Raddeanin a Suppresses Glioblastoma Growth by Inducing ROS Generation and Subsequent JNK Activation to Promote Cell Apoptosis

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
Fei PengShiguang Zhao

Abstract

Raddeanin A (RA), an active pharmacological ingredient from Anemone raddeana Regel, plays an important role in tumor suppression. In this study, we assessed the potentially therapeutic effect of RA on glioblastoma and its underlying mechanisms. Cell viability was examined using the MTT assay. Invasive and migratory capacities were examined using Transwell and wound healing assays. Apoptosis was determined by Hoechst staining, flow cytometry, DCFH-fluorescent probe and immunohistochemical staining. Autophagy was detected by transmission electron microscopy and western blotting. A U251 glioma xenograft model was established to evaluate the effect of RA in vivo. The data demonstrated that RA inhibited viability, and abrogated the invasive/migratory abilities of glioblastoma cells. In addition, RA induced apoptosis by reactive oxygen species (ROS)/ Jun N-terminal kinase (JNK) signaling in glioblastoma. Conversely, the antioxidant N-Acetyl-L-cysteine (NAC) and pan-caspase inhibitor z-VAD-fmk attenuated RA-induced apoptosis by scavenging ROS and inactivating caspase-3. Furthermore, the inhibition of autophagy by 3-MA exacerbated apoptosis through ROS generation and JNK phosphorylation. In vivo, RA exhibited a curative effect on U251-...Continue Reading

Citations

Feb 29, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Irum NazKwang Seok Ahn
Mar 25, 2019·Journal of Cellular and Molecular Medicine·Hongyan XiaYan Dong
Nov 18, 2018·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Milica LazarevićĐorđe Miljković
Nov 6, 2018·International Journal of Molecular Sciences·Xing-Xian GuoJing Li
May 8, 2021·Biochemical and Biophysical Research Communications·Yue-Yue WangJi-Yu Gong
Dec 31, 2021·Journal of Biochemical and Molecular Toxicology·Yu-Ye XueGuang Cheng

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