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题名SIRT1 Activation Reduces LPS-Induced Human Middle Ear Epithelial Cell Injury via Promoting Autophagy
作者
发表日期2024-02
发表期刊JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS   影响因子和分区
语种英语
原始文献类型Article
关键词otitis media SIRT1 inflammatory response autophagy human middle ear epithelial cells
其他关键词ACUTE OTITIS-MEDIA ; COCHLEAR HAIR CELL ; OXIDATIVE STRESS ; KAPPA-B ; INFLAMMATION
摘要Background: Otitis media (OM) is a prevalent pervasive illness among the pediatric population. Research on sirtuin 1 (SIRT1), a deacetylase sensitive to nicotinamide adenine dinucleotide (NAD(+)), has increasingly identified its pivotal role in various inflammatory conditions. Our study aims to elucidate the role of SIRT1 in inflammatory injury in OM and its potential action mechanism. Methods: Human middle ear epithelial cells (HMEECs) were stimulated with lipopolysaccharide (LPS) to establish in vitro models of OM. Western blot was used to assess SIRT1 expression. Following the addition of SIRT1 activator SRT1720, with or without the autophagy inhibitor 3-Methyladenine (3-MA), the Cell Counting Kit-8 (CCK-8) assay was used to evaluate cell viability. Terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) assay was used to assess cell apoptotic levels. Enzyme-linked immunosorbent assay (ELISA) was used to estimate inflammatory levels and dichloro-dihydro-fluorescein diacetate (DCFH-DA) staining was used to estimate reactive oxygen species (ROS) activity. Western blot was used to analyze the content of apoptosis-, inflammatory response-, autophagy-, and nuclear factor-kappaB (NF-kappa B) signaling-associated proteins. Results: SIRT1 expression was attenuated in LPS-treated HMEECs (p < 0.05). SRT1720 pretreatment significantly enhanced cell viability (p < 0.05), attenuated apoptosis (p < 0.05), suppressed the inflammatory response (p < 0.05), and reduced ROS production (p < 0.05). Additionally, it inhibited NF-kappa B signaling (p < 0.05) while inducing autophagy (p < 0.05) in HMEECs exposed to LPS in a concentration-dependent manner. Furthermore, 3-Methyladenine (3-MA) partially counteracted the suppressive effects of SRT1720 in LPS-induced viability loss, apoptosis (p < 0.05), inflammatory response (p < 0.05), NF-kappa B signaling activation (p < 0.05), and ROS generation (p < 0.05) in HMEECs. Conclusions: In summary, the activation of SIRT1 may mitigate the inflammatory response in LPS-induced HMEECs through the modulation of apoptosis, inflammatory signaling, and autophagic processes.
出版者BIOLIFE SAS
ISSN0393-974X
EISSN1724-6083
卷号38期号:2页码:1341-1350
DOI10.23812/j.biol.regul.homeost.agents.20243802.107
页数10
WOS类目Endocrinology & Metabolism ; Immunology ; Medicine, Research & Experimental ; Physiology
WOS研究方向Endocrinology & Metabolism ; Immunology ; Research & Experimental Medicine ; Physiology
WOS记录号WOS:001159366700001
收录类别SCIE
通讯作者地址[Liu, Fanli]Wenzhou Med Univ, Affiliated Hosp 2, Dept Otolaryngol Head & Neck Surg, Wenzhou 325027, Zhejiang, Peoples R China. ; [Liu, Fanli]Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou 325027, Zhejiang, Peoples R China.
引用统计
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/209890
专题附属第二医院_耳鼻咽喉科
第二临床医学院,附属第二医院、育英儿童医院
通讯作者Liu, Fanli
作者单位
1.Wenzhou Med Univ, Affiliated Hosp 2, Dept Otolaryngol Head & Neck Surg, Wenzhou 325027, Zhejiang, Peoples R China;
2.Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou 325027, Zhejiang, Peoples R China
第一作者单位附属第二医院_耳鼻咽喉科;  第二临床医学院,附属第二医院、育英儿童医院
通讯作者单位附属第二医院_耳鼻咽喉科;  第二临床医学院,附属第二医院、育英儿童医院
第一作者的第一单位附属第二医院_耳鼻咽喉科
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GB/T 7714
Zheng, Bo,Zheng, Lei,Liu, Fanli. SIRT1 Activation Reduces LPS-Induced Human Middle Ear Epithelial Cell Injury via Promoting Autophagy[J]. JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS,2024,38(2):1341-1350.
APA Zheng, Bo, Zheng, Lei, & Liu, Fanli. (2024). SIRT1 Activation Reduces LPS-Induced Human Middle Ear Epithelial Cell Injury via Promoting Autophagy. JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS, 38(2), 1341-1350.
MLA Zheng, Bo,et al."SIRT1 Activation Reduces LPS-Induced Human Middle Ear Epithelial Cell Injury via Promoting Autophagy".JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS 38.2(2024):1341-1350.

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