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RISS 인기검색어
- 검색키워드
- 저자 : Yongyong Li (검색결과 3 건)
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Li, Ruiwen,Zhou, Peijiang,Guo, Yongyong,Lee, Jae-Seong,Zhou, Bingsheng Elsevier 2017 Neurotoxicology Vol.58 No.-
<P>Tris (1, 3-dichloro-2-propyl) phosphate (TDCIPP, also known as TDCPP), an extensively used flame retardant, is frequently detected in the environment and biota. Recent studies have shown that TDCIPP has neurotoxic effects. In this study, we determined the mechanisms of TDCIPP-induced neurotoxicity in human neuroblastoma (SH-SY5Y) cells. By using morphological examination, flow cytometry, and mitochondrial membrane potential (Delta Ym) measurement, we confirmed that exposure to TDCIPP caused apoptosis accompanied by the activation of apoptosis-related genes (e.g. Bax and Bc1-2) and caspase 3 protein in SH-SY5Y cells. Increased reactive oxygen species (ROS) formation and intracellular calcium ions ([Ca2+](i)) were also observed in TDCIPP-treated SH-SY5Y cells. Exposure to TDCIPP led to the activation of protein markers of endoplasmic reticulum (ER) stress, including eukaryotic translation initiation factor 2a subunit (p-EIF2a), activation transcription factor (ATF4), glucose-regulated protein (GRP78), and the proapoptotic factor C/EBP homologous protein (CHOP). To determine the role of the ER in apoptosis, phenyl butyric acid (PBA), an ER stress inhibitor, was applied. Treatment with PBA effectively attenuated TDCIPP-induced ER stress and protected against apoptotic death in SH-SY5Y cells by inhibition of Bax expression and promotion of Bcl-2 expression. Furthermore, we found that pretreatment of the cells with the ROS scavenger N-acetyl cysteine (NAC) inhibited the ER stress response and prevented apoptosis. The combination of PBA and NAC pretreatment could further prevent TDCIPP induced ER-stress and apoptotic death compared with PBA or NAC pretreatment alone. Thus, in the present study, we demonstrated that TDCIPP induces cytotoxicity through a ROS-dependent mechanism involving ER stress and activation of mitochondrial apoptotic pathways in SH-SY5Y cells. (C) 2016 Elsevier B.V. All rights reserved.</P>
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Shuhui Zheng,Hang Zhou,Bo Gao,Yongyong Li,Zhiheng Liao,Taifeng Zhou,Chengjie Lian,Zizhao Wu,Deying Su,Tingting Wang,Peiqiang Su,Caixia Xu 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
This study aimed to verify the effects of estrogen on the onset and development of adolescent idiopathic scoliosis and the mechanisms associated with these effects by constructing a pubescent bipedal rat model. Experiments were conducted to investigate whether scoliosis progression was prevented by a Triptorelin treatment. One hundred twenty bipedal rats were divided into female, OVX (ovariectomy), OVX + E2, Triptorelin, sham, and male groups. According to a spinal radiographic analysis, the scoliosis rates and curve severity of the female and OVX + E2 groups were higher than those in the OVX, Triptorelin, and male groups. The measurements obtained from the sagittal plane of thoracic vertebrae CT confirmed a relatively slower growth of the anterior elements and a faster growth of the posterior elements between T11 and T13 in the female and OVX + E2 groups than in the OVX and Triptorelin groups. Histomorphometry and immunohistochemistry revealed a significantly longer hypertrophic zone of the vertebral cartilage growth plates that expressed more type X collagen and less type II collagen in the OVX and Triptorelin groups than in the female and OVX + E2 groups. Ki67 immunostaining confirmed an increase in the proliferation of vertebral growth plate chondrocytes in the OVX group compared with the female and OVX + E2 groups. In conclusion, estrogen obviously increased the incidence of scoliosis and curve severity in pubescent bipedal rats. The underlying mechanism may be a loss of coupling of the endochondral ossification between the anterior and posterior columns. Triptorelin decreased the incidence of scoliosis and curve magnitudes in bipedal female rats. Introduction Adolescent
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Zhendi Wang,Zhuo Zuo,Lu Li,Suping Ren,Tianchang Gao,Jingqi Fu,Yongyong Hou,Yanyan Chen,Jingbo Pi 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.3
White adipocytes play a key role in maintainingwhole body energy homeostasis by forming white adiposetissue (WAT). The impairment of WAT formation or WATdysfunction is clearly associated with severe metabolic disorders. Mature adipocytes are derived from differentiatedpreadipocytes and are pivotal in energy storage and metabolism. Nuclear factor erythroid 2-related factor 2 (Nrf2) isa member of a family of CNC-bZIP proteins which exerttheir transcriptional control on genes harboring antioxidantresponse elements (ARE) in partnership with smallmusculoaponeurotic fibrosarcoma proteins. The activationof Nrf2-ARE coordinated by specific repressor Kelch-likeECH-associated protein 1 (Keap1) regulates networks ofgenes controlling diverse homeostatic processes involvingadaptive antioxidant response and detoxification amongmany other adaptive responses. Interestingly, accumulatingevidence indicates that Nrf2 may act as a transcription factorin regulating the formation and function of adipose tissues,including adipogenesis, lipid metabolism and insulin sensitivity. In this mini-review, an overview on the distinct rolesof Nrf2 in adipocytes is provided. While highlighting the regulatory role of Nrf2 in adipogenesis, recent key findingson Nrf2 in insulin signal transduction and energy metabolismof adipocytes are also summarized.
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