n/a
Abstract Title:

Erinacerins, Novel Glioma Inhibitors from Hericium erinaceus, Induce Apoptosis of U87 Cells through Bax/Capase-2 Pathway.

Abstract Source:

Anticancer Agents Med Chem. 2020 Aug 3. Epub 2020 Aug 3. PMID: 32753025

Abstract Author(s):

Feng Zhang, Hui Lv, Xuhua Zhang

Article Affiliation:

Feng Zhang

Abstract:

BACKGROUND: Glioma is the most common tumor of the central nervous system. Hericium erinaceus, which has been reported to have a variety of pharmacological activities, is a kind of widely used Traditional Chinese Medicine (TCM), and also a kind of delicious food accepted by the public.

METHODS AND RESULTS: In this study, two new natural products, compounds 1 and 2, were isolated and identified from Hericium erinaceus. They were named erinacerin O and erinacerin P respectively after the structural identification, and their effects on human glioma cell line U87 were evaluated. Erinacerin P (2) exhibited an obvious cytotoxity on human glioma cell line U87. The IC50 value of 2 was 19.32μg/mL. The results showed that the apoptosis of U87 cells treated with 2 increased and the morphology of U87 cells altered significantly. Flow cytometry experiment showed that 2 could significantly increase the apoptosis rate of U87 cells and reduce DNA replication. Western blot results suggested the Bax/capase-3 pathway was involved in the U87 cell apoptosis induce by 2.

CONCLUSION: Erinacerin O and Erinacerin P are novel compounds from Hericium erinaceus and Erinacerin P could be a potential novel glioma inhibitor.

Study Type : In Vitro Study

Print Options


Key Research Topics

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2024 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.