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Protective effects of <i>p-</i>coumaric acid against acetaminophen-induced hepatotoxicity in mice
Cha, Hanvit,Lee, Seoyoon,Lee, Jin Hyup,Park, Jeen-Woo Elsevier 2018 Food and chemical toxicology Vol.121 No.-
<P><B>Abstract</B></P> <P>Acetaminophen (N-acetyl-p-aminophenol, AAP) is an effective analgesic and antipyretic drug with minimal toxicity when used at therapeutic doses. However, AAP overdose is the most common cause of drug-induced acute liver failure and one of the main causes of morbidity and mortality. <I>p-</I>Coumaric acid (PCA) is the most abundant isomer of hydroxycinnamic acid in nature, and it can be widely found in fruits, vegetables, and plants products. PCA has strong antioxidant activity and exhibits protective effects in numerous disease models associated with reactive oxygen species (ROS) generation. In this study, we investigated the protective effects of PCA on AAP-induced hepatotoxicity and the underlying mechanisms using an <I>in vivo</I> model. We found that PCA ameliorates AAP-induced hepatotoxicity as well as the reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity. Furthermore, we observed that PCA suppressed hepatic apoptosis via ROS-mediated DNA damage responses and inflammation by modulating the mitogen-activated protein kinase (MAPK) signaling axis in an ROS-dependent manner. These findings indicate that the administration of PCA protects against AAP-induced hepatotoxicity, suggesting it could be a novel therapeutic strategy for AAP-induced liver injury.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Acetaminophen (AAP) overdose causes drug-induced acute liver failure. </LI> <LI> <I>p-</I>Coumaric acid (PCA) ameliorates AAP-induced hepatotoxicity in mice model. </LI> <LI> PCA suppressed hepatic apoptosis via ROS-mediated DNA damage responses. </LI> <LI> PCA protected inflammation by modulating MAPK signaling axis. </LI> </UL> </P>
<i>Idh2</i> deficiency accelerates renal dysfunction in aged mice
Lee, Su Jeong,Cha, Hanvit,Lee, Seoyoon,Kim, Hyunjin,Ku, Hyeong Jun,Kim, Sung Hwan,Park, Jung Hyun,Lee, Jin Hyup,Park, Kwon Moo,Park, Jeen-Woo Academic Press 2017 Biochemical and biophysical research communication Vol. No.
<P><B>Abstract</B></P> <P>The free radical or oxidative stress theory of aging postulates that senescence is due to an accumulation of cellular oxidative damage, caused largely by reactive oxygen species (ROS) that are produced as by-products of normal metabolic processes in mitochondria. The oxidative stress may arise as a result of either increased ROS production or decreased ability to detoxify ROS. The availability of the mitochondrial NADPH pool is critical for the maintenance of the mitochondrial antioxidant system. The major enzyme responsible for generating mitochondrial NADPH is mitochondrial NADP<SUP>+</SUP>-dependent isocitrate dehydrogenase (IDH2). Depletion of IDH2 in mice (<I>idh2</I> <SUP>-<I>/</I>-</SUP>) shortens life span and accelerates the degeneration of multiple age-sensitive traits, such as hair grayness, skin pathology, and eye pathology. Among the various internal organs tested in this study, IDH2 depletion-induced acceleration of senescence was uniquely observed in the kidney. Renal function and structure were greatly deteriorated in 24-month-old <I>idh2</I> <SUP> <I>-/</I>-</SUP> mice compared with wild-type. In addition, disruption of redox status, which promotes oxidative damage and apoptosis, was more pronounced in <I>idh2</I> <SUP> <I>-/</I>-</SUP> mice. These data support a significant role for increased oxidative stress as a result of compromised mitochondrial antioxidant defenses in modulating life span in mice, and thus support the oxidative stress theory of aging.</P> <P><B>Highlights</B></P> <P> <UL> <LI> IDH2 is a major enzyme to maintain mitochondrial redox status. </LI> <LI> Depletion of IDH2 in mice shortens life span and accelerates aging. </LI> <LI> Renal function was greatly deteriorated in 24-month-old <I>idh2</I> <SUP>-<I>/</I>-</SUP> mice. </LI> </UL> </P>