Affiliation:
1. College of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, P. R. China
Abstract
Atractylodin is one of the main active ingredients of Atractylodis Rhizoma. It has various pharmacological properties, such as antigastric ulcer, immune regulation, antibacterial, anti-inflammatory, antitumor, anti-oxidant, and neuroprotective properties. In the past few decades, atractylodin has attracted the attention of researchers due to its excellent therapeutic effects. This paper aims to review the pharmacology of atractylodin, focusing mainly on its pharmacological effects in tumor treatment. Atractylodin exerts its antitumor effect by regulating different signaling pathways to induce important biological events such as apoptosis, cell cycle arrest, and autophagy, inhibiting cancer cell invasion and metastasis. In the process of cell apoptosis, atractylodin mainly induces cancer cell apoptosis by downregulating the Notch signaling pathway, affecting multiple upstream and downstream targets. In addition, atractylodin induces autophagy in cancer cells by regulating various signaling pathways such as PI3K/AKT/mTOR, p38MAPK, and hypothalamic Sirt1 and p-AMPK. Atractylodin effectively induces G1/M and G2/M phase arrest under the action of multiple signaling pathways. Among them, the pathways related to G1/M are more widely stagnated. In inhibiting the migration and invasion of cancer cells, atractylodin mainly regulates the Wnt signaling pathway, downregulates the expression of N-cadherin in cancer cells, and then blocks the PI3K/AKT/mTOR signaling pathway, inhibiting the phosphorylation of PI3K, AKT, and mTOR proteins, thereby having a significant impact on the invasion and migration of cancer cells. This paper systematically reviews the research progress on the antitumor effects and mechanisms of atractylodin, hoping to provide a reference and theoretical basis for its clinical application and new drug development.
Funder
the National Natural Science Foundation of China
Publisher
World Scientific Pub Co Pte Ltd