Catalpol ameliorates doxorubicin‑induced inflammation and oxidative stress in H9C2 cells through PPAR‑γ activation
Affiliations: Department of Pharmacology, Jinhua Institute for Food and Drug Control, Jinhua, Zhejiang 321017, P.R. China, Department of Pharmacy, Lianshui County People's Hospital, Huai'an, Jiangsu 223400, P.R. China
- Published online on: May 13, 2020 https://doi.org/10.3892/etm.2020.8743
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Drug‑induced cardiomyopathy is a severe disease that leads to refractory heart disease at late stages, with increasing detrimental effects. DOX‑induced cell damage is primarily induced via cellular oxidative stress. The present study investigated the effects of catalpol on doxorubicin (DOX)‑induced H9C2 cardiomyocyte inflammation and oxidative stress. The Cell Counting Kit‑8 assay was performed to detect cell viability, and western blotting was performed to detect the expression of peroxisome proliferator‑activated receptor (PPAR)‑γ in H9C2 cells. The expression levels of tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑1β and IL‑6 were measured using ELISAs. Furthermore, the oxidative stress kit was used to detect the levels of malondialdehyde, superoxide dismutase and glutathione peroxidase. A reactive oxygen species (ROS) kit and DCF‑DA staining were used to detect ROS levels. The results indicated that DOX treatment inhibited H9C2 cell expression of PPAR‑γ and decreased H9C2 cell viability. Various concentrations of catalpol exhibited a less potent effect on H9C2 cell viability compared with DOX; however, catalpol increased the viability of DOX‑induced H9C2 cells. Catalpol treatment also signiﬁcantly decreased the expression levels of inflammatory factors (TNF‑α, IL‑1β and IL‑6) in DOX‑induced H9C2 cells, which was reversed by transfections with short hairpin RNA targeting PPAR‑γ. Results from the present study indicated that catalpol ameliorated DOX‑induced inflammation and oxidative stress in H9C2 cardiomyoblasts by activating PPAR‑γ.