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Sulforaphane protects against acetaminophen-induced hepatotoxicity
Noh, Jung-Ran,Kim, Yong-Hoon,Hwang, Jung Hwan,Choi, Dong-Hee,Kim, Kyoung-Shim,Oh, Won-Keun,Lee, Chul-Ho Elsevier 2015 Food and chemical toxicology Vol.80 No.-
<P><B>Abstract</B></P> <P>Oxidative stress is closely associated with acetaminophen (APAP)-induced toxicity. Heme oxygenase-1 (HO-1), an antioxidant defense enzyme, has been shown to protect against oxidant-induced tissue injury. This study investigated whether sulforaphane (SFN), as a HO-1 inducer, plays a protective role against APAP hepatotoxicity <I>in vitro</I> and <I>in vivo</I>. Pretreatment of primary hepatocyte with SFN induced nuclear factor E2-factor related factor (Nrf2) target gene expression, especially HO-1 mRNA and protein expression, and suppressed APAP-induced glutathione (GSH) depletion and lipid peroxidation, which eventually leads to hepatocyte cell death. A comparable effect was observed in mice treated with APAP. Mice were treated with 300 mg/kg APAP 30 min after SFN (5 mg/kg) administration and were then sacrificed after 6 h. APAP alone caused severe liver injuries as characterized by increased plasma AST and ALT levels, GSH depletion, apoptosis, and 4-hydroxynonenal (4-HNE) formations. This APAP-induced liver damage was significantly attenuated by pretreatment with SFN. Furthermore, while hepatic reactive oxygen species (ROS) levels were increased by APAP exposure, pretreatment with SFN completely blocked ROS formation. These results suggest that SFN plays a protective role against APAP-mediated hepatotoxicity through antioxidant effects mediated by HO-1 induction. SFN has preventive action in oxidative stress-mediated liver injury.</P> <P><B>Highlights</B></P> <P> <UL> <LI> SFN pretreatment increases the cell viability against APAP-induced toxicity. </LI> <LI> SFN pretreatment protects depletion of cellular GSH after APAP treatment. </LI> <LI> SFN pretreatment enhances Nrf2 target gene expression, especially HO-1 after APAP treatment. </LI> <LI> SFN has protective effect against APAP overdose-induced liver injury <I>in vivo</I> model as well. </LI> </UL> </P>
Noh, Jung-Ran,Lee, In-Kyoung,Kim, Yong-Hoon,Gang, Gil-Tae,Hwang, Jung Hwan,Ly, Sun-Yung,Yun, Bong-Sik,Lee, Chul-Ho S. Karger AG 2011 Annals of nutrition & metabolism Vol.59 No.2
<P>Abstract</P><P><I>Aims:</I> The present study was carried out to investigate the antiatherosclerotic effect of antioxidant polyphenols from <I>Phellinus baumii</I> (PBE) in apolipoprotein E-deficient (apoE–/–) mice. <I>Methods and Results:</I> apoE–/– mice were randomly divided into three groups: mice on a normal chow diet comprised the normal group, mice on an atherogenic diet plus vehicle were the control group, and mice on an atherogenic diet plus PBE (500 mg/kg) comprised the PB500 group. After 8 weeks of treatment, the plasma lipids and cytokine levels were measured. Although no significant differences were found in cholesterol levels among groups, the triglyceride level was significantly decreased in the PBE-treated group compared with the control group. Plasma tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels were reduced by PBE treatment. Real-time PCR analysis of the aorta showed that PBE significantly prevented the upregulation of the vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, TNF-α, IL-6, and IL-1β expression. Furthermore, reduced macrophage infiltration, lipid accumulation and atherosclerotic lesions were observed in the aortic sinus and en face of the whole aorta in PBE-fed apoE–/– mice compared with atherogenic diet-fed control mice. <I>Conclusions:</I> Collectively, the findings of the present study suggest that the antiatherosclerotic effect of PBE is probably related to the inhibition of adhesion molecule and cytokine expression resulting in amelioration of lesion development.</P><P>Copyright © 2011 S. Karger AG, Basel</P>
Jung Hwan Hwang,Tae-Hwan Kim,Yong-Hoon Kim,Jung-Ran Noh,Dong-Hee Choi,Kyoung-Shim Kim,Eun-Young Lee,Byoung-Chan Kim,Myung Hee Kim,Ho Kim,Tae Geol Lee,Jong-Soo Lee,Chul-Ho Lee 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Dysregulated immune responses and impaired function in intestinal epithelial cells contribute to the pathogenesis ofinflammatory bowel disease (IBD). Growth arrest and DNA damage-inducible 45 beta (Gadd45β) has been implicatedin the pathogenesis of various inflammatory symptoms. However, the role of Gadd45β in IBD is completely unknown. This study aimed to evaluate the role of Gadd45β in IBD. Gadd45β-KO mice exhibited drastically greater susceptibilityto dextran sulfate sodium (DSS)-induced colitis and mortality than C57BL/6J mice. Bone marrow transplantationexperiments revealed that Gadd45β functions predominantly in the intestinal epithelium and is critical during therecovery phase. Gadd45β regulates the TGF-β signaling pathway in colon tissue and epithelial cells by inhibitingSmurf-mediated degradation of TGF-β receptor type 1 via competitive binding to the N-terminal domain of Smad7. Furthermore, these results indicate that the Gadd45β-regulated TGF-β signaling pathway is involved in wound healingby enhancing epithelial restitution. These results expand the current understanding of the function of Gadd45β and itstherapeutic potential in ulcerative colitis.