National Chung Hsing University

About: National Chung Hsing University is a education organization based out in Taichung, Taiwan. It is known for research contribution in the topics: Catalysis & Thin film. The organization has 19443 authors who have published 24060 publications receiving 540154 citations. The organization is also known as: NCHU.

Kaempferol induces autophagy through AMPK and AKT signaling molecules and causes G2/M arrest via downregulation of CDK1/cyclin B in SK-HEP-1 human hepatic cancer cells

Abstract: Kaempferol belongs to the flavonoid family and has been used in traditional folk medicine. Here, we investigated the antitumor effects of kaempferol on cell cycle arrest and autophagic cell death in SK-HEP-1 human hepatic cancer cells. Kaempferol decreased cell viability as determined by MTT assays and induced a G2/M phase cell cycle arrest in a concentration-dependent manner. Kaempferol did not induce DNA fragmentation, apoptotic bodies or caspase-3 activity in SK-HEP-1 cells as determined by DNA gel electrophoresis, DAPI staining and caspase-3 activity assays, respectively. In contrast, kaempferol is involved in the autophagic process. Double-membrane vacuoles, lysosomal compartments, acidic vesicular organelles and cleavage of microtubule-associated protein 1 light chain 3 (LC3) were observed by transmission electron microscopy, LysoΤracker red staining, GFP-fluorescent LC3 assays and acridine orange staining, respectively. In SK-HEP-1 cells, kaempferol increased the protein levels of p-AMPK, LC3-II, Atg 5, Atg 7, Atg 12 and beclin 1 as well as inhibited the protein levels of CDK1, cyclin B, p-AKT and p-mTOR. Taken together, CDK1/cyclin B expression and the AMPK and AKT signaling pathways contributed to kaempferol-induced G2/M cell cycle arrest and autophagic cell death in SK-HEP-1 human hepatic cancer cells. These results suggest that kaempferol may be useful for long-term cancer prevention.

Aluminum complexes supported by tridentate aminophenoxide ligand as efficient catalysts for ring-opening polymerization of epsilon-caprolactone

Abstract: Aluminum complexes bearing dianionic amine bis(phenolate) ligand are described. Reactions of ligand precursors H2O2NMe or H2O2NPr [H2O2NMe = (CH3)N-(CH2-2-HO-3,5-C6H2(tBu)2)2; H2O2NPr = (CH3CH2CH2)N-(CH2-2-HO-3,5-C6H2(tBu)2)2] with 1.1 mol equiv of AlMe3 in toluene afford MeAl(O2NMe) (1) and MeAl(O2NPr) (2) as four-coordinate aluminum methyl complexes. The molecular structures are reported for compounds 1 and 2. Both compounds show excellent catalytic activity toward the ring-opening polymerization of e-caprolactone in the presence of benzyl alcohol.

Mechanical properties, deformation behaviors and interface adhesion of (AlCrTaTiZr)Nx multi-component coatings

Abstract: In this study, (AlCrTaTiZr)N x multi-component coatings with quinary metallic elements were developed as protective hard coatings for tribological application. The mechanical properties, creep behaviors, deformation mechanisms and interface adhesion of the (AlCrTaTiZr)N x coatings with different N contents were characterized. With increasing the N 2 -to-total (N 2 + Ar) flow ratio, R N , during sputtering deposition, the (AlCrTaTiZr)N x coatings transformed from an amorphous metallic phase to a nanocomposite and finally a crystalline nitride structure. The hardness of the coatings accordingly increased from 13 GPa to a high value of about 30 GPa, but the creep strain rate also increased from 1.3 × 10 − 4 to 7.3 × 10 − 4 1/s. The plastic deformation of the amorphous metallic coating deposited with R N = 0% proceeded through the formation and extension of shear bands, whereas dislocation activities dominated the deformation behavior of the crystalline nitride coatings deposited with R N = 10% and 30%. With increasing R N , the interface adhesion energy between the coatings and the substrates was also enhanced from 6.1 to 22.9 J/m 2 .

Advanced glycation end-products induce skeletal muscle atrophy and dysfunction in diabetic mice via a RAGE-mediated, AMPK-down-regulated, Akt pathway.

Abstract: Diabetic myopathy, a less studied complication of diabetes, exhibits the clinical observations characterized by a less muscle mass, muscle weakness and a reduced physical functional capacity. Accumulation of advanced glycation end-products (AGEs), known to play a role in diabetic complications, has been identified in ageing human skeletal muscles. However, the role of AGEs in diabetic myopathy remains unclear. Here, we investigated the effects of AGEs on myogenic differentiation and muscle atrophy in vivo and in vitro. We also evaluated the therapeutic potential of alagebrium chloride (Ala-Cl), an inhibitor of AGEs. Muscle fibre atrophy and immunoreactivity for AGEs, Atrogin-1 (a muscle atrophy marker) and phosphorylated AMP-activated protein kinase (AMPK) expressions were markedly increased in human skeletal muscles from patients with diabetes as compared with control subjects. Moreover, in diabetic mice we found increased blood AGEs, less muscle mass, lower muscular endurance, atrophic muscle size and poor regenerative capacity, and increased levels of muscle AGE and receptor for AGE (RAGE), Atrogin-1 and phosphorylated AMPK, which could be significantly ameliorated by Ala-Cl. Furthermore, in vitro, AGEs (in a dose-dependent manner) reduced myotube diameters (myotube atrophy) and induced Atrogin-1 protein expression in myotubes differentiated from both mouse myoblasts and primary human skeletal muscle-derived progenitor cells. AGEs exerted a negative regulation of myogenesis of mouse and human myoblasts. Ala-Cl significantly inhibited the effects of AGEs on myotube atrophy and myogenesis. We further demonstrated that AGEs induced muscle atrophy/myogenesis impairment via a RAGE-mediated AMPK-down-regulation of the Akt signalling pathway. Our findings support that AGEs play an important role in diabetic myopathy, and that an inhibitor of AGEs may offer a therapeutic strategy for managing the dysfunction of muscle due to diabetes or ageing.

Genome-Wide Analysis of Heat-Sensitive Alternative Splicing in Physcomitrella patens

Abstract: Plant growth and development are constantly influenced by temperature fluctuations. To respond to temperature changes, different levels of gene regulation are modulated in the cell. Alternative splicing (AS) is a widespread mechanism increasing transcriptome complexity and proteome diversity. Although genome-wide studies have revealed complex AS patterns in plants, whether AS impacts the stress defense of plants is not known. We used heat shock (HS) treatments at nondamaging temperature and messenger RNA sequencing to obtain HS transcriptomes in the moss Physcomitrella patens. Data analysis identified a significant number of novel AS events in the moss protonema. Nearly 50% of genes are alternatively spliced. Intron retention (IR) is markedly repressed under elevated temperature but alternative donor/acceptor site and exon skipping are mainly induced, indicating differential regulation of AS in response to heat stress. Transcripts undergoing heat-sensitive IR are mostly involved in specific functions, which suggests that plants regulate AS with transcript specificity under elevated temperature. An exonic GAG-repeat motif in these IR regions may function as a regulatory cis-element in heat-mediated AS regulation. A conserved AS pattern for HS transcription factors in P. patens and Arabidopsis (Arabidopsis thaliana) reveals that heat regulation for AS evolved early during land colonization of green plants. Our results support that AS of specific genes, including key HS regulators, is fine-tuned under elevated temperature to modulate gene regulation and reorganize metabolic processes.