Search

Published in Khimiya Prirodnykh Soedinenii, No. 1, January-February, 2021, pp. 168-169 I Selaginella i is the sole genus of the Selaginellaceae, which consists of about 700 species and widely distributed in the world. By using extensive spectroscopic data, including UV I vis i , IR, HR-ESI-MS, and 1D/2D NMR and comparing the spectroscopic data with the reported literature, compounds B 1-18 b have been identified. Subfraction F7 was directly purified by semi-preparative HPLC (ACN-H SB 2 sb O, 45:55, 3.0 mL/min) to yield compounds B 1 b (2.3 mg), B 2 b (3.5 mg), B 3 b (3.3 mg), B 4 b (3.0 mg), B 5 b (2.4 mg), B 6 b (4.1 mg), B 9 b (2.1 mg), B 10 b (2.3 mg), B 11 b (5.1 mg), and B 12 b (5.3 mg). Fraction H was chromatographed over silica gel repeatedly and then subjected to Sephadex LH-20 with MeOH-H SB 2 sb O (60:40, isocratic elution) to afford six subfractions (Subfrs. [Extracted from the article]

l-glutamate plays a key role in neuronal cell death associated with many neurodegenerative conditions such as cerebral ischemia, hypoxia, Alzheimer's, Huntington’s, and Parkinson’s diseases. Selaginellin, a component extracted from Saussurea pulvinata (Hook.et Grev.) Maximo, was assessed for its ability to protect rat pheochromocytoma (PC12) cells against oxidative toxicity induced by glutamate. The differentiated PC12 cells were pretreated with various concentrations (10−7, 3 × 10−7, or 10−6 M) of selaginellin for 1 h prior to exposure to l-glutamate. Selaginellin was shown to protect PC12 cells against glutamate toxicity, as determined by characteristic morphological features, lactate dehydrogenase release and cell viability, and apoptosis as evaluated by Hoechst 33342 staining assay and caspase-3 activity. In addition, the increase in levels of reactive oxygen species and decrease in klotho gene expression induced by glutamate were significantly reversed by selaginellin. Our study suggests that selaginellin has a neuroprotective effect against l-glutamate-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis via scavenging reactive oxygen species and up-regulating the expression of klotho gene. [ABSTRACT FROM AUTHOR]

Monocyte adhesion to activated vascular endothelial cells is the critical event in the initiation of atherosclerosis. Adhesion molecules are inflammatory markers, which are upregulated by oxidized low-density lipoprotein (ox-LDL) and play a pivotal role in atherogenesis. In present study, the effect of reinioside C, a major compound of Polygala fallax Hemsl., on adhesion of monocytes to endothelial cells induced by ox-LDL was investigated. The results showed that incubation of endothelial cells with ox-LDL (100 µg/mL) for 24 h markedly increased the expression of ICAM-1 and P-selectin and enhanced the adhesion of monocytes to endothelial cells. Pretreatment with reinioside C (1, 3, or 10 µM) dose-dependently decreased ox-LDL-induced upregulation of expression of ICAM-1 and P-selectin and the enhanced adhesion of monocytes to endothelial cells. To determine the role of NADPH oxidase/reactive oxygen species (ROS)/nuclear factor-κB (NF-κB) pathway, endothelial cells were treated with ox-LDL (100 µg/mL) for 2 h, and NADPH oxidase subunit (Nox 2 and p22phox) mRNA expression, intracellular ROS level, and NF-κB activity were measured. The results showed that reinioside C attenuated ox-LDL-induced NADPH oxidase subunit (Nox 2 and p22phox) mRNA expression, generation of ROS, and activation of NF-κB in endothelial cells in a dose-dependent manner; the two latter effects were inhibited by pyrollidine dithiocarbamate, the inhibitor of NF-κB. These findings suggest that reinioside C attenuates ox-LDL-induced expression of adhesion molecules (P-selectin and ICAM-1) and the adhesion of monocytes to endothelial cells by inhibiting NADPH oxidase/ROS/NF-κB pathway. [ABSTRACT FROM AUTHOR]

Previous investigations have indicated that endogenous inhibitors of nitric oxide synthase (NOS) such as asymmetric dimethylarginine (ADMA) may play an important role in endothelium dysfunction, and some antioxidant drugs improve endothelium function via reduction of ADMA level. The present study examined the antioxidation and endothelial protection of daviditin A, a xanthone compound. Daviditin A significantly inhibited Cu2+-induced low-density lipoprotein (LDL) oxidation (EC50: 38.7 μM) and scavenged 2,2-diphenyl-1-picrylhydrazyl (DPPH) radicals (EC50: 57.5 μM). Vasodilator responses to acetylcholine in rings of the isolated thoracic aorta were impaired in the presence of lysophosphatidylcholine (LPC)(5 mg/l). Daviditin A (10 or 30 μM) significantly attenuated inhibition by LPC of endothelium-dependent relaxation. Incubation of ECV304 cells with LPC (5 mg/l) for 24 h markedly elevated lactate dehydrogenase (LDH) activity and the levels of malondialdehyde (MDA) and ADMA, and decreased the content of nitric oxide (NO) and the activity of dimethylarginine dimethylaminohydrolase (DDAH). Daviditin A (1, 3 or 10 μM) significantly attenuated the increased release of LDH, increased content of MDA, and decreased level of NO induced by LPC. Daviditin A (3 or 10 μM) significantly inhibited the increased concentration of ADMA. Daviditin A (10 μM) significantly attenuated the decreased activity of DDAH. The present results suggest that daviditin A preserves endothelial dysfunction elicited by LPC, and the protective effect of daviditin A on the endothelium is related to reduction of ADMA concentration. [ABSTRACT FROM AUTHOR]

The article focuses on the study regarding the isolation of compounds from Selaginella delicatula. The study has employed air-dried S. delicatula extraction with ethanol by heat, its crude oil extract is subjected to polyamide column chromatography with EtOH-H 2O (v/v) elution, and recrystallization. The study has yielded compounds including heveaflavone, amentoflavone, and emodin-8-O-Β-D-glucopyranoside.