Abstract
SC-E3 is a novel herbal formula composed of five oriental medicinal herbs that are used to treat a wide range of inflammatory diseases in Korean traditional medicine. In this study, we sought to determine the effects of SC-E3 on free radical generation and inflammatory response in lipopolysaccharide- (LPS-) treated RAW 264.7 macrophages and the molecular mechanism involved. The ethanol extract of SC-E3 showed good free radical scavenging activity and inhibited LPS-induced reactive oxygen species generation. SC-E3 significantly inhibited the production of the LPS-induced inflammatory mediators, nitric oxide and prostaglandin E2, by suppressing the expressions of inducible nitric oxide synthase and cyclooxygenase-2, respectively. SC-E3 also prevented the secretion of the proinflammatory cytokines, IL-1β, TNF-α, and IL-6, and inhibited LPS-induced NF-κB activation and the mitogen-activated protein kinase (MAPK) pathway. Furthermore, SC-E3 induced the expression of heme oxygenase-1 (HO-1) by promoting the nuclear translocation and transactivation of Nrf2. Taken together, these results suggest that SC-E3 has potent antioxidant and anti-inflammatory effects and that these effects are due to the inhibitions of NF-κB and MAPK and the induction of Nrf2-mediated HO-1 expression in macrophages. These findings provide scientific evidence supporting the potential use of SC-E3 for the treatment and prevention of various inflammatory diseases.
Highlights
Interest in diseases and health problems and desires for a better quality of life are rising along with an increase in life expectancy
We evaluated the effects of SC-E3 on the protein levels of iNOS and COX-2, which are involved in the productions of nitric oxide (NO) and prostaglandin E2 (PGE2), respectively, in LPS-stimulated RAW 264.7 macrophages
We confirmed that treatment with SnPP blocked the suppression of LPS-induced NO production by SC-E3. These results demonstrate that the antiinflammatory effects of SC-E3 are mediated by a multitargeting mechanism that involves the inhibitions of mitogen-activated protein kinase (MAPK) and NF-κB and Nrf2-mediated HO-1 induction in macrophages
Summary
Interest in diseases and health problems and desires for a better quality of life are rising along with an increase in life expectancy. Since most disease is associated with the disruption of homeostasis and chronic inflammation, oxidative stress and inflammation have become major health issues. Oxidative stress is defined as an imbalance between the production of reactive oxygen species (ROS) and the capacity of cellular antioxidant defenses [1]. Excessive ROS generation damages cellular macromolecules, including proteins, carbohydrates, lipids, and nucleic acids, dysregulates cellular signaling events, and leads to the pathogeneses and progressions of inflammatory diseases [2]. Inflammation and oxidative stress are often by-products of normal cellular processes, excessive oxidative stress and chronic inflammation can cause chronic diseases, such as diabetes, cancer, degenerative diseases, and obesity, and accelerate the aging process [3]. It is important that oxidative stress and inflammation be adequately controlled to prevent the progressions of chronic diseases
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