Wedelolactone alleviates doxorubicin-induced inflammation and oxidative stress damage of podocytes by IκK/IκB/NF-κB pathway

[Display omitted] •Wedelolactone, a natural compound, shows outstanding effects of anti-inflammation and anti-oxidative stress.•The alleviation to doxorubicin(DOX)-driven podocyte injury may contribute to the attenuation of renal damage.•Wedelolactone can regulate the IκK/IκB/NF-κB signaling pathway...

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Veröffentlicht in:Biomedicine & pharmacotherapy 2019-09, Vol.117, p.109088, Article 109088
Hauptverfasser: Zhu, Mao-mao, Wang, Long, Yang, Dang, Li, Chao, Pang, Shi-ting, Li, Xing-hua, Li, Ru, Yang, Bing, Lian, Yuan-pei, Ma, Liang, Lv, Qing-lin, Jia, Xiao-bin, Feng, Liang
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Sprache:eng
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Zusammenfassung:[Display omitted] •Wedelolactone, a natural compound, shows outstanding effects of anti-inflammation and anti-oxidative stress.•The alleviation to doxorubicin(DOX)-driven podocyte injury may contribute to the attenuation of renal damage.•Wedelolactone can regulate the IκK/IκB/NF-κB signaling pathway to alleviate levels of oxidative stress and inflammation. The acute kidney injury(AKI) caused by nephrotoxic drugs contributes to inflammation and oxidative injury in podocytes. Wedelolactone (WED), a natural compound, is found with activities as anti-inflammation, anti-oxidative, anti-free radical,and etc. In this present study, MPC-5 cells were exposed to the nephrotoxic drugs doxorubicin (DOX). The results showed that WED significantly increased the SOD activity, CAT and GSH-Px levels, while significantly decreased the MDA content and ROS levels in DOX-induced MPC-5 cells. WED could also significantly decrease the levels of cytokines IL-6, MCP-1, TNF-α, and TGF-β1. Additionally, the activation and phosphorylation of IκKα, IκBα and NF-κB p65 was inhibited by WED. The co-treatment of PDTC (NF-κB inhibitor) and WED significantly reduced NF-κB p65 phosphorylation. These findings suggested that WED alleviated inflammation and oxidative stress of doxorubicin-induced MPC-5 cells through IκK/IκB/NF-κB signaling pathway.
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2019.109088