Tuning the Cyclopropane Ring-Opening Reaction over Electronic Bias by Fusion to a Pre-Aromatic Ring: TfOH-Promoted Aromatization of Dibenzonorcaradienes to Dibenzo[<i>f</i>,<i>h</i>]isocoumarins

Fusion of the cyclopropane ring bearing two vicinal acceptors to the pre-aromatic dihydrophenanthrene ring, which is constructed by the Pd-catalyzed cross-coupling between the vicinal aromatic rings, is found to effectively direct the cleavage of the electronically unfavored cyclopropane bond between the vicinal acceptors. Consequently, a modular method for the rapid synthesis of dibenzo­[f,h]­isocoumarins from methyl ketones, aryl aldehydes, and α-keto esters via a reaction cascade of aldol condensation, Kukhtin–Ramirez cyclopropanation, Pd-catalyzed direct arylation, and acid-promoted aromatization has been realized

Tuning the Cyclopropane Ring-Opening Reaction over Electronic Bias by Fusion to a Pre-Aromatic Ring: TfOH-Promoted Aromatization of Dibenzonorcaradienes to Dibenzo[<i>f</i>,<i>h</i>]isocoumarins

Fusion of the cyclopropane ring bearing two vicinal acceptors to the pre-aromatic dihydrophenanthrene ring, which is constructed by the Pd-catalyzed cross-coupling between the vicinal aromatic rings, is found to effectively direct the cleavage of the electronically unfavored cyclopropane bond between the vicinal acceptors. Consequently, a modular method for the rapid synthesis of dibenzo­[f,h]­isocoumarins from methyl ketones, aryl aldehydes, and α-keto esters via a reaction cascade of aldol condensation, Kukhtin–Ramirez cyclopropanation, Pd-catalyzed direct arylation, and acid-promoted aromatization has been realized

Tuning the Cyclopropane Ring-Opening Reaction over Electronic Bias by Fusion to a Pre-Aromatic Ring: TfOH-Promoted Aromatization of Dibenzonorcaradienes to Dibenzo[<i>f</i>,<i>h</i>]isocoumarins

Fusion of the cyclopropane ring bearing two vicinal acceptors to the pre-aromatic dihydrophenanthrene ring, which is constructed by the Pd-catalyzed cross-coupling between the vicinal aromatic rings, is found to effectively direct the cleavage of the electronically unfavored cyclopropane bond between the vicinal acceptors. Consequently, a modular method for the rapid synthesis of dibenzo­[f,h]­isocoumarins from methyl ketones, aryl aldehydes, and α-keto esters via a reaction cascade of aldol condensation, Kukhtin–Ramirez cyclopropanation, Pd-catalyzed direct arylation, and acid-promoted aromatization has been realized

Three new triterpenoids with their bioactives from the roots of <i>Rosa cymosa</i>

Three new triterpenoids, 2α, 3α, 20β, 23-tetrahydroxyurs-13 (18)-en-28-oic-acid (1) (Figure 1), 2β, 3α, 20β, 23-tetrahydroxyurs-13(18)-en-28-oic-acid (2), and 2α, 3α-dihydroxyurs-12(13), 18(19)-dien-28-oic-acid (3) were isolated from the roots of R. cymosa. Their structures were elucidated by extensive spectroscopic methods, including NMR, MS, and IR spectroscopic analyses data. All the isolates were evaluated for their α-glucosidase inhibitory and anti-inflammatory activities in vitro. The results showed that compound 2 displayed moderate anti-inflammatory activity with IC50 value of 9.4 μM.</p

Image_1_Araloside C Prevents Hypoxia/Reoxygenation-Induced Endoplasmic Reticulum Stress via Increasing Heat Shock Protein 90 in H9c2 Cardiomyocytes.TIF

<p>Araloside C (AsC) is a cardioprotective triterpenoid compound that is mainly isolated from Aralia elata. This study aims to determine the effects of AsC on hypoxia-reoxygenation (H/R)-induced apoptosis in H9c2 cardiomyocytes and its underlying mechanisms. Results demonstrated that pretreatment with AsC (12.5 μM) for 12 h significantly suppressed the H/R injury in H9c2 cardiomyocytes, including improving cell viability, attenuating the LDH leakage and preventing cardiomyocyte apoptosis. AsC also inhibited H/R-induced ER stress by reducing the activation of ER stress pathways (PERK/eIF2α and ATF6), and decreasing the expression of ER stress-related apoptotic proteins (CHOP and caspase-12). Moreover, AsC greatly improved the expression level of HSP90 compared with that in the H/R group. The use of HSP90 inhibitor 17-AAG and HSP90 siRNA blocked the above suppression effect of AsC on ER stress-related apoptosis caused by H/R. Taken together, AsC could reduce H/R-induced apoptosis possibly because it attenuates ER stress-dependent apoptotic pathways by increasing HSP90 expression.</p

Image_3_Araloside C Prevents Hypoxia/Reoxygenation-Induced Endoplasmic Reticulum Stress via Increasing Heat Shock Protein 90 in H9c2 Cardiomyocytes.TIF

Araloside C (AsC) is a cardioprotective triterpenoid compound that is mainly isolated from Aralia elata. This study aims to determine the effects of AsC on hypoxia-reoxygenation (H/R)-induced apoptosis in H9c2 cardiomyocytes and its underlying mechanisms. Results demonstrated that pretreatment with AsC (12.5 μM) for 12 h significantly suppressed the H/R injury in H9c2 cardiomyocytes, including improving cell viability, attenuating the LDH leakage and preventing cardiomyocyte apoptosis. AsC also inhibited H/R-induced ER stress by reducing the activation of ER stress pathways (PERK/eIF2α and ATF6), and decreasing the expression of ER stress-related apoptotic proteins (CHOP and caspase-12). Moreover, AsC greatly improved the expression level of HSP90 compared with that in the H/R group. The use of HSP90 inhibitor 17-AAG and HSP90 siRNA blocked the above suppression effect of AsC on ER stress-related apoptosis caused by H/R. Taken together, AsC could reduce H/R-induced apoptosis possibly because it attenuates ER stress-dependent apoptotic pathways by increasing HSP90 expression.</p

Additional file 1: Figure S1. of Trichloromethane fraction of Incarvillea compacta induces lytic cytotoxicity and apoptosis in Epstein-Barr virus-positive gastric cancer AGS cells

UHPLC-MS chromatogram profile of dichloromethane fraction of I. compacta. (DOCX 23 kb

A new diterpene from <i>Clinopodium chinense</i>

<div><p>A new abietane diterpene, named as 3β-hydroxy-12-<i>O</i>-β-d-glucopyranosyl-8,11,13-abietatrien-7-one (<b>1</b>), together with four known flavonoids, was isolated from the hot water extract of the aerial parts of <i>Clinopodium chinense</i>. Their structures were determined by analysing the spectroscopic data including 1D, 2D NMR and HR-ESI-MS. Compound <b>1</b> tested against HepG-2 and A549 cancer cell lines expressed weak cytotoxicity. Cardioprotective effects of compounds <b>2</b>–<b>5</b> against H₂O₂-induced apoptosis in H9c2 cells were also evaluated; compounds <b>2</b> and <b>3</b> exhibited moderate cardioprotective effect.</p></div

Image_3_Araloside C Prevents Hypoxia/Reoxygenation-Induced Endoplasmic Reticulum Stress via Increasing Heat Shock Protein 90 in H9c2 Cardiomyocytes.TIF

<p>Araloside C (AsC) is a cardioprotective triterpenoid compound that is mainly isolated from Aralia elata. This study aims to determine the effects of AsC on hypoxia-reoxygenation (H/R)-induced apoptosis in H9c2 cardiomyocytes and its underlying mechanisms. Results demonstrated that pretreatment with AsC (12.5 μM) for 12 h significantly suppressed the H/R injury in H9c2 cardiomyocytes, including improving cell viability, attenuating the LDH leakage and preventing cardiomyocyte apoptosis. AsC also inhibited H/R-induced ER stress by reducing the activation of ER stress pathways (PERK/eIF2α and ATF6), and decreasing the expression of ER stress-related apoptotic proteins (CHOP and caspase-12). Moreover, AsC greatly improved the expression level of HSP90 compared with that in the H/R group. The use of HSP90 inhibitor 17-AAG and HSP90 siRNA blocked the above suppression effect of AsC on ER stress-related apoptosis caused by H/R. Taken together, AsC could reduce H/R-induced apoptosis possibly because it attenuates ER stress-dependent apoptotic pathways by increasing HSP90 expression.</p

DataSheet_2_Gut Microbiota Correlates With Clinical Responsiveness to Erythropoietin in Hemodialysis Patients With Anemia.xlsx

The main treatment for renal anemia in end-stage renal disease (ESRD) patients on hemodialysis is erythropoiesis (EPO). EPO hyporesponsiveness (EH) in dialysis patients is a common clinical problem, which is poorly understood. Recent searches reported that gut microbiota was closely related to the occurrence and development of ESRD. This study aims to explore the changes in gut microbiota between ESRD patients with different responsiveness to EPO treatment. We compared the gut microbiota from 44 poor-response (PR) and 48 good-response (GR) hemodialysis patients treated with EPO using 16S rDNA sequencing analysis. The results showed that PR patients displayed a characteristic composition of the gut microbiome that clearly differed from that of GR patients. Nine genera (Neisseria, Streptococcus, Porphyromonas, Fusobacterium, Prevotella_7, Rothia, Leptotrichia, Prevotella, Actinomyces) we identified by Lasso regression and ROC curves could excellently predict EH. In contrast, five genera (Faecalibacterium, Citrobacter, Bifidobacterium, Escherichia–Shigella, Bacteroides) identified by the same means presented a protective effect against EH. Analyzing the correlation between these biomarkers and clinical indicators, we found that gut microbiota may affect response to EPO through nutritional status and parathyroid function. These findings suggest that gut microbiota is altered in hemodialysis patients with EH, giving new clues to the pathogenesis of renal anemia.</p