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Kim, Kwang-Youn,Park, Kwang-Il,Lee, Seul Gi,Baek, Su Youn,Lee, Eun Hye,Kim, Sang Chan,Kim, Sang-Hun,Park, Sul-Gi,Yu, Sun-Nyoung,Oh, Tae Woo,Kim, Joung-Hee,Kim, Keuk-Jun,Ahn, Soon-Cheol,Kim, Young Woo Elsevier 2018 Chemico-biological interactions Vol.294 No.-
<P><B>Abstract</B></P> <P>Deoxypodophyllotoxin (DPT) is a naturally occurring flavolignan in <I>Anthriscus sylvestris</I> known as cow parsley or wild chervil, and has been reported to have inhibitory effects against several pathological processes including cancer, inflammation and infection. Here, we report the effects of DPT in the fatty liver induced by high fat diet <I>in vivo</I> as well as its regulatory mechanism related with the transcription factor for lipogenic genes such as sterol regulatory element binding protein-1c (SREBP-1c) <I>in vitro</I>. C57BL/6 mice were fed high fat diet for 10 weeks and also orally administrated with DPT for additional 4 weeks. 5 and 10 mg/kg of DPT decreased lipid accumulation in the liver induced by high fat diet, as indicated by histological parameters such as Oil Red O staining and hematoxylin & eosin as well as the contents of hepatic triglyceride and cholesterol. In hepatocytes, DPT inhibited the liver X receptor α-mediated SREBP-1c induction and expression of the lipogenic genes, including fatty acid synthase, acetyl-CoA carboxylase and stearoyl-CoA desaturase-1. Moreover, DPT induced AMP-activated protein kinase (AMPK) activation, which has been known to inhibit the expression of SREBP-1c in hepatocyte. Also this compound restored the dysregulation of AMPK and SREBP-1c induced by high fat diet in mice. In conclusion, we demonstrated that DPT significantly inhibited fatty liver by adjusting lipid metabolism coordinated with AMPK activation and SREBP-1c inhibition.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Deoxypodophyllotoxin (DPT), a chemopreventive flavolignan, inhibited diet-induced fatty liver. </LI> <LI> DPT inhibited the LXR-α-mediated sterol regulatory element binding protein (SREBP)-1c. </LI> <LI> DPT blocked the expression of <I>de novo</I> lipogenic genes including FAS and ACC. </LI> <LI> DPT activated AMPK related with SREBP-1c inhibition. </LI> <LI> DPT might be a pharmaceutical candidate for hepatic steatosis. </LI> </UL> </P>
Comparision of doxorubicin-induced cardiotoxicity in the ICR mice of different sources
Sou Hyun Kim,Keuk-Jun Kim,Joung-Hee Kim,Jae-Hwan Kwak,HyunKeun Song,Joon Young Cho,Dae Youn Hwang,Kil Soo Kim,Young-Suk Jung 한국실험동물학회 2017 Laboratory Animal Research Vol.33 No.2
Doxorubicin is a widely used chemotherapeutic agents and is now part of standard therapeutic regimens for a variety of cancers (eg, hematopoietic malignancies and advanced solid tumors of the breast, ovary, thyroid, and bone). However, a potentially lethal and dose-dependent cardiotoxicity that appears within a short time after treatment limits the usage of doxorubicin in cancer patients. Although the mechanism of doxorubicin-induced cardiotoxicity is not completely understood, it is thought that free radical-induced oxidative stress and excessive production of reactive oxygen species are primary drivers of its toxicity. In this study, we compared the doxorubicin-induced cardiotoxicity of ICR mice obtained from three different sources and evaluated the utility of Korl:ICR stock established by the Korean FDA. Because doxorubicin-induced cardiotoxicity is thought to involve the excessive generation of ROS followed by oxidative stress, we determined the representative tissue index of oxidation, lipid peroxidation, and antioxidant, glutathione (GSH), as well as the parameters of heart injury. Doxorubicin treatment successfully induced cardiotoxicity as evidenced by histological examination and serum parameters (eg, levels of LDH and CK activities) in ICR mice. It was accompanied by increased lipid peroxidation and a decrease in both cysteine and GSH, further supporting previous reports that oxidative stress is a potential mechanism of doxorubicin-induced cardiotoxicity. Of interest, we did not observe a significant difference in doxorubicin-induced cardiotoxicity among mice of different origins. Collectively, our results suggest that Korl:ICR strain may be useful in the research of doxorubicin-induced cardiotoxicity.
Byung Gyu Kim,Sung-Jin Hong,Byeong-Keuk Kim,Yong-Joon Lee,Seung-Jun Lee,Chul-Min Ahn,Dong-Ho Shin,Jung-Sun Kim,Young-Guk Ko,Donghoon Choi,Myeong-Ki Hong,Yangsoo Jang 대한심장학회 2023 Korean Circulation Journal Vol.53 No.12
Background and Objectives: We evaluated the effect of diabetes on the relationship between body mass index (BMI) and clinical outcomes in patients following percutaneous coronary intervention (PCI) with drug-eluting stent implantation. Methods: A total of 6,688 patients who underwent PCI were selected from five different registries led by Korean Multicenter Angioplasty Team. They were categorized according to their BMI into the following groups: underweight (<18.5 kg/m2), normal weight (18.5–24.9 kg/m2), overweight to obese (≥25.0 kg/m2). Major adverse cardiac and cerebrovascular events (MACCE), defined as a composite of death, nonfatal myocardial infarction, stroke, and target-vessel revascularization, were compared according to the BMI categories (underweight, normal and overweight to obese group) and diabetic status. All subjects completed 1-year follow-up. Results: Among the 6,688 patients, 2,561 (38%) had diabetes. The underweight group compared to normal weight group had higher 1-year MACCE rate in both non-diabetic (adjusted hazard ratio [HR], 2.24; 95% confidence interval [CI], 1.04–4.84; p=0.039) and diabetic patients (adjusted HR, 2.86; 95% CI, 1.61–5.07; p<0.001). The overweight to obese group had a lower MACCE rate than the normal weight group in diabetic patients (adjusted HR, 0.67 [0.49–0.93]) but not in non-diabetic patients (adjusted HR, 1.06 [0.77–1.46]), with a significant interaction (p-interaction=0.025). Conclusions: Between the underweight and normal weight groups, the association between the BMI and clinical outcomes was consistent regardless of the presence of diabetes. However, better outcomes in overweight to obese over normal weight were observed only in diabetic patients. These results suggest that the association between BMI and clinical outcomes may differ according to the diabetic status.
Lee, Kyunghee,Kim, Hyunsoo,Kim, Jin-Man,Kim, Jae-Ryong,Kim, Keuk-Jun,Kim, Yong-Jin,Park, Se-Il,Jeong, Jae-Ho,Moon, Young-mi,Lim, Hyun-Sook,Bae, Dong-Won,Kwon, Joseph,Ko, Chang-Yong,Kim, Han-Sung,Shin, Blackwell Publishing Ltd 2011 JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Vol.15 No.10
<P>Systemic transplantation of adipose-derived stem cells (ASCs) is emerging as a novel therapeutic option for functional recovery of diverse damaged tissues. This study investigated the effects of systemic transplantation of human ASCs (hASCs) on bone repair. We found that hASCs secrete various bone cell-activating factors, including hepatocyte growth factor and extracellular matrix proteins. Systemic transplantation of hASCs into ovariectomized mice induced an increased number of both osteoblasts and osteoclasts in bone tissue and thereby prevented bone loss. We also observed that conditioned medium from hASCs is capable of stimulating proliferation and differentiation of osteoblasts <I>via</I> Smad/extracellular signal-regulated kinase (ERK)/JNK (c-jun NH<SUB>2</SUB>-terminal kinase) activation as well as survival and differentiation of osteoclasts <I>via</I> ERK/JNK/p38 activation <I>in vitro</I>. Overall, our findings suggest that paracrine factors secreted from hASCs improve bone repair and that hASCs can be a valuable tool for use in osteoporosis therapy.</P>