New Indole Diketopiperazine Alkaloids from Soft Coral-Associated Epiphytic Fungus Aspergillus versicolor CGF 9-1-2.

Two new indole diketopiperazine alkaloids (IDAs), (+)19-epi-sclerotiamide (1) and (-)19-epi-sclerotiamide (2), along with 13 known analogs (3-15), were isolated from a soft coral-associated epiphytic fungus Aspergillus versicolor CGF 9-1-2. The structures of two new compounds were established based on the combination of HR-ESI-MS, 1D and 2D NMR spectroscopy, optical rotation measurements and quantum chemical 13 C-NMR, the absolute configurations were determined by experimental and electronic circular dichroism (ECD) calculations. The results of molecular docking showed that all the compounds had a good binding with TDP1, TDP2, TOP1, TOP2, Ache, NLRP3, EGFR, EGFR L858R, EGFR T790M and EGFR T790/L858. Biological evaluation of compounds 3, 6, 8, 11 showed that 3 exerted a strong inhibitory effect on TDP2 with a rate of 81.72 %.

Heat stress induced IPEC-J2 cells barrier dysfunction through endoplasmic reticulum stress mediated apoptosis by p-eif2α/CHOP pathway.

Heat stress (HS) induced by high ambient temperatures compromises intestinal epithelial cell. However, the underlying mechanisms by which HS causes intestinal barrier dysfunction remain unclear. In this study, we established an in vitro acute-HS-induced intestinal damage using porcine small intestinal epithelial cell (IPEC-J2) that exposed to the high temperatures (43°C) for 2 h. The cell proliferation, apoptosis, tight junction (TJ) barrier integrity and transcriptomic profiles were measured. The results showed that HS decreased cell viability while increased proapoptotic signaling evidenced by Bax/bcl2 ratio, cytochrome C release to cytosol and active-caspase 3 increases (p < 0.01). HS led to decreased transepithelial electrical resistance, increased cell permeability, and downregulated TJ proteins including ZO1, occludin, and claudin 3 (p < 0.05). Transcriptome sequencing and KEGG pathway analysis revealed HS-induced cell cycle arrest and activation of endoplasmic reticulum stress (ERS) response mediated by a critical transcript eif2α and proapoptotic molecule DDIT3 (known as CHOP). Furthermore, inhibition of ERS by 4-phenylbutyrate (4-PBA) administration and knockdown of eif2α and CHOP significantly attenuated IPEC-J2 cells apoptosis (p < 0.05). Transmission electron microscopy analysis suggested that 4-PBA inhibited HS-induced increase in ER lumen diameter, indicating ultrastructural sign of ERS. In addition, HS-induced impairment of TJs was significantly attenuated by 4-PBA (p < 0.05). Collectively, HS induces ERS and activates the p-eif2α/CHOP signaling pathway to impair epithelial barrier integrity through triggering the intestinal epithelial cell apoptosis.

Bioactive Aspergteroids G-J from Soft-Coral-Associated Symbiotic and Epiphytic Fungus Aspergillus terreus EGF7-0-1.

Two new disubstituted maleimides, aspergteroids G-H (1-2), and two trisubstituted butenolides aspergteroids I-J (3-4), along with four known analogs, were isolated and structurally identified from the fermentation extract of soft-coral-associated symbiotic and epiphytic fungus Aspergillus terreus EGF7-0-1. The structures of the new compounds were established mainly via spectroscopic data analyses, and their absolute configurations were determined via X-ray diffraction analysis and comparison of the calculated and experimental electronic circular dichroism. Myocardial protection assays showed that compounds 1, 2, 5, and 6 possess protective effects against tert-butyl hydroperoxide (TBHP)-induced H9c2 (rat myocardial cells) apoptosis at low concentrations. Based on the analyses of the protein-protein interaction (PPI) network and Western blotting, compound 1 may inhibit the apoptosis and inflammatory response of cardiomyocytes after TBHP induction and improve the antioxidant capacity of cardiomyocytes. We speculate that the anti-inflammatory response of compound 1 is suppressed by the glycogen synthase kinase-3 beta (GSK-3ß), downregulated by the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome activation, and suppressed by the expression of cysteinyl aspartate specific proteinase-3 (caspase-3) and B-cell lymphoma-2 associated X protein (Bax).

[Effects of seasonal temperature variation on nitrogen removal from a tidal flow constructed wetland system with CANON process]. / 季节性温度变化对CANON型潮汐流人工湿地脱氮的影响.

We investigated the effects of seasonal temperature variation on the treatment perfor-mance and underlying mechanisms of nitrogen transformation in a tidal flow constructed wetland (TFCW) with the complete autotrophic nitrogen removal over nitrite (CANON) process. Different temperatures resulted in periodical variations in nitrogen transformation pathways and removal performance of the TFCW with CANON process, which was mainly due to the changes of dominant bacterial communities for nitrogen removal in the system. When temperature was higher than 20.0 ℃, nitrogen transformation and associated microbial characteristics in the TFCW were significantly affected, and the CANON process remained to be the principal pathway for nitrogen removal. The abundance and activity of anammox bacteria experienced different degrees of reduction when temperature dropped below 20.0 ℃. At the temperature of 9.3-20.0 ℃, the proliferation and increased activities of nitrite oxidizing bacteria (NOB) made the nitrification/denitrification process instead of the CANON process became the primary total nitrogen (TN) removal route in the TFCW, and the TN removal efficiency of the system declined to 34.8%±13.0%. Under the temperature range of 2.2-9.0 ℃, anammox bacteria, which was inhibited at the low temperatures, presented competitive advantage in comparison with NOB and denitrifiers, resulting that nitrogen removal in the TFCW relied on the CANON process again. Correspondingly, nitrogen removal rate of the system was 54.8%±4.8%. This study was conductive to the optimization of the TFCW with CANON process, as well as its engineering application.