

Baicalin inhibited the proliferation of myeloma cell lines and the survival of primary myeloma cells, especially MPC-1- immature myeloma cells, and induced apoptosis in myeloma cell lines via a mitochondria-mediated pathway by reducing mitochondrial membrane potential and activating caspase-9 and caspase-3. Further experiments confirmed that Scutellaria radix was responsible for the suppressive effect on myeloma cell proliferation, and the baicalein in Scutellaria radix showed strong growth inhibition and induction of apoptosis in comparison with baicalin or wogonin. Baicalein as well as baicalin suppressed the survival in vitro of MPC-1- immature myeloma cells rather than MPC-1+ myeloma cells from myeloma patients. Baicalein inhibited the phosphorylation of IkB-, which was followed by decreased expression of the IL-6 and XIAP genes and activation of caspase-9 and caspase-3. Therefore, HLJDT and Scutellaria radix have an antiproliferative effect on myeloma cells, especially MPC-1- immature myeloma cells, and baicalein may be responsible for the suppressive effect of Scutellaria radix by blocking IkB-degradation.

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