Dysfunctional phagocytosis capacity, granulocyte recruitment and inflammatory factor secretion of Kupffer cells in diabetes mellitus reversed by Lidocaine
机构：[1]Department of Emergency, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China[2]Department of Gynaecology and Obstetrics, China- Japan Union Hospital of Jilin University, Changchun, Jilin 130033, China[3]Department of Pathology, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China[4]Department of Medical Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China[5]Department of Medical Records and Statistics, Xuanwu Hospital, Capital Medical University, Beijing 100045, China首都医科大学宣武医院[6]Department of Infection Control, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China[7]Department of Gynaecology and Obstetrics, Beijing Key Laboratory of Cancer Therapeutic Vaccine, Beijing 100038, China[8]Department of Evidence-based Medicine, Oncology School of Capital Medical University, Beijing 100038, China[9]Department of Science and Technology, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China
Purpose: Kupffer cells (KCs) present dysfunctional immunity capacity among the diabetes mellitus patients. This study aims to investigate whether Lidocaine could reverse dysfunctions of KCs, in terms of phagocytosis, granulocyte recruitment and inflammatory mediator secretion. Methods: db/db and C57BL/6 mice were employed to establish diabetic and nondiabetic models. Upon intravenous injection of Lidocaine, KCs were isolated and cultured ex vivo. The functions of phagocytosis, recruiting granulocytes and inflammatory mediator secretion in KCs were compared between Lidocaine-treated and untreated (control) groups. Results: Comparing with nondiabetic mice, KCs in diabetic mice presented reduced phagocytosis, activated granulocyte recruitment, increased expression of intercellular cell adhesion molecule-1 (ICAM-1) and activated levels of inflammatory mediators. With Lidocaine injection, phagocytic functions of KCs in diabetic mice were improved significantly; in contrast, recruitment of granulocytes, expression of ICAM-1 and secretion of inflammatory mediators were reduced markedly. However, Lidocaine intervention did not alter KC functions in phagocytosis, granulocyte recruitment, ICAM-1 expression or inflammatory mediator secretion among nondiabetic mice. Conclusion: Lidocaine reversed diabetes-related dysfunctions of KCs in terms of phagocytosis, granulocyte recruitment, ICAM-1 expression or inflammatory mediator secretion.
基金：
This study was supported by Beijing Shijitan Hospital
(RW. 2016-Q18), Ministry of Railway (QS. grant number
J2017Z604) and Beijing Municipal Administration of
Hospitals (QS. grant number PX2018029).
第一作者机构：[1]Department of Emergency, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China
通讯作者：
通讯机构：[*1]Department of Science and Technology, Beijing Shijitan Hospital, Capital Medical University, Tieyi Road 10, Haidian District, Beijing 100038, China[*2]Department of Gynaecology and Obstetrics, China-Japan Union Hospital of Jilin University, No.126 Xiantai Road, Changchun 130033, China
推荐引用方式(GB/T 7714)：
Wang Ruibin,Sheng Minjia,Shi Feng,et al.Dysfunctional phagocytosis capacity, granulocyte recruitment and inflammatory factor secretion of Kupffer cells in diabetes mellitus reversed by Lidocaine[J].DIABETES METABOLIC SYNDROME AND OBESITY-TARGETS AND THERAPY.2018,11:827-834.doi:10.2147/DMSO.S186695.
APA：
Wang, Ruibin,Sheng, Minjia,Shi, Feng,Zhao, Yanjie,Zhao, Lin...&Song, Qingkun.(2018).Dysfunctional phagocytosis capacity, granulocyte recruitment and inflammatory factor secretion of Kupffer cells in diabetes mellitus reversed by Lidocaine.DIABETES METABOLIC SYNDROME AND OBESITY-TARGETS AND THERAPY,11,
MLA：
Wang, Ruibin,et al."Dysfunctional phagocytosis capacity, granulocyte recruitment and inflammatory factor secretion of Kupffer cells in diabetes mellitus reversed by Lidocaine".DIABETES METABOLIC SYNDROME AND OBESITY-TARGETS AND THERAPY 11.(2018):827-834
