MOESM3 of Alpha-mangostin induces endoplasmic reticulum stress and autophagy which count against fatty acid synthase inhibition mediated apoptosis in human breast cancer cells

Additional file 3: Figure S3. α-Mangostin inhibited intracellular FAS activity and reduced the amount of free fatty acids. (A) MDA-MB-231 cells were treated with 0, 1, 2, and 4 μM α-mangostin for 24 h, then intracellular FAS activity was determined spectrophotometrically by measuring the decrease of absorbance at 340 nm due to oxidation of NADPH. (B) MDA-MB-231 cells were treated with 0, 1, 2, and μM α-mangostin for 24 h. Then cells were harvested using trypsin–EDTA, washed twice with PBS. Intracellular fatty acid was determined with a Free Fatty Acid Quantification Kit (Bivision) according to the manufacturer’s instructions. Data represented the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01

MOESM1 of Alpha-mangostin induces endoplasmic reticulum stress and autophagy which count against fatty acid synthase inhibition mediated apoptosis in human breast cancer cells

Additional file 1: Figure S1. The effects of α-mangostin on ER stress, autophagy, cell viabilities in MCF-7 cells. (A) MCF-7 cells were treated with 0, 1, 2, and 4 μM α-mangostin for 24 h, and then the relative expression levels of CHOP, BIP, LC3II/LC31 and P62 were analyzed by western blot and were quantified densitometrically with the software ImageJ and calculated according to the reference bands of GAPDH. Data represented the mean ± SD of three independent experiments. **p < 0.01. (B) MCF-7 cells were treated with 4 μm α-mangostin, 5 mM 4PBA, 5 mM 3MA or a combination of them. Cell viabilities were then determined by the CCK-8 assay. Data represented the mean ± SD of three independent experiments. **p < 0.01. (C) MCF-7 cells were treated with/without 4 μm α-mangostin followed 24 h incubation with/without 10 μM PA. Cell viabilities were then determined by the CCK-8 assay. Data represented the mean ± SD of three independent experiments. **p < 0.01

MOESM2 of Alpha-mangostin induces endoplasmic reticulum stress and autophagy which count against fatty acid synthase inhibition mediated apoptosis in human breast cancer cells

Additional file 2: Figure S2. The time-dependent effects of α-mangostin on ER stress and autophagy in MDA-MB-231 cells. Cells were treated with 4 μm α-mangostin for 0, 6, 12, 18, and 24 h, and then the relative expression levels of CHOP, BIP, LC3II/LC31 and P62 were analyzed by western blot and were quantified densitometrically with the software ImageJ and calculated according to the reference bands of GAPDH. Data represented the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01

Stereoselective Synthesis of 2-<i>C</i>-Acetonyl-2-Deoxy-d-Galactosides using 1,2-Cyclopropaneacetylated Sugar as Novel Glycosyl Donor

1,2-Cyclopropaneacetylated sugar is an effective glycosyl donor, which reacted with various glycosyl acceptors including monosaccharides, amino acids and other alcohols in the presence of BF3•OEt2 or TMSOTf. The glycosylation is stereoselective in favor of β-anomeric products with BF3•OEt2 as catalyst, whereas TMSOTf-catalyzed glycosylation prefers the α-anomeric products. 2-C-Acetonyl-2-deoxy-d-galactosides were obtained in good yields.</b

A Novel and Highly Stereoselective Synthesis of 2-Substituted Perhydrofuro[2,3-<i>b</i>]pyran Derivatives

An effective and facile method for the synthesis of 2-substituted perhydrofuro[2,3-b]pyran derivatives is described. The cyclization of 2-C-aldehydo-2-deoxy-d-thioglucoside in the presence of N-iodosuccinimide (NIS) is highly stereoselective. 2-Substituted cyclization products were obtained in good to excellent yields

One-Pot Synthesis of 2‑<i>C</i>‑Branched Glycosyl Triazoles by Integrating 1,2-Cyclopropanated Sugar Ring-Opening Azidation and CuAAC Reaction

A series of 2-C-branched glycosyl triazoles including triazole-tethered oligosaccharides and glycopeptides were synthesized in one pot from 1,2-cyclopropanated sugars or 2′-acetonyl-2-O-Ts-C-furanosides, NaN3, and alkynes using PEG-400 as a single solvent. Nucleophilic ring-opening azidation of 1,2-cyclopropanated sugars (or 2′-acetonyl group 1,2-migration-azidation of C-furanosides) obtained glycosyl azides, which upon reaction with alkynes under CuAAC conditions achieved glycosyl triazoles in good yields and high stereoselectivity without the need to change the solvent and isolate any intermediates

Efficacy of the sphingosine-1-phosphate receptor agonist fingolimod in animal models of stroke: an updated meta-analysis

Objective: Neuroinflammation is a central part of cerebral ischemia/reperfusion injury. The novel immune suppressant, fingolimod, is a promising candidate to ameliorate stroke-induced damage. Fingolimod is efficacious in experimental ischemic models, but a rigorous meta-analysis is lacking that considers how different experiment variables affect outcomes. Methods: We conducted a systematic literature review of fingolimod in stroke models, with the aim of rigorously evaluating fingolimod’s effects on reducing infarct volume improving neurological outcomes. Seventeen variables were evaluated as covariates for the source of heterogeneity, and effect sizes were combined by using normalized mean difference meta-analysis to evaluate efficacy. Study quality was evaluated by the CAMARADES ten-item checklist, and publication bias was evaluated by funnel plots and Egger’s tests. Results: About 123 unduplicated articles were identified in the literature research. Of these papers, 118 articles were excluded after reading titles and abstracts. Another 17 articles were selected in this study. Study quality was moderate (median = 6; interquartile range = 4), and publication bias was statistically insignificant. fingolimod reduced infarct volume by 30.4% (95% CI 22.4%−38.3%; n = 24; I2 = 90.0%; p n = 14; I2 = 76.5%; p  Conclusions: Our rigorous statistical evaluation confirmed the neuroprotective properties of fingolimod. New data can be used in designing future clinical trials.</p

Table_1_Shared Biological Pathways Between Alzheimer’s Disease and Ischemic Stroke.XLSX

Alzheimer’s disease (AD) and ischemic stroke (IS) are an immense socioeconomic burden worldwide. There is a possibility that shared genetic factors lead to their links at epidemiological and pathophysiological levels. Although recent genome-wide association studies (GWAS) have provided profound insights into the genetics of AD and IS, no shared genetic variants have been identified to date. This prompted us to initiate this study, which sought to identify shared pathways linking AD and IS. We took advantage of large-scale GWAS summary data of AD (17,008 AD cases and 37,154 controls) and IS (10,307 cases and 19,326 controls) to conduct pathway analyses using genetic pathways from multiple well-studied databases, including GO, KEGG, PANTHER, Reactome, and Wikipathways. Collectively, we discovered that AD and IS shared 179 GO categories (56 biological processes, 95 cellular components, and 28 molecular functions); and the following pathways: six KEGG pathways; two PANTHER pathways; four Reactome pathways; and one in Wikipathways pathway. The more fine-grained GO terms were mainly summarized into different functional categories: transcriptional and post-transcriptional regulation, synapse, endocytic membrane traffic through the endosomal system, signaling transduction, immune process, multi-organism process, protein catabolic metabolism, and cell adhesion. The shared pathways were roughly classified into three categories: immune system; cancer (NSCLC and glioma); and signal transduction pathways involving the cadherin signaling pathway, Wnt signaling pathway, G-protein signaling and downstream signaling mediated by phosphoinositides (PIPs). The majority of these common pathways linked to both AD and IS were supported by convincing evidence from the literature. In conclusion, our findings contribute to a better understanding of common biological mechanisms underlying AD and IS and serve as a guide to direct future research.</p

Table_2_Shared Biological Pathways Between Alzheimer’s Disease and Ischemic Stroke.xlsx

Alzheimer’s disease (AD) and ischemic stroke (IS) are an immense socioeconomic burden worldwide. There is a possibility that shared genetic factors lead to their links at epidemiological and pathophysiological levels. Although recent genome-wide association studies (GWAS) have provided profound insights into the genetics of AD and IS, no shared genetic variants have been identified to date. This prompted us to initiate this study, which sought to identify shared pathways linking AD and IS. We took advantage of large-scale GWAS summary data of AD (17,008 AD cases and 37,154 controls) and IS (10,307 cases and 19,326 controls) to conduct pathway analyses using genetic pathways from multiple well-studied databases, including GO, KEGG, PANTHER, Reactome, and Wikipathways. Collectively, we discovered that AD and IS shared 179 GO categories (56 biological processes, 95 cellular components, and 28 molecular functions); and the following pathways: six KEGG pathways; two PANTHER pathways; four Reactome pathways; and one in Wikipathways pathway. The more fine-grained GO terms were mainly summarized into different functional categories: transcriptional and post-transcriptional regulation, synapse, endocytic membrane traffic through the endosomal system, signaling transduction, immune process, multi-organism process, protein catabolic metabolism, and cell adhesion. The shared pathways were roughly classified into three categories: immune system; cancer (NSCLC and glioma); and signal transduction pathways involving the cadherin signaling pathway, Wnt signaling pathway, G-protein signaling and downstream signaling mediated by phosphoinositides (PIPs). The majority of these common pathways linked to both AD and IS were supported by convincing evidence from the literature. In conclusion, our findings contribute to a better understanding of common biological mechanisms underlying AD and IS and serve as a guide to direct future research.</p

A Novel and Highly Stereoselective Synthesis of 2-Substituted Perhydrofuro[2,3-<i>b</i>]pyran Derivatives

An effective and facile method for the synthesis of 2-substituted perhydrofuro[2,3-b]pyran derivatives is described. The cyclization of 2-C-aldehydo-2-deoxy-d-thioglucoside in the presence of N-iodosuccinimide (NIS) is highly stereoselective. 2-Substituted cyclization products were obtained in good to excellent yields