Correction: Melatonin as an inducer of arecoline and their coordinated roles in anti-oxidative activity and immune responses.

Correction for 'Melatonin as an inducer of arecoline and their coordinated roles in anti-oxidative activity and immune responses' by Xiaojian Yin , , 2020, , 8788-8799, https://doi.org/10.1039/D0FO01841D.

Omics and Transgenic Analyses Reveal that Salvianolic Acid B Exhibits its Anti-Inflammatory Effects through Inhibiting the Mincle-Syk-Related Pathway in Macrophages.

Salvianolic acid B (Sal B), the main water-soluble compound in , is known to exhibit anti-inflammatory activity, however, the underlying mechanism(s) is not completely uncovered. In this study, Sal B inhibited lipopolysaccharide (LPS)-induced M1 activation and promoted the transformation of macrophages from M1- to M2-type polarization. The altered lipid profiles of LPS-induced RAW 264.

Melatonin as an inducer of arecoline and their coordinated roles in anti-oxidative activity and immune responses.

Arecoline is one of the main medicinal constituents in areca. Melatonin is an amine molecule with multiple functions in plants and animals. However, the interaction between arecoline and melatonin remains unknown.

Integrative omic and transgenic analyses reveal the positive effect of ultraviolet-B irradiation on salvianolic acid biosynthesis through upregulation of SmNAC1.

Salvianolic acids (SalAs), a group of secondary metabolites in Salvia miltiorrhiza, are widely used for treating cerebrovascular diseases. Their biosynthesis is modulated by a variety of abiotic factors, including ultraviolet-B (UV-B) irradiation; however, the underlying mechanisms remain largely unknown. Here, an integrated metabolomic, proteomic, and transcriptomic approach coupled with transgenic analyses was employed to dissect the mechanisms underlying UV-B irradiation-induced SalA biosynthesis.

Compounds containing trace element copper or zinc exhibit as potent hyperuricemia inhibitors via xanthine oxidase inactivation.

Compounds containing trace elements copper or zinc are potential gout and hyperuricemia suppressant by virtue of their inhibiting effect on xanthine oxidase/xanthine dehydrogenase (XOD/XDH) and anti-inflammatory and anti-oxidative function. In this study, compounds Cu(hmy-paa)·SO·HO (simplified as CuHP) and Zn(hmy-paa)·SO·HO (simplified as ZnHP) are synthesized, where hmy-paa stands for 3-(4-hydroxy-3-methoxyphenyl)-N-(1H-pyrazol-3-yl)acrylamide). The ligand hmy-paa is composed of functional ferulic acid and 3-aminopyrazole.

Succinate induces aberrant mitochondrial fission in cardiomyocytes through GPR91 signaling.

Altered mitochondrial metabolism acts as an initial cause for cardiovascular diseases and metabolic intermediate succinate emerges as a mediator of mitochondrial dysfunction. This work aims to investigate whether or not extracellular succinate accumulation and its targeted G protein-coupled receptor-91 (GPR91) activation induce cardiac injury through mitochondrial impairment. The results showed that extracellular succinate promoted the translocation of dynamin-related protein 1 (Drp1) to mitochondria via protein kinase Cδ (PKCδ) activation, and induced mitochondrial fission factor (MFF) phosphorylation via extracellular signal-regulated kinases-1/2 (ERK1/2) activation in a GPR91-dependent manner.

Inhibition of lipolysis by ilexgenin A via AMPK activation contributes to the prevention of hepatic insulin resistance.

Adipose dysfunction links tightly to hepatic insulin resistance and gluconeogenesis. Ilexgenin A is reported with the ability to regulate lipid profile and protect the liver against high fat diet (HFD) -induced impairment. Here, we propose that ilexgenin A ameliorates hepatic insulin signaling and gluconeogenesis by regulating lipolysis in white adipose tissue (WAT).

Succinate accumulation impairs cardiac pyruvate dehydrogenase activity through GRP91-dependent and independent signaling pathways: Therapeutic effects of ginsenoside Rb1.

Altered mitochondrial oxidation increases vulnerability to cardiac ischemia/reperfusion (I/R) injury in metabolic disorders. However, the metabolic signaling responsible for the dysfunction remains partly unknown. We sought to test whether or not hypoxic succinate accumulation could inhibit pyruvate dehydrogenase (PDH) activity and subsequently aggravate I/R injury.