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The Brassicaceae is an economically and scientifically important family distributed globally, including oilseed rape and the model plant, Arabidopsis thaliana. Although growing molecular data have been used in phylogenetic studies, the relationships among major clades and tribes of Brassicaceae are still controversial. Here, we investigated the core Brassicaceae phylogenetics using 222 plastomes and 235 nrDNA cistrons, including 106 plastomes and 112 nrDNA cistrons assembled from newly sequenced genome skimming data of 112 taxa. The sampling covered 73 genera from 61.5% tribes and four unassigned genera and species. Three well supported lineages LI, LII, and LIII were revealed in our plastomic analyses, with LI sister to LII + LIII. In addition, the monophyly of the newly delimitated LII was strongly supported by three different partition strategies, concatenated methods under Bayesian and Maximum Likelihood analyses. LII comprised 13 tribes, including four tribes previously unassigned to any lineage, that is Biscutelleae as the earliest diverging clade and Cochlearieae as the sister to Megacarpaeeae + Anastaticeae. Within LII, the intertribal relationships were also well resolved, except that a conflicting position of Orychophragmus was detected among different datasets. In LIII, Shehbazia was resolved as a member of Chorisproreae, but Chorisproreae, Dontostemoneae, and Euclidieae were all resolved as paraphyletic, which was also confirmed by nrDNA analyses. Moreover, the loss of the rps16 gene was detected as likely to be a synapomorphy of the tribes Arabideae and Alysseae. Overall, using genome skimming data, we resolved robust phylogenetic relationships of core Brassicaceae and shed new light on the complex evolutionary history of this family. [ABSTRACT FROM AUTHOR]

Introduction: The effects of edaravone against pentylenetetrazole (PTZ)‐induced epilepsy in male albino rats were investigated. Edaravone is a well‐known commercial drug used in the treatment of strokes and amyotrophic lateral sclerosis (ALS). Antioxidant and free radical scavenging activities of edaravone have been reported in patients with ALS. Methods: In this study, the experimental groups were as follows: sham, control, 5 mg/kg edaravone, and 10 mg/kg edaravone. Behavioral assessment, determination of biochemical markers, apoptosis, nitric oxide (NO), and mRNA and protein expression of cyclooxygenase‐II (COX‐II) were carried out. Seizure incidence, including generalized tonic–clonic seizure (GTCS) and minimal clonic seizure (MCS), was directly associated with PTZ administration in rats. Results: Edaravone supplementation substantially increased MCS and GTCS latency in rats, and biochemical markers were significantly altered in the brain tissue of PTZ‐treated rats. Edaravone treatment normalized altered biochemical markers compared with the untreated control. Apoptosis and NO levels were significantly reduced by more than 50% compared to their respective controls. COX‐II mRNA was increased by 130% in PTZ‐treated rats, while edaravone supplementation reduced mRNA and protein expression of COX‐II by more than 20% and 40%, respectively. Immunohistochemistry indicated that COX‐II protein expression was reduced by 13.2% and 33.7% following supplementation with 5 and 10 mg/kg edaravone, respectively. Conclusion: Taken together, our results suggest that edaravone functions by downregulating the levels of COX‐II and NO and is a potential candidate for the treatment of PTZ‐induced epilepsy. Edaravone supplementation significantly normalized altered lipid peroxidation and antioxidant biochemical markers. Apoptosis and NO levels were reduced compared to their respective controls. mRNA and protein expression of COX‐II was substantially reduced following edaravone supplementation. Taken together, our results suggest that edaravone is a potential candidate for the treatment of PTZ‐induced epilepsy and functions by downregulating the levels of COX‐II and NO. [ABSTRACT FROM AUTHOR]