Targeted Metabolomics Provide Chemotaxonomic Insights of Medicago ruthenica, with Coupled Transcriptomics Elucidating the Mechanism Underlying Floral Coloration.

Medicago ruthenica, a wild legume forage widely distributed in the Eurasian steppe, demonstrates high genetic and phenotypic variation. M. ruthenica with a purely yellow flower (YFM), differing from the general phenotype of M. ruthenica with a purple flower (PFM), was recently discovered. The similar characteristics of YFM with Medicago falcata have led to conflicting opinions on its taxonomy using traditional morphological methods. The lack of chemotaxonomy information about M. ruthenica species and the unclear flower coloration mechanisms have hampered their study. Here, we investigated M. ruthenica using targeted metabolomics based on the chemotaxonomy method and elaborated the floral coloration mechanisms using transcriptomics. The identified flavonoids were the same types, but there were different contents in YFM and PFM, especially the contents of cyanidin-3-O-glucoside (C3G), an anthocyanin that causes the purple-reddish color of flowers. The over-accumulation of C3G in PFM was 1,770 times more than YFM. Nineteen anthocyanin-related genes were downregulated in YFM compared with their expression in PFM. Thus, YFM could be defined as a variety of M. ruthenica rather than a different species. The loss of purple flower coloration in YFM was attributed to the downregulation of these genes, resulting in reduced C3G accumulation. The taxonomic characteristics and molecular and physiological characteristics of this species will contribute to further research on other species with similar external morphologies.

The PPARγ agonist rosiglitazone prevents neuronal loss and attenuates development of spontaneous recurrent seizures through BDNF/TrkB signaling following pilocarpine-induced status epilepticus.

Hippocampal neuronal loss plays an important role in epileptogenesis, and it is considered a trigger of repeated spontaneous recurrent seizures (SRS). The BDNF/TrkB signaling pathway regulates neuronal plasticity in the CNS, and promotes epileptogenesis. Previous studies have shown that Peroxisome proliferator-activated receptor gamma (PPARγ) agonists exert neuroprotective effects by inhibiting oxidative stress and inflammation in epilepsy. In the present study, the PPARγ agonist rosiglitazone inhibited increases in BDNF and TrkB after status epilepticus (SE), and also prevented hippocampal neuronal loss. More importantly, our study showed that rosiglitazone suppressed SRS. However, the effects of rosiglitazone were significantly reversed by cotreatment with K252a, an antagonist of TrkB. Additionally, rosiglitazone did not affect the development and severity of SE. Thus, our data provide evidence that rosiglitazone exerts neuroprotective and antiepileptic effects involve BDNF/TrkB signaling. Our study also offers new perspectives for the treatment of epilepsy.