Can Magnoflorine Improve Memory? Immunohistochemical Studies on Parvalbumin Immunoreactive Neurons and Fibers of Mice Hippocampus.

: We assessed the influence of long-term injection of magnoflorine (MAG) on memory acquisition in mice for the first time. : This isoquinoline alkaloid that belongs to the aporphines was isolated from the roots of by centrifugal partition chromatography (CPC) using a biphasic solvent system composed of chloroform: methanol: water in the ratio 4:3:3 (//) with 20 mM of hydrochloric acid and triethylamine, within 64 min. : Our results indicated that long-term injection of MAG 20 mg/kg dose improve the long-term memory acquisition in mice that were evaluated in the passive avoidance (PA) test with no toxicity records.

The Vacuolar Inositol Transporter BvINT1;1 Contributes to Raffinose Biosynthesis and Reactive Oxygen Species Scavenging During Cold Stress in Sugar Beet.

Despite a high sucrose accumulation in its taproot vacuoles, sugar beet (Beta vulgaris subsp. vulgaris) is sensitive to freezing. Earlier, a taproot-specific accumulation of raffinose was shown to have beneficial effects on the freezing tolerance of the plant.

The Activity of 1,8-Dihydroanthraquinone Derivatives in Nervous System Cancers.

Primary and metastatic tumors of the nervous system represent a diverse group of neoplasms, each characterized by distinct biological features, prognostic outcomes, and therapeutic approaches. Due to their molecular complexity and heterogeneity, nervous system cancers (NSCs) pose significant clinical challenges. For decades, plants and their natural products with established anticancer properties have played a pivotal role in the treatment of various medical conditions, including cancers.

Adipocyte-derived small extracellular vesicles exacerbate diabetic ischemic heart injury by promoting oxidative stress and mitochondrial-mediated cardiomyocyte apoptosis.

Background: Diabetes increases ischemic heart injury via incompletely understood mechanisms. We recently reported that diabetic adipocytes-derived small extracellular vesicles (sEV) exacerbate myocardial reperfusion (MI/R) injury by promoting cardiomyocyte apoptosis. Combining in vitro mechanistic investigation and in vivo proof-concept demonstration, we determined the underlying molecular mechanism responsible for diabetic sEV-induced cardiomyocyte apoptosis after MI/R.

S100A1ct: A Synthetic Peptide Derived From S100A1 Protein Improves Cardiac Performance and Survival in Preclinical Heart Failure Models.

Background: The EF-hand Ca sensor protein S100A1 has been identified as a molecular regulator and enhancer of cardiac performance. The ability of S100A1 to recognize and modulate the activity of targets such as SERCA2a (sarcoplasmic reticulum Ca ATPase) and RyR2 (ryanodine receptor 2) in cardiomyocytes has mostly been ascribed to its hydrophobic C-terminal α-helix (residues 75-94). We hypothesized that a synthetic peptide consisting of residues 75 through 94 of S100A1 and an N-terminal solubilization tag (S100A1ct) could mimic the performance-enhancing effects of S100A1 and may be suitable as a peptide therapeutic to improve the function of diseased hearts.