p-Coumaric acid protects cardiac function against lipopolysaccharide-induced acute lung injury by attenuation of oxidative stress.
Iran J Basic Med Sci. 2019 Aug ;22(8):949-955. PMID: 31579452
Objectives: Acute lung injury (ALI) has a high mortality rate and is characterized by damage to pulmonary system giving rise to symptoms such as histological alteration, lung tissue edema and production of proinflammatory cytokine. p-Coumaric acid (p-CA), as a phenolic compound, that is found in many types of fruits and vegetables has been reported to exhibit a therapeutic effect in several inflammatory disorders. The aim of our study was evaluation of pretreatment with p-CA against heart dysfunction, oxidative stress and nuclear factor-erythroid 2 -related factor 2 (Nrf2) modifications following lipopolysaccharide (LPS)-induced acute lung inflammation.
Materials and Methods: The rats were divided into four groups (n=8): Control, LPS (5 mg/kg, it), p-CA (100 mg/kg, IP), and LPS+pCA. Inflammatory response and oxidative stress were evaluated by measurement of interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and malondialdehyde (MDA) levels in heart tissue. For evaluation of the effect of LPS on cardiac response, electrocardiography (ECG) and hemodynamic parameters were recorded.
Results: A significant increase in lipid peroxidation (<0.001, cytokine parameters (TNF-α and IL-6 (<0.01), gene expression of Nrf2 (<0.05), and antioxidant activity of superoxide dismutase and glutathione (<0.05) in addition to glutathione peroxidase (<0.01) was demonstrated in heart tissue of ALI rats. LPS can impair cardiac function (inmeasurement of hemodynamic parameters by using Langendorff setup, and inmeasurement of ECG parameters), and pretreatment with p-CA recovered these parameters to control levels in heart. Pretreatment with p-CA causes modulation of cytokines and MDA level that protected cardiac injury caused by LPS in ALI model.
Conclusion: Our results showed anti-inflammatory and antioxidative effect of p-CA on LPS-induced ALI.