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      Remifentanil Protects against Lipopolysaccharide-Induced Inflammation through PARP-1/NF- κB Signaling Pathway

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          Abstract

          Sepsis is a leading cause of death in patients with severe infection worldwide. Remifentanil is an ultra-short-acting, potent opioid analgesic. In the study, we aimed to investigate the role and underlying mechanism of remifentanil in lipopolysaccharide- (LPS-) induced inflammation in human aortic endothelial cells (HAECs). HAECs were pretreated with phosphate-buffered saline (PBS) or remifentanil (2.5  μM) for 30 min, then stimulated by LPS (10  μg/ml) for another 24 h. Poly(ADP-ribose) polymerase 1 (PARP-1) was inhibited by small interfering RNA (siRNA). Superoxide anion production and DNA damage were analyzed by dihydroethidium (DHE) staining and comet assay. The inducible nitric oxide synthase (iNOS), intercellular adhesion molecule 1 (ICAM-1), PARP-1, poly(ADP-ribose) (PAR), and nuclear factor-kappa B p65 (NF- κB p65) expressions were analyzed by RT-PCR or western blotting analysis. NF- κB p65 nuclear translocation was assessed by immunofluorescence. Compared with the control group, pretreatment with remifentanil significantly reduced superoxide anion production and DNA damage, with downregulation of iNOS, ICAM-1, and PARP-1 expressions as well as PAR expression. Moreover, pretreatment with PARP-1 siRNA or remifentanil inhibited LPS-induced NF- κB p65 expression and nuclear translocation. Remifentanil reduced LPS-induced inflammatory response through PARP-1/NF- κB signaling pathway. Remifentanil might be an optimal choice of analgesia in septic patients.

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          Most cited references28

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          Poly(ADP-ribose): novel functions for an old molecule.

          The addition to proteins of the negatively charged polymer of ADP-ribose (PAR), which is synthesized by PAR polymerases (PARPs) from NAD(+), is a unique post-translational modification. It regulates not only cell survival and cell-death programmes, but also an increasing number of other biological functions with which novel members of the PARP family have been associated. These functions include transcriptional regulation, telomere cohesion and mitotic spindle formation during cell division, intracellular trafficking and energy metabolism.
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            Mechanisms and treatment of organ failure in sepsis

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              Biology of Poly(ADP-Ribose) Polymerases: The Factotums of Cell Maintenance.

              Péter Bai (2015)
              The protein family of poly(ADP-ribose) polymerases (PARPs) or diphtheria toxin-type ADP-ribose transferases (ARTDs) are multidomain proteins originally identified as DNA repair factors. There are 17 PARP enzymes in humans, and it is now evident that PARPs undertake more tasks than DNA repair. The aim of this review is to give a comprehensive view of the biological roles of the PARP family starting from the simplest biochemical reactions to complex regulatory circuits. Special attention will be laid on discussing linkage of PARP enzymes with tumor biology, oxidative stress, inflammatory, and metabolic diseases. A better understanding of PARP-mediated processes and pathologies may help in identifying new pathways and, by these, new targets to combat diseases that affect large populations and seriously shorten life expectancy and the quality of life, such as cancer, metabolic, or inflammatory diseases.
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                Author and article information

                Contributors
                Journal
                Mediators Inflamm
                Mediators Inflamm
                MI
                Mediators of Inflammation
                Hindawi
                0962-9351
                1466-1861
                2019
                31 December 2019
                : 2019
                : 3013716
                Affiliations
                1Department of Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, Shandong, China
                2State Key Laboratory of Biobased Material and Green Papermaking, Key Laboratory of Pulp & Paper Science and Technology of Shandong Province/Ministry of Education, Qilu University of Technology, Shandong Academy of Sciences, Jinan, China
                3The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of Shandong University, Jinan, Shandong, China
                Author notes

                Academic Editor: Antonella Fioravanti

                Author information
                https://orcid.org/0000-0001-7238-6860
                Article
                10.1155/2019/3013716
                7012251
                32082073
                f024cb0b-a950-44da-83d7-caaa4158c5de
                Copyright © 2019 Jian-ning Zhang et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 6 July 2019
                : 29 November 2019
                : 11 December 2019
                Funding
                Funded by: Natural Science Foundation of Shandong Province
                Award ID: ZR2019PH007
                Award ID: ZR201807061161
                Funded by: China Postdoctoral Science Foundation
                Award ID: 2018M630788
                Categories
                Research Article

                Immunology
                Immunology

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