一二三四区视频,亚洲少妇熟女色,日本久热无码视频网,欧美国产日韩大尺度,亚洲a视频,久久少妇一区二区,日韩999无码视频,刺激久久久久久久,啊啊啊啊不要啊在线

ChemicalBook >> journal list >> Neural Regeneration Research >>article
Neural Regeneration Research

Neural Regeneration Research

IF: 5.9
Download PDF

TMEM16F may be a new therapeutic target for Alzheimer’s disease

Published:1 March 2023 DOI: 10.4103/1673-5374.350211 PMID: 36018189
Zhi-Qiang Cui, Xiao-Ying Hu, Tuo Yang, Jing-Wei Guan, Ying Gu, Hui-Yuan Li, Hui-Yu Zhang, Qing-Huan Xiao, Xiao-Hong Sun

Abstract

TMEM16F is involved in many physiological processes such as blood coagulation, cell membrane fusion and bone mineralization. Activation of TMEM16F has been studied in various central nervous system diseases. High TMEM16F level has been also found to participate in microglial phagocytosis and transformation. Microglia-mediated neuroinflammation is a key factor in promoting the progression of Alzheimer's disease. However, few studies have examined the effects of TMEM16F on neuroinflammation in Alzheimer's disease. In this study, we established TMEM16F-knockdown AD model in vitro and in vivo to investigate the underlying regulatory mechanism about TMEM16F-mediated neuroinflammation in AD. We performed a Morris water maze test to evaluate the spatial memory ability of animals and detected markers for the microglia M1/M2 phenotype and NLRP3 inflammasome. Our results showed that TMEM16F was elevated in 9-month-old APP/PS1 mice. After TMEM16F knockdown in mice, spatial memory ability was improved, microglia polarization to the M2 phenotype was promoted, NLRP3 inflammasome activation was inhibited, cell apoptosis and Aβ plaque deposition in brain tissue were reduced, and brain injury was alleviated. We used amyloid-beta (Aβ25-35) to stimulate human microglia to construct microglia models of Alzheimer's disease. The levels of TMEM16F, inducible nitric oxide synthase (iNOS), proinflammatory cytokines and NLRP3 inflammasome-associated biomarkers were higher in Aβ25-35 treated group compared with that in the control group. TMEM16F knockdown enhanced the expression of the M2 phenotype biomarkers Arg1 and Socs3, reduced the release of proinflammatory factors interleukin-1, interleukin-6 and tumor necrosis factor-α, and inhibited NLRP3 inflammasome activation through reducing downstream proinflammatory factors interleukin-1β and interleukin-18. This inhibitory effect of TMEM16F knockdown on M1 microglia was partially reversed by the NLRP3 agonist Nigericin. Our findings suggest that TMEM16F participates in neuroinflammation in Alzheimer's disease through participating in polarization of microglia and activation of the NLRP3 inflammasome. These results indicate that TMEM16F inhibition may be a potential therapeutic approach for Alzheimer's disease treatment.

Substances (4)

Materials
Procduct Name CAS Molecular Formula Supplier Price
NIGERICIN SODIUM SALT 28380-24-7 C40H68O11 152 suppliers Inquiry
NIGERICIN SODIUM SALT 28380-24-7 C40H68O11 152 suppliers Inquiry
NIGERICIN SODIUM SALT 28380-24-7 C40H68O11 152 suppliers Inquiry
NIGERICIN SODIUM SALT 28380-24-7 C40H68O11 152 suppliers Inquiry

Similar articles

IF:3.2

Frontiers | Tauroursodeoxycholic acid: a bile acid that may be used for the prevention and treatment of Alzheimer’s disease

Frontiers in Neuroscience Honghu Song, Jiancheng Liu,etc Published: 7 February 2024
IF:3.9

Magnesium may be an effective therapy for Alzheimer's disease.

World Journal of Psychiatry Dao-Yun Lei, Jie Sun,etc Published: 19 September 2022
IF:4.4

Palmitoylethanolamide (PEA) as a Potential Therapeutic Agent in Alzheimer’s Disease

Frontiers in Pharmacology S. Beggiato,?M. C. Tomasini,etc Published: 24 July 2019
无锡市| 临泽县| 温泉县| 防城港市| 明溪县| 邹平县| 磐安县| 桐乡市| 周宁县| 遂平县| 杨浦区| 印江| 疏附县| 江门市| 临汾市| 子长县| 武陟县| 新民市| 伊通| 漳州市| 阳东县| 宁夏| 天门市| 宾川县| 浮山县| 乌审旗| 海伦市| 桐庐县| 永新县| 闽侯县| 宜君县| 新田县| 寻甸| 江油市| 剑阁县| 马关县| 开平市| 高阳县| 大名县| 永安市| 青冈县|