Silencing Akt1 enhances the resistance of prostate cancer cells to starvation and inhibits starvation-induced lung metastasis through epithelial-mesenchymal transition in prostate cancer.

Nutritional starvation (NST) is the basis of tumor anti-angiogenesis and metabolic therapy strategy. Silencing Akt1 inhibits prostate cancer (PCa) cells growing; slow-growing cells tend to consume less nutrition. It is suggested that Akt1-silenced cancer cells will have a more substantial tolerance to NST.

Neuroglobin expression and function in the temporal cortex of bilirubin encephalopathy rats.

Bilirubin encephalopathy (BE) is a neurological syndrome in newborns, mainly caused by neuronal injury due to excessive oxidative stress produced by unconjugated bilirubin (UCB). Neuroglobin (NGB) can protect the brain by removing oxidative stress species, but its expression and significance in BE are not clear. To address this question, the neonatal BE model was established by injecting UCB into the cerebellomedullary cistern of 7-day-old SD rats.

[Effect of electroacupuncture of different acupoint groups on learning-memory ability and expression of IL-1β and TNF-α in hippocampus and prefrontal cortex in rats with Alzheimer's disease].

Objective: To compare the effect of electroacupuncture (EA) of acupoint group for "reinforcing the kidney and regulating Governor Vessel" and acopoint group for "reinforcing the kidney and lung and regulating Governor Vessel" on lear-ning-memory ability and expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) proteins in the hippocampus and prefrontal cortex (PFC) in Alzheimer's disease （AD） rats, so as to explore the efficacy of the two acupoint groups and mechanisms underlying improvement of AD.

Methods: Forty male SD rats were randomly divided into control, sham operation, model, "Baihui" + "Shenshu" (GV20+BL23, for "reinforcing the kidney and regulating Governor Vessel") EA and GV20+BL23+ "Feishu" (BL13, GV20+BL23+BL13, for "reinforcing the kidney and lung and regulating Governor Vessel") EA groups (=8 rats in each group). The AD model was established by bilateral injection of amyloid β peptide （Aβ，10 μL) into bilateral hippocampus, and rats of the sham operation group received injection of normal saline.

[Effect of electroacupuncture on the P35/P25-cyclin-dependent kinase 5-Tau pathway in hippocampus of rats with Alzheimer's disease].

Objective: To investigate the effect of electroacupuncture on the P35/P25-cyclin-dependent kinase 5 (CDK5)-Tau pathway in rats with Alzheimer's disease (AD), as well as the mechanism of electroacupuncture in the prevention and treatment of AD.

Methods: Sprague-Dawley rats were randomly divided into control group, sham-operation group, model group, and electroacupuncture treatment group, with 12 rats in each group. A rat model of AD was established by injection of Aβ into the bilateral hippocampus.

Curcumin Ameliorates Memory Deficits by Enhancing Lactate Content and MCT2 Expression in APP/PS1 Transgenic Mouse Model of Alzheimer's Disease.

Curcumin is a natural product with several anti-Alzheimer's disease (AD) neuroprotective properties. This study aimed to investigate the effects of curcumin on memory deficits, lactate content, and monocarboxylate transporter 2 (MCT2) in APP/PS1 mouse model of AD. APP/PS1 transgenic mice and wild-type (WT) C57BL/6J mice were used in the present study.

Both endoplasmic reticulum and mitochondrial pathways are involved in oligodendrocyte apoptosis induced by capsular hemorrhage.

Objective: The white matter injury caused by intracerebral hemorrhage (ICH) includes demyelination and axonal injury. Oligodendrocyte apoptosis is reported to be involved in triggering demyelination. Experimental observations indicate that both endoplasmic reticulum and mitochondrial pathways could mediate cell apoptosis.

Loss of AQP4 polarized localization with loss of β-dystroglycan immunoreactivity may induce brain edema following intracerebral hemorrhage.

The aquaporin-4 (AQP4) water channel contributes to brain water homeostasis in perivascular and subpial membrane domains of astrocytes where it is concentrated. These membranes form the interface between the neuropil and the extracellular liquid spaces. The brain-selective deletion of the dystroglycan (DG) gene causes a disorganization of AQP4 on the astroglial endfeet.

Internalization of aquaporin-4 after collagenase-induced intracerebral hemorrhage.

Brain edema formation following intracerebral hemorrhage (ICH) appears to be related with aquaporin-4 (AQP4), which is critically involved in brain volume homeostasis and water balance. Despite its importance, the regulation of AQP4 expression involved in transmembrane water movements still remains rudimentary. Many studies suggest that the internalization of several membrane-bound proteins, including AQP4, may occur with or without lysosomal degradation.

Upregulation and lysosomal degradation of AQP4 in rat brains with bacterial meningitis.

Brain edema is among the major complications in children with bacterial meningitis. Aquaporins are integral membrane pore proteins that form channels to regulate cellular water content. Aquaporin-4 (AQP4), which is enriched in parts of astrocytic membranes that are apposed to pial or perivascular basal laminae, is the predominant aquaporin in the central nervous system.

The internalization and lysosomal degradation of brain AQP4 after ischemic injury.

The membrane-bound water channel aquaporin-4 (AQP4) plays a significant role in maintaining brain water homeostasis. In ischemic brain, changes in the expression level of AQP4 have been reported. Previous studies suggest that the internalization of several membrane-bound proteins, including AQP4, may occur with or without lysosomal degradation.

Demyelination initiated by oligodendrocyte apoptosis through enhancing endoplasmic reticulum-mitochondria interactions and Id2 expression after compressed spinal cord injury in rats.

Background: Demyelination is one of the most important pathological factors of spinal cord injury. Oligodendrocyte apoptosis is involved in triggering demyelination. However, fewer reports on pathological changes and mechanism of demyelination have been presented from compressed spinal cord injury (CSCI).

Aquaporin 9 in rat brain after severe traumatic brain injury.

Objective: To reveal the expression and possible roles of aquaporin 9 (AQP9) in rat brain, after severe traumatic brain injury (TBI).

Methods: Brain water content (BWC), tetrazolium chloride staining, Evans blue staining, immunohistochemistry (IHC), immunofluorescence (IF), western blot, and real-time polymerase chain reaction were used.

Results: The BWC reached the first and second (highest) peaks at 6 and 72 hours, and the blood brain barrier (BBB) was severely destroyed at six hours after the TBI.