Abstract
Background Oxidative stress, inflammation and cardiac apoptosis were closely involved in doxorubicin (DOX)-induced cardiac injury. Piperine has been reported to suppress inflammatory response and pyroptosis in macrophages. However, whether piperine could protect the mice against DOX-related cardiac injury remain unclear. This study aimed to investigate whether piperine inhibited DOX-related cardiac injury in mice. Methods To induce DOX-related acute cardiac injury, mice in DOX group were intraperitoneally injected with a single dose of DOX (15 mg/kg). To investigate the protective effects of piperine, mice were orally treated for 3 weeks with piperine (50 mg/kg, 18:00 every day) beginning two weeks before DOX injection. Results Piperine treatment significantly alleviated DOX-induced cardiac injury, and improved cardiac function. Piperine also reduced myocardial oxidative stress, inflammation and apoptosis in mice with DOX injection. Piperine also improved cell viability, and reduced oxidative damage and inflammatory factors in cardiomyocytes. We also found that piperine activated peroxisome proliferator-activated receptor-γ (PPAR-γ), and the protective effects of piperine were abolished by the treatment of the PPAR-γ antagonist in vivo and in vitro. Conclusions Piperine could suppress DOX-related cardiac injury via activation of PPAR-γ in mice.
Highlights
A medical survey conducted by National Health and Nutrition Examination, which included 1807 cancer survivors, showed that 33% died of heart diseases [1]
DOX injection resulted in a marked increase in the level of Cardiac troponin I (cTnI), and piperine treatment signi cantly decreased this elevation in DOX-injected mice (Figure 1(c)). e level of NTproBNP was increased in DOX group, and piperine treatment decreased the increased level of NT-proBNP (Figure 1(d))
We found that piperine activated peroxisome proliferator-activated receptor-γ (PPAR-γ) receptors and PPAR-γ receptors inhibition could o set piperine-mediated protection in mice
Summary
A medical survey conducted by National Health and Nutrition Examination, which included 1807 cancer survivors, showed that 33% died of heart diseases [1]. E pathogenesis of DOX-induced cardiotoxicity are not completely understood, but increasing evidence suggests that oxidative stress, in ammation accumulation and cardiac apoptosis are closely involved [3, 4]. It has been reported that activation of peroxisome proliferator-activated receptor-γ (PPAR-γ) by pioglitazone ameliorated cardiac oxidative stress and in ammation in rats with metabolic syndrome [6]. In ammation and cardiac apoptosis were closely involved in doxorubicin (DOX)-induced cardiac injury. Whether piperine could protect the mice against DOX-related cardiac injury remain unclear. Is study aimed to investigate whether piperine inhibited DOX-related cardiac injury in mice. Piperine treatment signi cantly alleviated DOX-induced cardiac injury, and improved cardiac function. Piperine reduced myocardial oxidative stress, in ammation and apoptosis in mice with DOX injection. Piperine could suppress DOX-related cardiac injury via activation of PPAR-γ in mice
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