Research on glucose oxidase nanoparticles combined with dexmedetomidine in regulating oxygen metabolism and improving damaged cells in hypoxic-ischenmia reperfusion brain damage

Author:

Wang Jun1,Fang Meng2,Li Jingjing2

Affiliation:

1. Department of Anesthesiology, Huaian Second People’s Hospital, Huaian Hospital Affiliated to Xuzhou Medical University, Huaian City, Jiangsu Province, 223299, China

2. Department of Anesthesiology, First People’s Hospital of Zaoyang City, Zaoyang City, Hubei Province, 441299, China

Abstract

The aim of this study was to assess GOX-NPs (glucose oxidase nanoparticles) combined with dexmedetomidine in regulating oxygen metabolism and improving the damaged cells in HIRBD (hypoxic-ischenmia reperfusion brain damage, HIRBD). Model of hippocampal neurons injured by hypoxia and reoxygenation was prepared in vitro. The groups were randomly divided into control set, DEX (dexmedetomidine) set, GOX-NPs (glucose oxidase nanoparticles) set and set of DEX and GOX-NPs. Proliferative and apoptotic activity, expression of Cyt-c (cytochrome-c) and APAF-1 (Apoptotic protease activating factor-1), quantity of total adenine nucleotide, activity of reactive oxygen species (ROS) and SOD (Superoxide dismutase), and expression of HMGB1 (High mobility group box 1 protein) were all observed, proliferation was prompted in DEX set and GOX-NPs set, while apoptotic activity was restrained. The expressions of Cyt-c and APAF-1 (Apoptotic protease activating factor-1) were restrained. ROS content was reduced, and SOD activity was increased, and HMGB1 presentation was reduced. The action in the DEX and GOX-NPs sets was notable, while proliferation of nerve cells in cerebral injury with hypoxia and reoxygenation was prompted by oxidase nanoparticles combined with dexmedetomidine, and apoptosis was restrained. The energy metabolism was improved effectively through restraining inflammatory pathway and oxidative stress. The nerve cells in the cerebral injury with hypoxia and reoxygenation was effectively improved.

Publisher

American Scientific Publishers

Subject

General Materials Science

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