Iridoid Glycosides and Flavonoids Isolated from the Twigs and Leaves of Callicarpa nudiflora and Their Anti-Inflammatory Activities.

A new iridoid glycoside, named 6'-O-trans-feruloyl-8-epiloganic acid, together with fifteen known compounds were isolated from the twigs and leaves of Callicarpa nudiflora, a traditional Chinese medicine to treat inflammatory-related diseases. Their structures were identified by comprehensive spectroscopic analysis and comparison with reported data. Bioassay results revealed that twelve of the isolates could obviously inhibit nitric oxide (NO) production in lipopolysaccharide (LPS)-induced RAW 264.7 cell lines with IC50 values from 0.64 to 38.72 µM. Among them, compounds 1 (3.27 µM), 6 (5.23 µM), 13 (1.56 µM) and 14 (0.64 µM) exhibited significantly higher activities than that of the positive control (27.13 µM). Additionally, it was supposed that the presence of the carboxy group at the C-4 position of iridoid glycosides and glycosylation at C-3 position of flavonoids might impact their inhibitory activities against NO production.

Delayed exposure to environmental enrichment improves functional outcome after stroke.

Stroke is one of the leading causes of long-term disabilities worldwide. Although exposure to an enriched environment (EE) initiated in the acute phase after stroke has neuroprotective effects and improves stroke outcome, it remains unclear whether EE has positive effects when started in a delayed time frame. Here we show that exposure to EE in the delayed phase notably ameliorates the ischemia-induced impairments in neurological functions and spatial learning and memory. In addition, delayed EE exposure after stroke significantly promotes the survival and neuronal fate choice of hippocampal newborn cells, increases synaptic density of hippocampal mature neurons, and enhances the migration of subventricular zone (SVZ)-derived cells towards the ischemic striatum. Histone deacetylase 2 (HDAC2), synapse-associated proteins and brain-derived neurotrophic factor (BDNF) may respectively mediate these roles of delayed EE. Our findings provide the suggestion that exposure to EE initiated in the delayed phase after stroke promotes plastic changes via affecting neurogenesis, synaptogenesis and neuronal migration, and thus improves stroke outcome. Because EE initiated earlier than 24 h is clinically feasible, our work could be introduced into clinical studies of stroke directly and may provide stroke survivors with a new strategy for their functional recovery.