Creatine Phosphate Sodium

Sepsis-associated encephalopathy (SAE) is a severe neurological complication stemming from sepsis, characterized by cognitive impairment. The underlying mechanisms involve oxidative stress, neuroinflammation, and disruptions in copper/iron homeostasis. This study introduces magnesium hexacyanoferrate (MgHCF) as a novel compound and explores its therapeutic potential in SAE. Our investigation reveals that MgHCF features intriguing properties in effectively scavenging reactive oxygen species (ROS), and chelating excess copper and iron. Treatment with MgHCF significantly attenuates microglia activation, and protects neuronal cells from oxidative damage and cytotoxicity induced by activated microglia in vitro and in vivo. Furthermore, the cognitive impairment in SAE mice is effectively alleviated by MgHCF treatment, mechanically through a reduction in the copper/iron-responsive histone methylation, and neuronal cuproptosis. These findings suggest MgHCF as a promising therapeutic agent for SAE, targeting the copper/iron signaling pathway to alleviate neuroinflammation, and neuronal cuproptosis.

The leaves of Annona muricata Linn. have long been utilized in traditional medicine for diabetes treatment, and there is no study that has employed a metabolomics approach to investigate the plant's effects in managing the disease. We aimed to explore the antidiabetic effects of the standardised A. muricata leaf extract on diabetes-induced rats by alloxan monohydrate (Ax) and nicotinamide (NA) using a proton nuclear magnetic resonance (¹H-NMR)-based metabolomics approach. Absolute quantification was performed on the leaf extract using ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). Two different doses of the extract were administered orally for four weeks to diabetic rats induced with Ax + NA, and physical evaluations, biochemical analyses, and ¹H-NMR metabolomics of urine and serum were assessed. The results showed that quercetin 3-rutinoside was the most abundant compound in the 80 % ethanolic extract of A. muricata leaf. The induction of type 2 diabetes mellitus (T2DM) in the rat model was confirmed by the clear metabolic distinction between normal rats, diabetic rats, and metformin-treated diabetic rats. The low-dose of A. muricata leaf extract (200 mg/kg) was found to exhibit better results, significantly reducing serum urea levels in diabetic rats, with effects comparable to those of metformin. Additionally, metabolite analysis from ¹H-NMR metabolomics of serum and urine showed a slight shift toward normal metabolic profiles in the treated diabetic rats. Pathway analysis revealed alterations in the tricarboxylic acid cycle (TCA), pyruvate metabolism, and glycolysis/gluconeogenesis pathways in the diabetic rat model, which were improved following treatment with the A. muricata leaf extract. Overall, this study provides scientific support for its traditional use in diabetes management and offers new insights into the underlying molecular mechanisms.