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Brassinosteroids (BRs) have been shown to enhance stress tolerance by inducing antioxidant defense systems. However, the mechanisms of BR-induced antioxidant defense in plants remain to be determined. In this study, the role of calcium (Ca(2+)) and maize calcium/calmodulin-dependent protein kinase (CCaMK), ZmCCaMK, in BR-induced antioxidant defense, and the relationship between ZmCCaMK and Ca(2+) in BR signaling were investigated. BR treatment led to a significant increase in cytosolic Ca(2+) concentration in protoplasts from maize mesophyll, and Ca(2+) was shown to be required for BR-induced antioxidant defense. Treatment with BR induced increases in gene expression and enzyme activity of ZmCCaMK in maize leaves. Transient overexpression and silencing of ZmCCaMK in maize protoplasts demonstrated that ZmCCaMK was required for BR-induced antioxidant defense. The requirement for CCaMK was further investigated using a loss-of-function mutant of OsCCaMK, the orthologous gene of ZmCCaMK in rice. Consistent with the findings in maize, BR treatment could not induce antioxidant defense in the rice OsCCAMK mutant. Furthermore, Ca(2+) was required for BR-induced gene expression and activation of ZmCCaMK, while ZmCCaMK was shown to enhance the BR-induced increase in cytosolic Ca(2+) concentration. Moreover, our results also showed that ZmCCaMK and H2O2 influenced each other. These results indicate that Ca(2+) works together with ZmCCaMK in BR-induced antioxidant defense, and there are two positive feedback loops between Ca(2+) or H2O2 and ZmCCaMK in BR signaling in maize.

Two new tetrahydrofuran-type lignans, (-)-gentioluteol 9-O-β-d-glucopyranoside (1), (-)-berchemol 9-O-β-d-apiofuranosyl-(1→6)-O-β-d-glucopyranoside (2), along with sixteen known compounds 3 - 18 were isolated from the 95% EtOH extract of the stems of Periploca forrestii. The structures of the new tetrahydrofuran-type lignans were determined by HR-ESI-MS and various NMR techniques in combination with CD method. Then, their antioxidant abilities were evaluated by 1,1-diphenyl-2-picrylhydrazyl (DPPH), 2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging activity, and ferric-reducing antioxidant power (FRAP) assays. Meanwhile, a similar trend was obtained in tripartite antioxidant assays, which compounds 7 - 9 and 11 exhibited potent abilities. Subsequently, the evaluation of all compounds against the α-melanocyte-stimulating hormone (α-MSH) induced melanogenesis on the B16F10 cell line, compounds 5 - 11, 15, and 16 exhibited inhibitory effects with no or weak toxicity at low concentration. Of these, compound 8 exhibited the strongest inhibition melanogenesis ability. Furthermore, Western blot analysis suggested that compound 8 could inhibit melanogenesis by suppressing the protein expression of microphthalmia-associated transcription factor (MITF) and tyrosinase.

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