n/a
Article Publish Status: FREE
Abstract Title:

Chlorogenic acid promotes the Nrf2/HO-1 anti-oxidative pathway by activating p21to resist dexamethasone-induced apoptosis in osteoblastic cells.

Abstract Source:

Free Radic Biol Med. 2019 Apr 17 ;137:1-12. Epub 2019 Apr 17. PMID: 31004750

Abstract Author(s):

Dandan Han, Xiaolong Gu, Jian Gao, Zhi Wang, Gang Liu, Herman W Barkema, Bo Han

Article Affiliation:

Dandan Han

Abstract:

In a previous study, p21(p21) promoted activation of the nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, which has an important role in regulating apoptosis triggered by oxidative stress and inhibiting development of osteoporosis. Chlorogenic acid (CGA) has a strong protective effect on osteoporosis, closely related to activating the Nrf2/HO-1 pathway. However, whether CGA can resist apoptosis by regulating p21 and consequently promote activation of the Nrf2/HO-1 pathway needs further investigation. MC3T3-E1 cells were treated with dexamethasone (Dex), with or without CGA pre-treatment. Cell proliferation and cytotoxicity were measured using MTT assay and LDH release assay, respectively, and apoptosis assessed by flow cytometry. CGA significantly attenuated mitochondrial apoptosis and reversed down-regulation of p21 in osteoblastic MC3T3-E1 cells exposed to Dex. Additionally, CGA decreased Keap1 expression and promoted activation of the Nrf2/HO-1 pathway, quenching intracellular reactive oxygen species (ROS), hydrogen peroxide (HO) and mitochondrial superoxide overproduction boosted by Dex. Importantly, depletion of p21 by siRNA blocked activation of the Nrf2/HO-1 pathway, enhanced oxidative stress and increased apoptosis induced by CGA in MC3T3-E1 cells challenged with Dex. Therefore, CGA promoted the Nrf2/HO-1 anti-oxidative pathway by activating p21 to prevent Dex-induced mitochondrial apoptosis in osteoblastic cells. This pathway has potential as a therapeutic target for prevention and treatment of osteoporosis.

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.