Protective effect of puerarin against burn‑induced heart injury in rats
- Junling Liu
- Jianyun Liu
- Mingming Bai
- Hui Wang
Affiliations: Department of Burn, Gansu Provincial Hospital, Lanzhou, Gansu 730000, P.R. China
- Published online on: April 29, 2020 https://doi.org/10.3892/etm.2020.8696
Copyright: © Liu
et al. This is an open access article distributed under the
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Commons Attribution License.
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The present study evaluated the potential protective effects of puerarin and its associated mechanism on burn-induced myocardial damage. A total of 40 healthy adult Wistar rats were randomly divided into four groups: i) Sham; ii) burn; iii) burn + puerarin; and iv) puerarin. Serum levels of interleukin (IL)‑1β, tumor necrosis factor‑α (TNF‑α) and IL‑6 were measured using ELISA. Myeloperoxidase (MPO) activity and malondialdehyde (MDA) levels were determined in myocardial homogenates using a commercial assay kit. TUNEL staining and western blot analysis of cleaved and pro‑caspase‑3 were also performed to assess apoptosis. Activation of p38‑MAPK, ERK, JNK and AKT were measured using western blot analysis. Left ventricular systolic pressure, maximum rates of increase/decrease in left ventricular pressure, creatine kinase MB activity and cardiac troponin T levels were found to be altered in the burn group 12 h after burn, which were reversed by puerarin treatment. Injection of puerarin following burn injury also reduced heart water content. Serum levels of IL‑1β, TNF‑α and IL‑6 were significantly higher in the burn group compared with those in the sham group. Puerarin treatment reduced serum levels of IL‑1β, TNF‑α and IL‑6, in addition to reducing MPO activity and MDA levels in myocardial tissues. Puerarin inhibited the activation of caspase‑3, p38, ERK and JNK following severe burn, but elevated Akt activation following severe burn. In conclusion, puerarin improved cardiac function in rats following severe burn injury, which may be due to reduced myocardial injury, inhibition of cardiomyocyte apoptosis and reduced oxidative inflammatory stress; the MAPK and AKT signaling pathways are proposed to the underlying mechanism of these findings.