Global profiling of protein lactylation in microglia in experimental high-altitude cerebral edema.

Background: High-altitude cerebral edema (HACE) is considered an end-stage acute mountain sickness (AMS) that typically occurs in people after rapid ascent to 2500 m or more. While hypoxia is a fundamental feature of the pathophysiological mechanism of HACE, emerging evidence suggests that inflammation serves as a key risk factor in the occurrence and development of this disease. However, little is known about the molecular mechanism underlying their crosstalk.

Gypenoside-14 Reduces Depression via Downregulation of the Nuclear Factor Kappa B (NF-kB) Signaling Pathway on the Lipopolysaccharide (LPS)-Induced Depression Model.

Neuroinflammation is a common pathogenetic sign of depression and is closely linked to the development of depression. Many clinical anti-inflammatory drugs act as antidepressants by reducing the neuroinflammatory response. Previous research found that gypenosides and their bioactive compound gypenoside-14 (GP-14) had neuroprotective effects against hypoxia-induced injury and reduced neuroinflammation-related high-altitude cerebral edema.

Expression profile of cytokines and chemokines in a mouse high-altitude cerebral edema model.

Introduction: High-altitude cerebral edema (HACE) is considered to be the end-stage of acute mountain sickness (AMS); however, its pathophysiological mechanism remains unknown. Increasing evidences support that inflammation is an important risk factor for the occurrence of HACE. Including our published papers, previous studies demonstrated that the levels of IL-6, IL-1β, and TNF-α in both serum and hippocampus were increased in the mouse HACE model induced by LPS stimulation combined with hypobaric hypoxia exposure; however, the expression profile of other cytokines and chemokines remains unknown.

[Hypoxia promotes lipopolysaccharide-induced CXCL10 expression in microglia].

This study was aimed to investigate the effect of hypoxia on lipopolysaccharide (LPS)-induced CXC-chemokine ligand-10 (CXCL10) expression and the underlying mechanism. C57BL/6J mice were randomly divided into control, hypoxia, LPS, and hypoxia combined with LPS groups. The LPS group was intraperitoneally injected with 0.

[Effects of blocking lactate production by 2-DG on hypoxic injury of HT22 neurons and its mechanisms].

Objective: To investigate the effects of blocking lactate synthesis on the HT22 cell injuries caused by hypoxia.

Methods: 2-deoxy-D-glucose (2-DG) is a non-metabolized glucose analogue that can inhibit lactate synthesis by blocking glycolysis. HT22 cells were divided into 4 groups: Control group, 2-DG group, Hypoxia group and 2-DG+Hypoxia group.

Cyclooxygenase‑2 contributes to the hypoxia‑induced aggravation of the neuroinflammation response stimulated by lipopolysaccharide in microglia.

Hypoxia and neuroinflammation are key risk factors involved in various pathophysiological neural disorders. Hypoxia can aggravate neuroinflammation and ; however, the underlying mechanisms remain unknown. In the present study, hypoxia [either 3 or 1% oxygen (O)] increased lipopolysaccharide (LPS)-induced expression of the IL-6, IL-1β and TNF-α proinflammatory cytokines in BV2 cells.