Intervention of exogenous VEGF protect brain microvascular endothelial cells from hypoxia-induced injury by regulating PLCγ/RAS/ERK and PI3K/AKT pathways.

Ischemic stroke rapidly increases the expression level of vascular endothelial growth factor (VEGF), which promotes neovascularization during hypoxia. However, the effect and mechanism of VEGF intervention on cerebrovascular formation remain unclear. Therefore, our research discussed the protective effect of exogenous VEGF on cells in hypoxia environment in cerebral microvascular endothelial cells, simulating ischemic stroke in hypoxic environment. Firstly, we detected the proliferation and apoptosis of cerebral microvascular endothelial cells under hypoxia environment, as well the expression levels of VEGF-E, vascular endothelial growth factor re-ceptor-2 (VEGFR-2), BCL2, PRKCE and PINK1. Moreover, immunofluorescence and western blotting were used to verify the regulation of exogenous VEGF-E on VEGFR-2 expression in hypoxic or normal oxygen environment. Lastly, we manipulated the concentration of VEGF-E in the culture medium to investigate its impact on phospholipase Cγ1 (PLCγ1)/extracellular signaling regulatory protein kinase (ERK) -1/2 and protein kinase B (AKT) pathways. Additionally, we employed a PLCγ1 inhibitor (U73122) to investigate its impact on proliferation and PLCγ1/ERK pathways. The results show that hypoxia inhibited the proliferation of cerebral microvascular endothelial cells, promoted cell apoptosis, significantly up-regulated the expression of VEGF-E, VEGFR-2, PRKCE and PINK1, but down-regulated the expression of BCL2. Interference from exogenous VEGF-E activated PLCγ1/ERK-1/2 and AKT pathways, promoting cell proliferation and inhibiting apoptosis of hypoxic brain microvascular endothelial cells. In summary, exogenous VEGF-E prevents hypoxia-induced damage to cerebral microvascular endothelial cells by activating the PLCγ1/ERK and AKT pathways. This action inhibits the apoptosis pathway in hypoxic cerebral microvascular endothelial cells, thereby safeguarding the blood-brain barrier and the nervous system.

Markers of brain injury in patients with aneurysmal subarachnoid hemorrhage.

AIM: To investigate the correlation of serum changes and markers of brain injury (BI) in cerebrospinal fluid (CSF) with postoperative cognitive dysfunction (POCD) in patients with cerebral aneurysmal subarachnoid haemorrhage (aSAH). METHODS: 120 patients diagnosed with aSAH were included. 3 months after surgery, these patients were divided into a normal cognition group and a cognitive dysfunction (CD) group relying on the Montreal Cognitive Assessment (MoCA) Scale. RESULTS: The correlations were analysed between the serological changes and the levels of BI markers, such as neurofilament-light (NF-L) protein, Ubisquitin C-terminal hydrolase L1(UCH-L1), Glial Fibrillary Acidic Protein (GFAP), and neuron specific enolase (NSE) in patients after surgery. Hunt-Hess grading standard was employed to determine the severity of aSAH in patients. The mean values of NF-L, UCH-L1, GFAP, and NSE were (8.2 ± 4.3) pg/mL, (0.7 ± 0.3) ng/mL, (2.2 ± 0.4) ng/mL, and (48.5 ± 10.9) ng/mL in patients with severe aSAH, which were remarkably higher than those in patients with mild aSAH [(3.5 ± 0.7) pg/mL, (0.5 ± 0.2) ng/mL, (1.3 ± 0.7) ng/mL, (30.7 ± 8.2) ng/mL]. The sensitivity, specificity, and accuracy of the combined prediction of four detections for POCD were 90.80%, 84.20%, and 82.80%, respectively, which were greatly higher than those of four independent predictions (p < 0.05). The combined prediction effect of the four items, with the area under the curve (AUC) of 0.938 and the 95% confidence interval (CI) of 0.851-0.926. CONCLUSIONS: BI markers NF-L, UCH-L1, GFAP, and NSE could be utilized as predictors of POCD in patients with aSAH, deserving a reference value.

[Lower capsular contracture of miniprostheses as compared with the conventional silicone implant].

OBJECTIVE: To determine if miniprostheses would form a capsule of significantly different biophysical, biochemical and histologic properties than the conventional silicone implant. METHODS: Four miniprostheses (experimental group) and one big silicone implants (control 1 group) were separately implanted beneath the panniculus carnosus muscle of 30 rabbits. After 3 months, measures related to contracture and capsular histology were performed on anesthetized animals. RESULTS: Baker ranking, capsular incision width and capsular thickness of the control groups were evidently higher than that of experimental groups (P < 0.01). Implant compression of the control groups was evidently lower than that of the experimental group. Histology revealed a thinner, more flexed capsule around the miniprostheses as compared with big silicone implants. CONCLUSIONS: The miniprostheses form a looser and thinner capsule than the conventional silicone implant.

[The experimental researches on the use of triamcinolone acetonide for the prevention of implant capsular contracture].

OBJECTIVE: To explore the use of triamcinolone acetonide for the prevention of implant capsular contracture. METHODS: 20 rabbits were randomly undivided into 2 groups of 10 animals each. Every 10 ml silicone implant was implanted beneath the panniculus carnosus muscle of one rabbit. At the same time, a modified expander catheter was mounted on the implant. This catheter has many lateral holes and the end was blind. Triamcinolone acetonide (10 mg/3 ml) was infused through the expander pot and catheter as the experimental groups. On the other hand, 3 ml saline was used as the control group at 1, 2, and 3 months. At 6 months, measures related to contracture and capsular histology examinations were performed on anesthetized animals. RESULTS: Baker scores, capsular incision width and capsular thickness of the saline groups were evidently higher than that of triamcinolone acetonide groups (P < 0.01). Implant compression of the saline groups was evidently lower than that of triamcinolone acetonide group. Histology revealed a thinner capsules and less fibrous tissue deposition around the triamcinolone acetonide group, as compared with saline group. CONCLUSIONS: It is effective to deliver triamcinolone acetonide to reduction of capsular contracture through the catheter and its pot.