1.Effect of isoflurane pretreatment on hypoxia/reoxygenation-induced syndecan-1 shedding from human umbilical vein endothelial cells
Changyin YAO ; Shengyuan TONG ; Zeping DAI
Chinese Journal of Anesthesiology 2011;31(5):627-629
Objective To investigate the effect of isoflurane pretreatment on hypoxia/reoxygenation (H/R)-induced syndecan-1 shedding from human umbilical vein endothelial cells (HUVECs) . Methods HUVECs were cultured in EMB-2 medium and randomly divided into 3 groups ( n = 32 each) : control group (group C), H/R group and isoflurane pretreatment group (group I). H/R was produced by 4 h exposure of HUVECs to hypoxia followed by 2 h reoxygenation in H/R and I groups. HUVECs were exposed to the mixture of 5% CO2 and 95% O2 for 30 min and then cultured in normal culture atmosphere (21% O2) in group C. In group I, HUVECs were expased to 1.73% isoflurane and incubated for 30 min before H/R. The syndecan-1 expression, concentrations of shed syndecan-1 in the medium, and cell permeability and viability were measured at the end of reoxygenation. Results Compared with group C, the shed syndecan-1 concentration in the medium and cell permeability were significantly increased, while the syndecan-1 expression and cell viability decreased in H/R and Ⅰ groups ( P < 0.01) . Compared with group H/R, the shed syndecan-1 concentration in the medium and cell permeability were significantly decreased, while the syndecan-1 expression and cell viability increased in group Ⅰ (P < 0.01) . Conclusion Isoflurane pretreatment can protect HUVECs against H/R injury through inhibiting the syndecan-1 shedding.
2.Recent advance in Aβ tolerance in Alzheimer's disease
Jiayue CHEN ; Xueyan HUANG ; Qianqian YAO ; Changyin YU
Chinese Journal of Neuromedicine 2024;23(8):837-841
Beta-amyloid (Aβ) is considered to be a central event in Alzheimer's disease (AD). However, it has been found that some population have Aβ deposition in the brain and even AD related pathology without obvious cognitive impairment, which indicates that there are factors in the body to avoid or cope with Aβ damage, and this phenomenon is called Aβ tolerance. Starting from the concepts of resilience and reserve, this paper intends to sort out the epidemiology and quantitative methods, brain characteristics and influencing factors of Aβ tolerance, in order to further deepen clinicians' understanding of Aβ tolerance in AD diagnosis and treatment, so as to provide new ideas for prevention and treatment of the disease.