RESUMEN
BACKGROUND: Gastrodia elata is a widely distributed achlorophyllous orchid and is highly valued as both medicine and food. Gastrodia elata produces dust-like seeds and relies on mycorrhizal fungi for its germination and growth. In its life cycle, G. elata is considered to switch from a specific single-fungus relationship (Mycena) to another single-fungus relationship (Armillaria). However, no studies have investigated the changes in the plant-fungus relationship during the growth of G. elata in the wild. In this study, high-throughput sequencing was used to characterize the fungal community of tubers in different growth phases as well as the soils surrounding G. elata. RESULTS: The predominant fungi were Basidiomycota (60.44%) and Ascomycota (26.40%), which exhibited changes in abundance and diversity with the growth phases of G. elata. Diverse basidiomycetes in protocorms (phase P) were Hyphodontia, Sistotrema, Tricholoma, Mingxiaea, Russula, and Mycena, but the community changed from a large proportion of Resinicium bicolor (40%) in rice-like tubers (phase M) to an unidentified Agaricales operational taxonomic unit 1(OTU1,98.45%) in propagation vegetation tubers (phase B). The soil fungi primarily included Simocybe, Psathyrella, Conocybe, and Subulicystidium. Three Mycena OTUs obtained in this study were differentially distributed among the growth phases of G. elata, accounting for less than 1.0% of the total reads, and were phylogenetically close to Mycena epipterygia and M. alexandri. CONCLUSIONS: Our data indicated that G. elata interacts with a broad range of fungi beyond the Mycena genus. These fungi changed with the growth phases of G. elata. In addition, these data suggested that the development of the fungal community during the growth of G. elata was more complex than previously assumed and that at least two different fungi could be involved in development before the arrival of Armillaria.
Asunto(s)
Gastrodia , Interacciones Microbiota-Huesped , Micobioma/genética , Agaricales/genética , Agaricales/aislamiento & purificación , Basidiomycota/genética , Basidiomycota/aislamiento & purificación , ADN Espaciador Ribosómico/genética , Gastrodia/crecimiento & desarrollo , Gastrodia/microbiología , Secuenciación de Nucleótidos de Alto Rendimiento , Metagenómica , Filogenia , Microbiología del Suelo , SimbiosisRESUMEN
Scutellarin (SCU), a flavonoid from a traditional Chinese medicinal plant. Our previous study has demonstrated that SCU relaxes mouse aortic arteries mainly in an endothelium-depend-ent manner. In the present study, we investigated the vasoprotective effects of SCU against HR-induced endothelial dysfunction (ED) in isolated rat CA and the possible mechanisms involving cyclic guanosine monophosphate (cGMP) dependent protein kinase (PKG). The isolated endothelium-intact and endothelium-denuded rat CA rings were treated with HR injury. Evaluation of endothelium-dependent and -independent vasodilation relaxation of the CA rings were performed using wire myography and the protein expressions were assayed by Western blotting. SCU (10-1 000 µmol·L(-1)) could relax the endothelium-intact CA rings but not endothelium-denuded ones. In the intact CA rings, the PKG inhibitor, Rp-8-Br-cGMPS (PKGI-rp, 4 µmol·L(-1)), significantly blocked SCU (10-1 000 µmol·L(-1))-induced relaxation. The NO synthase (NOS) inhibitor, NO-nitro-L-arginine methylester (L-NAME, 100 µmol·L(-1)), did not significantly change the effects of SCU (10-1 000 µmol·L(-1)). HR treatment significantly impaired ACh-induced relaxation, which was reversed by pre-incubation with SCU (500 µmol·L(-1)), while HR treatment did not altered NTG-induced vasodilation. PKGI-rp (4 µmol·L(-1)) blocked the protective effects of SCU in HR-treated CA rings. Additionally, HR treatment reduced phosphorylated vasodilator-stimulated phosphoprotein (p-VASP, phosphorylated product of PKG), which was reversed by SCU pre-incubation, suggesting that SCU activated PKG phosphorylation against HR injury. SCU induces CA vasodilation in an endothelium-dependent manner to and repairs HR-induced impairment via activation of PKG signaling pathway.