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Background Artemisinin-based combination therapy has become the preferred approach for treating malaria and has successfully reduced malaria-related mortality. Currently, the main source of artemisinin is Artemisia annua L., and thus, it is of strategic importance to enhance artemisinin contents in A. annua plants. Phytohormones and illumination are known to be important external environmental factor that can have notable effects on the production of secondary metabolite. The activities of different hormones can be influenced to varying degrees by light, and thus light and hormones may jointly regulate various processes in plants. Here, we performed transcriptome and metabolome analyses revealed that ultraviolet B irradiation and phytohormone gibberellins coordinately promoted the accumulation of artemisinin in Artemisia annua. Methods Artemisinin analysis was performed by ultra-high performance liquid chromatography-tandem quadrupole mass spectrometry (UPLC-ESI-QqQ-MS/MS). RNA sequencing, GO and KEGG enrichment analysis were applied to analyzing the differentially expressed genes (DEGs) under ultraviolet B irradiation and gibberellins treatments. Weighted gene co-expression network (WGCNA) analyzed the genes in artemisinin‑related modules and identified candidate hub genes in these modules. Results In this study, we found that cross-talk between UV-B and GA induced processes leading to modifications in artemisinin accumulation. A total of 14,762 genes differentially expressed (DEGs) among different treatments were identified by transcriptome analysis. UV-B and GA treatments enhanced the accumulation of artemisinin by up-regulating the expression of the key artemisinin biosynthesis genes ADS and CYP71AV1. According to the high degree value and high expression level, a total of 84 co-expressed transcription factors were identified. Among them, MYB and NAC TFs mainly involved in regulating the biosynthesis of artemisinin. Weighted gene co-expression network analysis revealed that GA + UV in blue modules was positively correlated with artemisinin synthesis, suggesting that the candidate hub genes in these modules should be up-regulated to enhance artemisinin synthesis in response to GA + UV treatment. Conclusion Our study demonstrated the co-regulation of artemisinin biosynthetic pathway genes under ultraviolet B irradiation and phytohormone gibberellins treatment. The co-expression was analysis revealed that the selected MYB and NAC TFs might have regulated the artemisinin biosynthesis gene expression with ADS and CYP71AV1 genes. Weighted gene co-expression network analysis revealed that GA + UV treatment in blue modules was positively correlated with artemisinin synthesis. We established the network to distinguish candidate hub genes in blue modules might be up-regulated to enhance artemisinin synthesis in response to GA + UV treatment.

Two new 2-arylbenzofurans, 2-(4-methoxyphenyl)-3,5-dimethylbenzofuran-7-ol (1) and 2-(4-methoxyphenyl)-3,5-dimethylbenzofuran-6-ol (2), were isolated from the stems of Nicotiana tabacum. Their structures were determined by means of HR-ESI-MS and extensive 1D and 2D NMR spectroscopic studies. Compounds 1 and 2 were tested for their anti-TMV and cytotoxicity activities. The results showed that compounds 1 and 2 exhibited high anti-TMV activities with inhibition rates of 29.2% and 30.8% at the concentration of 20 μM. These rates are close to that of positive control (31.1%). Compounds 1 and 2 also showed moderate to weak cytotoxicities against the tested human tumor cell lines with IC50 values in the range of 2.2–8.2 μM.

Two new isobenzofurans, 1-(3-hydroxypropanoyl)-2-methoxy-isobenzofuran-1(3H)-one (1) and 2-methoxy-1-prenyl-isobenzofuran-1(3H)-one (2), were isolated from the leaves of Yunnan local sun-cured tobacco. Their structures were determined by means of HR-ESI-MS and extensive 1D and 2D NMR spectroscopic studies. Compounds 1 and 2 were tested for their cytotoxicity. The results revealed that compound 1 exhibited cytotoxicity for NB4, A549, SHSY5Y, PC3, and MCF7 cells with IC50 values of 2.8, 5.4, 6.9, 3.8, and 4.9 μM, and compound 2 exhibited cytotoxicity for NB4, A549, SHSY5Y, PC3, and MCF7 cells with IC50 values of 6.6, 7.8, 9.4, 7.0, and 9.2 μM, respectively.

The asymmetric unit of the title compound, [Zn(C3H7NO)2(H2O)4][Zn(C13H10N2O5)Cl]2, is composed of a single anion and half a cation. The ZnII atom in the monoanion has a distorted triganol–pyramidal geometry, being coordinated by three O atoms and one N atom from one 2-{3-[2-(carboxylatomethoxy)phenyl]pyrazol-1-yl}acetate ligand and one Cl atom. In the dication, the ZnII atom is located on an inversion center and is coordinated by six O atoms in a slightly distorted octahedral geometry. In the crystal, the ions are linked by O—H...O hydrogen bonds, forming a two-dimensional network lying parallel to the ab plane. There are also C—H...O and C—H...Cl interactions present, which lead to the formation of a three-dimensional structure.