Establishment of LC-MS/MS Methodology for the Determination of Rapamycin Concentration in Rat Whole Blood.

Background: The establishment and validation of methods for testing biological samples are crucial steps in pharmacokinetic studies. Currently, several methodological reports have been published on the detection of rapamycin plasma concentrations.

Objective: The objective of this study was to explore an effective method for detecting rapamycin in rat whole blood biological samples.

RIPK1 inhibition mitigates neuroinflammation and rescues depressive-like behaviors in a mouse model of LPS-induced depression.

Background: Depression is often linked to inflammation in the brain. Researchers have been exploring ways to reduce this inflammation to improve depression symptoms. One potential target is a protein called RIPK1, which is known to contribute to brain inflammation.

Ceftriaxone averts neuroinflammation and relieves depressive-like behaviors via GLT-1/TrkB signaling.

The beneficial effect of a beta-lactam antibiotic, Ceftriaxone (CEF), to improve depressive-like symptoms has been documented previously, attributed to its modulation of glutamate neurotransmission. Here, we aimed to determine whether CEF could improve LPS-altered glutamatergic signaling associated with neuroinflammation-allied depression. To assess our goals, we established a neuroinflammation-allied depression mice model by injecting lipopolysaccharides (LPS), followed by behavioral and biochemical analysis.

EPO prevents neuroinflammation and relieves depression via JAK/STAT signaling.

Aims: Erythropoietin (EPO) is a glycoprotein cytokine that exerts therapeutic potential on neurological disorders by promoting neurogenesis and angiogenesis. However, its role as an antidepressant via anti-inflammatory axes is poorly explored. Furthermore, chronic inflammation can induce neuroinflammation, concurrent with depressive-like behaviors that anti-inflammatory and antidepressant agents could avert.

Neuronal lack of PDE7a disrupted working memory, spatial learning, and memory but facilitated cued fear memory in mice.

Background: PDEs regulate cAMP levels which is critical for PKA activity-dependent activation of CREB-mediated transcription in learning and memory. Inhibitors of PDEs like PDE4 and Pde7 improve learning and memory in rodents. However, the role of PDE7 in cognition or learning and memory has not been reported yet.

Cytotoxic effects of extracts and isolated compounds from (forssk.) sch. bip against HepG-2 cancer cell line: Supported by ADMET analysis and molecular docking.

The purpose of this study was to determine the anticancer potential of () against HepG-2 cell line. To assess cytoxicity, brine shrimp lethality and MTT assays were performed. In the brine shrimp bioassay, the ethyl acetate fraction had a significant impact with an IC of 10 μg/ml.

miR-214-3p Deficiency Enhances Caspase-1-Dependent Pyroptosis of Microglia in White Matter Injury.

White matter injury (WMI) is the most frequent impairment of neurodevelopment in preterm infants. Here, we report that the caspase-1 inflammasome is abundantly activated in the microglia of WMI mice and results in increased pyroptosis of microglia. Pharmacology inhibition of caspase-1 cleavage alleviated the pathogenesis of WMI mice.

Clinical Manifestations of Neonatal Hyperbilirubinemia Are Related to Alterations in the Gut Microbiota.

Background And Purpose: Neonatal hyperbilirubinemia, also known as neonatal jaundice, is a common and frequent clinical condition with a complex etiology that can lead to brain damage in severe cases. Early recognition of hyperbilirubinemia and timely intervention and treatment can help reduce the occurrence of sequelae. This study was conducted to identify whether the gut microbiota composition can distinguish neonates with hyperbilirubinemia.

Knockdown of G protein-coupled receptor-17 (GPR17) facilitates the regeneration and repair of myelin sheath post-periventricular leukomalacia (PVL).

The G protein-coupled receptor-17 (GPR17) plays an important role in regulating the differentiation of oligodendrocytes and remyelination, which is a key negative regulator of oligodendrocyte differentiation. The present study aimed to investigate the function of GPR17 in the white matter of periventricular leukomalacia (PVL) neonatal rats. The PVL model was established in 2-day old neonatal rats by intracerebral injection of LPS (1 mg/kg).

[Correlation between end-tidal carbon dioxide and partial pressure of arterial carbon dioxide in ventilated newborns].

Objective: To study the correlation between end-tidal carbon dioxide (PetCO2) and partial pressure of arterial carbon dioxide (PaCO2) in ventilated newborns.

Methods: Thirty-one ventilated newborn underwent mainstream PetCO2 monitoring; meanwhile, arterial blood gas analysis was performed. The correlation and consistency between PetCO2 and PaCO2 were assessed.

Diphenyleneiodonium protects preoligodendrocytes against endotoxin-activated microglial NADPH oxidase-generated peroxynitrite in a neonatal rat model of periventricular leukomalacia.

The contribution of microglial activation to preoligodendroglial (preOL) damage in the central nervous system (CNS) is considered to be one of the principal causes of periventricular leukomalacia (PVL) pathogenesis. The present study explores the effect of diphenyleneiodonium (DPI), a NADPH oxidase (NOX) inhibitor, on protection of preOLs from bacterial lipopolysaccharide (LPS)-induced microglial toxicity in vivo and in vitro. In vitro, preOLs co-cultured with microglia exhibited increased preOL apoptosis, accompanied by overproduction of superoxide anion (O(2)(-)) and the formation of peroxynitrite (ONOO(-)) after LPS exposure.

Curcumin protects pre-oligodendrocytes from activated microglia in vitro and in vivo.

Infection and inflammation leading to injury or death of pre-oligodendrocytes (preOLs) is one of the principal initiating mechanisms in the pathogenesis of preterm periventricular leukomalacia (PVL). The present study explores the possible protective effect of curcumin against the toxicity of lipopolysaccharide (LPS)-activated microglia on preOLs in vitro and in vivo. In vitro, preOLs in coculture with microglia exhibited increased apoptosis after exposure to LPS.

[The construction and identification of siRNA expression vector against hypoxia inducible factor -1 alpha in vitro].

Objective: Previous studies have suggested that under hypoxic conditions hypoxia inducible factor-1 alpha (HIF-1 alpha) contributes to the progression of neonatal pulmonary hemorrhage (NPH) by increasing the expression of endothelin-1 (ET-1) gene. RNA interference (RNAi) refers to the process of sequence-specific post-transcriptional gene-silencing mediated by double-stranded RNA. This new gene-silencing technique has recently been shown to be a powerful approach for studying gene function.

[Effect of NADPH oxidase on hypoxia-inducible factor-1alpha and endothelin-1 expression in human umbilical endothelial cells and its possible mechanism].

Objective: To study the effect of NADPH oxidase on hypoxia-inducible factor (HIF)-1alpha and endothelin (ET)-1 expression in human umbilical endothelia cells (HUVECs) and its possible mechanism.

Methods: Twenty-five bottles of HUVECs culture fluid were randomly assigned into five groups: group A (normoxic control), group B (hypoxic), group C (NADPH oxidase inhibitor apocynin + normoxic), group D (H2O2 which can degrade HIF-1alpha rapidly+hypoxic) and group E (H2O2+apocynin+normoxic), with five bottles in each group. The culture supernates were collected and the total protein was extracted 3 hrs after treatment.