Dexmedetomidine attenuates ferroptosis by Keap1-Nrf2/HO-1 pathway in LPS-induced acute kidney injury.

Previous research has demonstrated that Dexmedetomidine (DEX), an α2 adrenergic agonist commonly used for its sedative and analgesic properties, can attenuate lipopolysaccharide (LPS)-induced acute kidney injury (AKI). This study explores the possibility that DEX's protective effects in LPS-induced AKI are mediated through the inhibition of ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation, and the activation of the antioxidant response through the Keap1/Nrf2/HO-1 signaling pathway. We induced AKI in 42 mice using LPS and divided them into six groups: saline control, LPS, LPS + DEX, LPS + Ferrostatin-1 (LPS + Fer-1; a ferroptosis inhibitor), LPS + DEX with α2-receptor antagonist Altipamizole (LPS + DEX + ATI), and LPS + DEX with Nrf2 inhibitor ML385 (LPS + DEX + ML385). After 24 h, we analyzed blood and kidney tissues. LPS exposure resulted in AKI, with increased serum creatinine, BUN, and cystatin C, and tubular damage, which DEX and Fer-1 ameliorated. However, Altipamizole and ML385 negated these improvements. The LPS group exhibited elevated oxidative stress markers and mitochondrial damage, reduced by DEX and Fer-1, but not when α2-adrenergic or Nrf2 pathways were blocked. Nrf2 and HO-1 expression declined in the LPS group, rebounded with LPS + DEX and LPS + Fer-1, and fell again with inhibitors; inversely, Keap1 expression varied. Our results demonstrate that DEX may protect against LPS-induced AKI, at least partially by regulating ferroptosis and the α2-adrenergic receptor/Keap1/Nrf2/HO-1 pathway, suggesting a potential therapeutic role for DEX in AKI management by modulating cell death and antioxidant defenses.

Novel hydrocortisone magnetic molecularly imprinted polymers: Preparation, characterization, and application.

In this work, magnetic molecularly imprinted polymers (MMIPs) were prepared by a surface imprinting method using Fe3O4 nanoparticles as a support. The products were characterized by FT-IR spectroscopy, VSM, TGA, SEM, and TEM. Combined with HPLC, hydrocortisone in milk powder and milk were separated and purified, and their contents were monitored. The results showed that MMIPs with a particle size of approximately 1000 nm were successfully prepared. The adsorption mechanism of MMIPs was confirmed by kinetic adsorption and thermodynamic adsorption experiments; the maximum adsorption capacity was found to be 17.2 mg g-1, and adsorption equilibrium could be reached within 40 min. In the actual sample application, the recovery rates of milk powder and milk were 93.88-99.15% and 95.80-98.10%, respectively. These results showed that MMIPs had good performance in selectively identifying hydrocortisone and were suitable for determining hydrocortisone in milk products.

Ginger polysaccharides enhance intestinal immunity by modulating gut microbiota in cyclophosphamide-induced immunosuppressed mice.

In this study, the immunity-enhancing effect of ginger polysaccharides UGP1 and UGP2 on CTX-induced immunosuppressed mice was evaluated. The results showed that ginger polysaccharide could effectively alleviate the symptoms of weight loss and dietary intake reduction induced by CTX, increase fecal water content, reduce fecal pH, and protect immune organs of immunosuppressed mice. In addition, ginger polysaccharides also stimulated the secretion of cytokines IL-2, IL-4, TNF-α and immunoglobulin Ig-G in the serum of mice, increased the expression of Occludin and Claudin-1, and restored the level of short-chain fatty acids in the intestine to improve immune deficiency. Furthermore, ginger polysaccharides significantly reduced the relative abundance ratio of the Firmicutes and Bacteroidetes in mice and increased the relative abundance of Verrucomicrobia and Bacteroidetes at the phylum level. At the family level, ginger polysaccharides increased the relative abundance of beneficial bacteria such as Muribaculaceae, Bacteroidaceae and Lactobacillaceae, and decreased the relative abundance of harmful bacteria such as Rikenellaceae and Lachnospiraceae. Spearman correlation analysis indicated that ginger polysaccharides could enhance intestinal immunity by modulating gut microbiota associated with immune function. These results indicated that ginger polysaccharides have the potential to be a functional food ingredients or a natural medicine for the treatment of intestinal barrier injury.

3-(2-Amino-ethyl)-2-(4-chloro-anilino)-quinazolin-4(3H)-one methanol 0.75-solvate.

In the asymmetric unit of the title compound, C(16)H(15)ClN(4)O·0.75CH(3)OH, there are two independent quinazolin-4(3H)-one mol-ecules and one and a half methanol mol-ecules. One of the methanol mol-ecules is disordered over two positions with equal occupancies. The dihedral angles between the quinazoline ring system and the chloro-benzene ring in the two quinazolin-4(3H)-one mol-ecules are essentially the same, at 39.83 (1) and 39.84 (1)°. Intra-molecular N-H⋯N and O-H⋯O, and inter-molecular N-H⋯O and N-H⋯N hydrogen bonds are observed. In addition, π-π stacking inter-actions, with centroid-to-centroid distances of 3.654 (1), 3.766 (1) and 3.767 (1) Å, and weak C-H⋯π inter-actions, are observed.