Flavonoids Identified from Korean Scutellaria baicalensis Induce Apoptosis by ROS Generation and Caspase Activation on Human Fibrosarcoma Cells

Author:

Zhang Jue1,Park Hyeon-Soo2,Kim Jin-A3,Hong Gyeong-Eun2,Nagappan ArulKumar2,Park Kwang-Il4,Kim Gon-Sup2

Affiliation:

1. Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi, Jiangsu 214063, China

2. Research Institute of Life Science and College of Veterinary Medicine, Gyeongsang National University, Gazwa, Jinju 660-701, Republic of Korea

3. Korea National Animal Research Resource Center and Korea National Animal Bio-Resource Bank, Gyeongsang National University, Gazwa, Jinju 660-701, Republic of Korea

4. Department of Biological Science, Center for Colon Cancer Research, University of South Carolina, Columbia, SC 29208, USA

Abstract

The effects of flavonoids from Korean Scutellaria baicalensis on fibrosarcoma HT1080 cells and their underlying molecular mechanism were investigated in this study. Flavonoids affected HT1080 cell proliferation by interrupting cell cycle progress, obviously augmenting the proportion of sub-G1 and diminishing that of G1 phase, and undergoing apoptosis at the tested dosage (100–400 μg/mL). In addition, the mediated apoptosis was mainly caused by total reactive oxygen species (ROS) generation and by up-regulating the ratio of Bax/Bcl-xL, triggering caspase cascades (caspase-3, -9 and -8), and inactivating PARP, dose-dependently. The proteomics results showed that AP-4, ARID 5B, HNRNP K, PLOG, Prdx6, and myosin-1, associated with cell growth, differentiation and development, and overexpressed in gastric cancer, colorectal cancer, pancreatic cancer, etc., were statistically down-regulated after the flavonoids treatment. Taken together, our data demonstrated that flavonoids from Korean S. baicalensis induced apoptosis in HT1080 cells, which involved a hierarchy of cellular pathways and multiple signal proteins, and might be a potential anticancer therapeutic agent.

Publisher

World Scientific Pub Co Pte Lt

Subject

Complementary and alternative medicine,General Medicine

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