An apoptosis inhibitor suppresses microglial and astrocytic activation after cardiac ischemia/reperfusion injury.

Objective: Microglial hyperactivation and apoptosis were observed following myocardial infarction and ischemia reperfusion (I/R) injury. This study aimed to test the hypothesis that the apoptosis inhibitor, Z-VAD, attenuates microglial and astrocytic hyperactivation and brain inflammation in rats with cardiac I/R injury.

Materials And Methods: Rats were subjected to either sham or cardiac I/R operation (30 min-ischemia followed by 120-min reperfusion), rats in the cardiac I/R group were given either normal saline solution or Z-VAD at 3.

Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury.

Growing evidence demonstrated that cell death pathways including ferroptosis, apoptosis and necroptosis contribute to cardiac ischaemia/reperfusion (I/R) injury. We hypothesized that ferroptosis, apoptosis and necroptosis contribute differently to myocardial damage during acute cardiac I/R injury. Rats underwent cardiac I/R or sham operation.

Cell death inhibitors protect against brain damage caused by cardiac ischemia/reperfusion injury.

Cognitive impairment has been reported in patients with myocardial infarction despite a successful reperfusion therapy. Several modes of cell death are involved in brain damage during cardiac ischemia/reperfusion (I/R) injury. Although apoptosis, necroptosis, and ferroptosis inhibitors provided neuroprotection against cerebral I/R injury, the effects of these cell death inhibitors on the brain following cardiac I/R injury have never been investigated.

The possible roles of necroptosis during cerebral ischemia and ischemia / reperfusion injury.

Cell death is a process consequential to cerebral ischemia and cerebral ischemia/reperfusion (I/R) injury. Recent evidence suggest that necroptosis has been involved in the pathogenesis of ischemic brain injury. The mechanism of necroptosis is initiated by an activation of inflammatory receptors including tumor necrosis factor, toll like receptor, and fas ligands.

Notch1 inhibition enhances DNA damage induced by cisplatin in cervical cancer.

The expression of Notch1 plays an important role in the occurrence and development of various tumors. Previous studies have shown that Notch1 plays a negative regulatory role in response to radiation-induced DNA damage responses. It also has been reported that Notch1 was highly expressed in cervical cancer.

Over-expression of BAG-1 in head and neck squamous cell carcinomas (HNSCC) is associated with cisplatin-resistance.

Background: In order to improve therapy for head and neck squamous cell carcinoma (HNSCC), biomarkers associated with local and/or distant tumor relapses and cancer drug resistance are urgently needed. This study identified a potential biomarker, Bcl-2 associated athanogene-1 (BAG-1), that is implicated in HNSCC insensitive to cisplatin and tumor progression.

Methods: Primary and advanced (relapsed from parental) University of Michigan squamous cell carcinoma cell lines were tested for sensitivity to cisplatin and gene expression profiles were compared between primary (cisplatin sensitive) and the relapsed (cisplatin resistant) cell lines by using Agilent microarrays.

Silica-encapsulated Gd3+-aggregated gold nanoclusters for in vitro and in vivo multimodal cancer imaging.

Gd(3+)-aggregated gold nanoclusters (AuNCs) encapsulated by silica shell (Gd(3+)-A-AuNCs@SiO2NPs) were strategically designed and prepared. The as-prepared nanoparticles exhibit aggregation-enhanced fluorescence (AEF), with an intensity that is up to 3.8 times that of discrete AuNCs.