Xuanfu Daizhe Tang alleviates reflux esophagitis in rats by inhibiting the STAT1/TREM-1 pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Reflux esophagitis (RE) is a common chronic inflammatory disease of the esophageal mucosa with a high prevalence and recurrence rate, for which a satisfactory therapeutic strategy is still lacking. Chinese medicine has its characteristics and advantages in treating RE, and the clinical application of Xuanfu Daizhe Tang (XDT) in treating RE has achieved sound therapeutic effects. However, there needs to be more research on its mechanism of action. AIM OF THE STUDY: The present work aimed to investigate the mechanism of XDT action in RE through the Signal Transducer and Activator of Transcription 1 (STAT1)/Triggering Receptor Expressed on Myeloid cells-1 (TREM-1) pathway. MATERIALS AND METHODS: The main active components of XDT were analyzed by ultra-performance liquid chromatography-mass spectrometer (UPLC-MS). The effect of XDT on RE was evaluated in a rat model of RE induced by "Cardioplasty + pyloric ligation + Roux-en-Y esophagojejunostomy". Each administration group was treated by gavage. The degree of damage to the esophageal mucosa was evaluated by visual observation, and the Potential of Hydrogen (PH) method and Hematoxylin-eosin staining (HE) staining were performed. Serum levels of Interleukin-1ß (IL-1ß), Interleukin-6 (IL-6), Tumor Necrosis Factor alpha (TNF-α), and Inducible Nitric Oxide Synthase (iNOS) were measured by ELISA. Quantitative Real-time PCR (qPCR), Western Blot (WB), and Immunofluorescence (IF) methods were used to detect Claudin-4, Claudin-5, TREM-1, and p-STAT1 in esophageal tissues for studying the mechanism of action and signaling pathway of XDT. Immunohistochemistry (IHC) analysis was used to detect the expression of TREM-1 and CD68 in esophageal tissues. Flow Cytometry (FC) was used to detect the polarization of macrophages in the blood. After conducting preliminary experiments to verify our hypothesis, we performed molecular docking between the active component of XDT and STAT1 derived from rats and parallel experiments with STAT1 inhibitor. The selective increaser of STAT1 transcription (2-NP) group was used to validate the mechanism by which XDT acts. RESULTS: XDT alleviated esophageal injury and attenuated histopathological changes in RE rats. XDT also inhibited the inflammatory response and decreased serum IL-1ß, IL-6, TNF-α, and iNOS levels in RE rats. qPCR and WB results revealed that XDT inhibited the expression of Claudin-4, Claudin-5, TREM-1, and STAT1 in the esophageal mucosa of RE rats. IHC and FC results showed that XDT reduced TREM-1 levels in esophageal tissues and polarized macrophages toward M2. The molecular docking results showed that rat-derived STAT1 can strongly bind to Isochronogenic acid A in XDT. The parallel experimental results of STAT1 inhibitor showed that XDT has anti-inflammatory effects similar to STAT1 inhibitors. The 2-NP group confirmed that XDT exerts its therapeutic effect on reflux esophagitis through the STAT1/TREM-1 pathway, with STAT1 as the upstream protein. CONCLUSIONS: This study suggests that XDT may treat reflux esophagitis by modulating the STAT1/TREM-1 pathway.

Proteomic analysis of anti-aging effects of Dendrobium nobile Lindl. alkaloids in aging-accelerated SAMP8 mice.

Senescence-accelerated mouse prone 8 (SAMP8) mice exhibit cognitive defects and neuron loss with aging, and were used to study anti-aging effects of Dendrobium nobile alkaloids (DNLA). DNLA (20 and 40 mg/kg) were orally administered to SAMP8 mice from 6 to 10 months of age. At 10-month of age, behavioral tests via Y-maze and Open-field and neuron damage via Nissl staining were evaluated. Protein was extracted and subjected to phosphorylated proteomic analysis followed by bioinformatic analysis. The cognitive deficits and neuron loss in hippocampus and cortex of aged SAMP8 mice were improved by DNLA. Hippocampal proteomic analysis revealed 196 differentially expressed protein/genes in SAMP8 compared to age-matched senescence-accelerated resistant SAMR1 mice. Gene Oncology enriched the tubulin binding, microtubule binding, and other activities. Kyoto Encyclopedia of Genes and Genomes (KEGG) revealed endocytosis, mRNA surveillance, tight junction, protein processing in endoplasmic reticulum, aldosterone synthesis and secretion, and glucagon signaling pathway changes. Upregulated protein/genes in the hippocampus of SAMP8 mice, such as Lmtk3, Usp10, Dzip1, Csnk2b, and Rtn1, were attenuated by DNLA; whereas downregulated protein/genes, such as Kctd16, Psd3, Bsn, Atxn2l, and Kif1a, were rescued by DNLA. The aberrant protein/gene expressions of SAMP8 mice were correlated with transcriptome changes of Alzheimer's disease in the Gene Expression Omnibus (GEO) database, and the scores were attenuated by DNLA. Thus, DNLA improved cognitive dysfunction and ameliorated neuronal injury in aged SAMP8 mice, and attenuated aberrant protein/gene expressions.

Gastrodin Improves Cognitive Dysfunction in REM Sleep-Deprived Rats by Regulating TLR4/NF-κB and Wnt/ß-Catenin Signaling Pathways.

Gastrodin is the active ingredient in Gastrodia elata. Our previous studies demonstrated that gastrodin ameliorated cerebral ischemia-reperfusion and hypoperfusion injury and improved cognitive deficit in Alzheimer's disease. This study aims to examine the effects of gastrodin on REM sleep deprivation in rats. Gastrodin (100 and 150 mg/kg) was orally administered for 7 consecutive days before REM sleep deprivation. Seventy-two hours later, pentobarbital-induced sleep tests and a Morris water maze were performed to measure REM sleep quality and learning and memory ability. Histopathology was observed with hematoxylin-eosin staining, and the expression of the NF-κB and Wnt/ß-catenin signaling pathways was examined using Western blot. After REM sleep deprivation, sleep latency increased and sleep duration decreased, and the ability of learning and memory was impaired. Neurons in the hippocampal CA1 region and the cortex were damaged. Gastrodin treatment significantly improved REM sleep-deprivation-induced sleep disturbance, cognitive deficits and neuron damage in the hippocampus CA1 region and cerebral cortex. A mechanism analysis revealed that the NF-κB pathway was activated and the Wnt/ß-catenin pathway was inhibited after REM sleep deprivation, and gastrodin ameliorated these aberrant changes. Gastrodin improves REM sleep-deprivation-induced sleep disturbance and cognitive dysfunction by regulating the TLR4/NF-κB and Wnt/ß-catenin signaling pathways and can be considered a potential candidate for the treatment of REM sleep deprivation.

The Strategy of How to Deeply Integrate Technology and Finance in the Internet Environment.

To solve some problems existing in the mechanism of the combination of science and technology and finance, this study studies the deep integration of science and technology and finance combined with the Internet. At present, there are many problems in the development of science and technology finance in terms of bank credit, capital market, service system, and risk supervision. To solve these problems, we need to innovate bank credit products and service modes, expand the breadth and depth of capital market services, establish a new science and technology financial service system, improve science and technology financial supervision regulations and means, and comprehensively promote the deep integration of science and technology and finance in the new era. Based on this, this study first expounds on the importance of the deep integration of science and technology and finance, comprehensively analyzes the problems existing in the deep integration of science and technology and finance, and finally puts forward the construction strategy of science and technology and finance integration platform. In the development of market economy, the deep integration of science and technology and finance and the development of platform model effectively improve the innovation ability of science and technology enterprises. The research shows that the high integration of science and technology and finance is the inevitable trend of the future development of the economic market. Therefore, enterprises need to constantly improve their financial operation ability, pay attention to the ways and means of the development of science and technology finance, strengthen the construction of their own platform, improve their operation ability, and improve their development status, so that enterprises can obtain a higher position in the market competition and achieve the purpose of sustainable development.

Antitumor effects of cadmium against diethylnitrosamine-induced liver tumors in mice.

Cadmium (Cd) has been reported to exhibit antitumor effects against chemically induced liver tumors. However, the antitumor effects of Cd are not completely understood. Metallotherapy, the use of a toxic metal to attack liver tumors, could be a viable strategy. In the present study, 8-week old, male, C57BL/6 mice were administered injections of diethylnitrosamine (DEN) (90 mg/kg, and then 50 mg/kg 2 weeks later), followed by liver tumor promotion with carbon tetrachloride. Cadmium chloride was administered in the drinking water (1000 ppm) from 21-40 weeks after DEN initiation. Body weights were recorded and liver tumor formation was monitored via ultrasound. At the end of experiments, livers were removed, weighed, and the tumor incidence, tumor numbers and tumor size scores were recorded. Liver histology and metallothionein (MT) immunostaining were performed. After DEN injection, animal body weight decreased, and then slowly recovered with time. Cd treatment did not affect animal body weight gain. Ultrasound analysis detected liver tumors 35 weeks after DEN injection, and the mice were necropsied at 40 weeks. Liver/body weight ratios increased in the DEN and DEN + Cd groups. Cd treatment decreased the tumor incidence (71 vs. 17%), tumor numbers (15 vs. 2) and tumor scores (22 vs. 3) when compared with the DEN only group. Histopathology showed hepatocyte degeneration in all groups, and immunohistochemistry showed MT-deficiency in the liver tumors, while MT staining was intensified in the surrounding tissues. Reverse transcription-quantitative PCR showed increases in α-fetoprotein level in DEN-treated livers, and increases in MT-2 and tumor necrosis factor α (TNFα) levels in Cd-treated livers. Thus, it was concluded that Cd is effective in the suppression of DEN-induced liver tumors, and that the mechanisms may be related to MT-deficiency in tumors and the induction of TNFα to kill tumor cells.

Beneficial effects of Dendrobium nobile Lindl. Alkaloids (DNLA) on anxiety and depression induced by chronic unpredictable stress in rats.

Dendrobium nobile Lindl. alkaloid (DNLA) is effective against animal models of Alzheimer's disease. This study further examined its effect on anxiety and depression produced by chronic unpredictable stress (CUS). Rats were subjected to CUS for 42 days, followed by DNLA treatment (20 mg/kg/day, po) for 28 days. The behavioral tests, histopathology, neurotransmitters and RNA-Seq were examined. DNLA attenuated body weight loss and CUS-induced anxiety/depressive-like behaviors, as evidenced by the elevated-plus-maze test, open-field test and sucrose preference. DNLA alleviated neuronal damage and loss and increased Nissl bodies in the hippocampus CA2 region and cortex. DNLA decreased CUS-elevated 5-hydroxytryptamine, dopamine and monoamine oxidase and catechol-O-methyltransferase activities in the brain. DNLA attenuated HPA activation by decreasing adrenocorticotropic hormones and the expression of corticotropin-releasing hormone receptor-1, and increased the expression of glucocorticoid receptor in the brain. RNA-Seq revealed distinct gene expression patterns among groups. Gene ontology revealed the cell projection assembly, postsynapse and centrosome as top biological processes, and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment showed the cAMP, cGMP-PKG, glutamatergic synapse and circadian as major pathways for DNLA effects. Using DESeq2, CUS modulated 1700 differentially expressed genes (DEGs), which were prevented or attenuated by DNLA. CUS-induced DEGs were highly correlated with the Gene Expression Omnibus (GEO) database for anxiety and depression and were ameliorated by DNLA. Taken together, DNLA attenuated anxiety/depression-like behavior and neuronal damage induced by CUS in rats. The mechanisms could be related to regulation of the monoamine neurotransmitters and the HPA axis, and modulation of gene expression in the hippocampus.

Dendrobium nobile Lindl. Alkaloids Ameliorate Cognitive Dysfunction in Senescence Accelerated SAMP8 Mice by Decreasing Amyloid-ß Aggregation and Enhancing Autophagy Activity.

BACKGROUND: Dendrobium nobile is a well-known traditional Chinese herbal medicine used for age-related diseases. Dendrobium nobile Lindl. alkaloid (DNLA) is the active ingredient to improve learning and memory deficits in laboratory animals. OBJECTIVE: The aim of the present study was to examine the anti-aging effects of long-term administration of DNLA and metformin during the aging process in senescence-accelerated mouse-prone 8 (SAMP8) mice. METHODS: SAMP8 mice were orally given DNLA (20 and 40 mg/kg) or metformin (80 mg/kg) starting at 6 months of age until 12 months of age. Age-matched SAMR1 mice were used as controls. DNLA and metformin treatments ameliorated behavioral deficits of 12-month-old SAMP8 mice, as determined by Rotarod, Y-maze, and Open-field tests. RESULTS: DNLA and metformin treatments prevented brain atrophy and improved morphological changes in the hippocampus and cortex, as evidenced by Nissl and H&E staining for neuron damage and loss, and by SA-ß-gal staining for aging cells. DNLA and metformin treatments decreased amyloid-ß1-42, AßPP, PS1, and BACE1, while increasing IDE and neprilysin for Aß clearance. Furthermore, DNLA and metformin enhanced autophagy activity by increasing LC3-II, Beclin1, and Klotho, and by decreasing p62 in the hippocampus and cortex. CONCLUSION: The beneficial effects of DNLA were comparable to metformin in protecting against aging-related cognitive deficits, neuron aging, damage, and loss in SAMP8 mice. The mechanisms could be attributed to increased Aß clearance, activation of autophagy activity, and upregulation of Klotho.

[Research progress of effect of anxiolytic traditional Chinese medicines and formulas on neurotransmitters].

Anxiety disorders are a common mental illness that seriously endangered physical and mental health of human beings. The etiology of anxiety disorders is closely related to the abnormality of monoamines neurotransmitters, amino acids neurotransmitters and neuropeptides. The long-term use of anti-anxiety chemical drugs has some adverse effects, such as constipation, muscle relaxation, lethargy, tolerance and withdrawal symptoms. However, traditional Chinese medicines have advantages of multi-component, multi-target coordination, with less adverse reactions. Therefore, it is a promising prospect to develop novel anti-anxiety drugs from traditional Chinese medicines and formulas. This article reviewed some traditional Chinese medicines and formulas that can relieve anxiety symptoms. These include traditional Chinese medicines(Panax ginseng, Lycium ruthenium, Morus alba, Bupleurum plus dragon bone oyster soup, Chailong Jieyu Pills, and Naogongtai Formulas) with the effect on monoamine neurotransmitters, such as serotonin, dopamine, and norepinephrine; traditional Chinese medicines(Rehmannia glutinosa, Ziziphus jujuba Mill. var. spinosa, Jielv Anshen Decoction, Baixiangdan Capsules, Antianxietic Compound Prescription Capsules) with the effect on amino acid neurotransmitters, such as glutamic acid, γ-aminobutyrc acid; and traditional Chinese medicines(P. ginseng, Xiaoyao San, Shuyu Ningxin Decoction)with the effect on neuropeptide Y pathway, with the aim to provide theoretical basis for the further development of some novel and more effective anti-anxiety therapeutics from traditional Chinese medicine and formulas.

PDL1-targeted vaccine exhibits potent antitumor activity by simultaneously blocking PD1/PDL1 pathway and activating PDL1-specific immune responses.

Despite the clinical success of immune checkpoint blockade, only a subset of people exhibits durable responses, suggesting that an alternative immunotherapeutic strategy is required. This paper reported a two-in-one cancer vaccine that targets programmed death ligand 1 (PDL1) that blocks the PD1/PDL1 pathway and also activates antitumor immune response. The PDL1- NitraTh vaccine, which consists of the extracellular domain of PDL1 and nitrated T cell epitope, effectively broke the immune tolerance of PDL1 and elicited PDL1-specific humoral and cellular immunity. The treatment of PDL1-NitraTh exhibited potent antitumor activity. Moreover, immunization of PDL1 vaccine increased the infiltration of tumor lymphocytes and decreased the proportion of Treg cells in tumor tissues, suggesting that the vaccine may remodel the tumor microenvironment. The upregulation of PDL1 in tumor tissues was induced by PDL1-NitraTh vaccine but not in spleen and lymphomas. This upregulation of PDL1 is beneficial to the antitumor activity of PDL1-specific humoral and cellular immunity induced by PDL1-NitraTh. In summary, PDL1-targeted vaccine exhibits potent antitumor activity and may provide an alternative immunotherapy strategy for patients who are not sensitive to PDL1 antibody drugs.

Dendrobium alkaloids decrease Aß by regulating α- and ß-secretases in hippocampal neurons of SD rats.

BACKGROUND: Alzheimer's disease (AD) is the primary cause of dementia in the elderly. The imbalance between production and clearance of amyloid ß (Aß) is a very early, often initiating factor in AD. Dendrobium nobile Lindl. alkaloids (DNLA) extracted from a Chinese medicinal herb, which have been shown to have anti-aging effects, protected against neuronal impairment in vivo and in vitro. Moreover, we confirmed that DNLA can improve learning and memory function in elderly normal mice, indicating that DNLA has potential health benefits. However, the underlying mechanism is unclear. Therefore, we further explored the effect of DNLA on neurons, which is closely related to learning and memory, based on Aß. METHODS: We exposed cultured hippocampal neurons to DNLA to investigate the effect of DNLA on Aß in vitro. Cell viability was evaluated by MTT assays. Proteins were analyzed by Western blot analysis. RESULTS: The cell viability of hippocampal neurons was not changed significantly after treatment with DNLA. But DNLA reduced the protein expression of amyloid precursor protein (APP), disintegrin and metalloprotease 10 (ADAM10), ß-site APP cleaving enzyme 1 (BACE1) and Aß1-42 of hippocampal neurons in rats and increased the protein expression of ADAM17. CONCLUSIONS: DNLA decreases Aß by regulating α- and ß-secretase in hippocampal neurons of SD rats.

Icariin Delays Brain Aging in Senescence-Accelerated Mouse Prone 8 (SAMP8) Model via Inhibiting Autophagy.

Icariin (ICA), a major flavonoid extracted from the Chinese tonic herb Epimedium, exerts beneficial effects in a variety of age-dependent diseases, such as Alzheimer's disease (AD). However, the antiaging mechanisms remain unclear. The senescence-accelerated mouse-prone 8 (SAMP8) model has been used to study age-related neurodegenerative changes associated with aging and the pathogenesis of AD. Hence, the current study was designed to examine the effect of ICA on age-related cognitive decline in SAMP8 mice and explore the role of autophagy in the ICA-mediated neuroprotection. SAMP8 mice were administered with ICA starting at 5 months of age, and the treatment lasted for 3 consecutive months. Morris water maze was used to evaluate cognitive function. The senescence-associated ß-galactosidase staining was used to determine the number of senescence cells. The neuronal morphologic changes were examined via Nissl staining. The hippocampal neuronal ultrastructure was examined by transmission electron microscopy. The expression of autophagy protein was examined by Western blot. ICA-treated SAMP8 mice exhibited a robust improvement in spatial learning and memory function. Meanwhile, ICA reduced the number of senescence cells in the brains of SAMP8 mice, inhibited neuronal loss, and reversed neuronal structural changes in the hippocampi of SAMP8 mice. Moreover, ICA treatment also decreased the formation of autophagosomes in the hippocampus of SAMP8 mice, and reduced the expression of autophagy-related proteins LC3-II and p62. These results demonstrate that ICA possesses the ability to delay brain aging in SAMP8 mice, and the mechanisms are possibly mediated through the regulation of autophagy.

Flexible decapyrrylcorannulene hosts.

The assembly of spherical fullerenes, or buckyballs, into single crystals for crystallographic identification often suffers from disordered arrangement. Here we show a chiral configuration of decapyrrylcorannulene that has a concave 'palm' of corannulene and ten flexible electron-rich pyrryl group 'fingers' to mimic the smart molecular 'hands' for self-adaptably cradling various buckyballs in a (+)hand-ball-hand(-) mode. As exemplified by crystallographic identification of 15 buckyball structures representing pristine, exohedral, endohedral, dimeric and hetero-derivatization, the pyrryl groups twist with varying dihedral angles to adjust the interaction between decapyrrylcorannulene and fullerene. The self-adaptable electron-rich pyrryl groups, susceptible to methylation, are theoretically revealed to contribute more than the bowl-shaped palm of the corannulene in holding buckyball structures. The generality of the present decapyrrylcorannulene host with flexible pyrryl groups facilitates the visualization of numerous unknown/unsolved fullerenes by crystallography and the assembly of the otherwise close-packed spherical fullerenes into two-dimensional layered structures by intercalation.

Dendrobium nobile Lindl. alkaloids regulate metabolism gene expression in livers of mice.

OBJECTIVES: In our previous studies, Dendrobium nobile Lindl. alkaloids (DNLA) has been shown to have glucose-lowering and antihyperlipidaemia effects in diabetic rats, in rats fed with high-fat diets, and in mice challenged with adrenaline. This study aimed to examine the effects of DNLA on the expression of glucose and lipid metabolism genes in livers of mice. METHODS: Mice were given DNLA at doses of 10-80 mg/kg, po for 8 days, and livers were removed for total RNA and protein isolation to perform real-time RT-PCR and Western blot analysis. KEY FINDINGS: Dendrobium nobile Lindl. alkaloids increased PGC1α at mRNA and protein levels and increased glucose metabolism gene Glut2 and FoxO1 expression. DNLA also increased the expression of fatty acid ß-oxidation genes Acox1 and Cpt1a. The lipid synthesis regulator Srebp1 (sterol regulatory element-binding protein-1) was decreased, while the lipolysis gene ATGL was increased. Interestingly, DNLA increased the expression of antioxidant gene metallothionein-1 and NADPH quinone oxidoreductase-1 (Nqo1) in livers of mice. Western blot on selected proteins confirmed these changes including the increased expression of GLUT4 and PPARα. CONCLUSIONS: DNLA has beneficial effects on liver glucose and lipid metabolism gene expressions, and enhances the Nrf2-antioxidant pathway gene expressions, which could play integrated roles in regulating metabolic disorders.

Dendrobium nobile Lindl alkaloid, a novel autophagy inducer, protects against axonal degeneration induced by Aß25-35 in hippocampus neurons in vitro.

AIMS: Axonal degeneration is a pathological symbol in the early stage of Alzheimer's disease (AD), which can be triggered by amyloid-ß (Aß) peptide deposition. Growing evidence indicates that deficit of autophagy eventually leads to the axonal degeneration. Our previous studies have shown that Dendrobium nobile Lindl alkaloid (DNLA) had protective effect on neuron impairment in vivo and in vitro; however, the underlying mechanisms is still unclear. METHODS: We exposed cultured hippocampus neurons to Aß25-35 to investigate the effect of DNLA in vitro. Axonal degeneration was evaluated by immunofluorescence staining and MTT assay. Neurons overexpressing GFP-LC3B were used to measure the formation of autophagosome. Autophagosome-lysosome fusion, the lysosomal pH, and cathepsin activity were assessed to reflect autophagy process. Proteins of interest were analyzed by Western blot. RESULTS: DNLA pretreatment significantly inhibited axonal degeneration induced by Aß25-35 peptide in vitro. Further studies revealed DNLA treatment increased autophagic flux through promoting formation and degradation of autophagosome in hippocampus neurons. Moreover, enhancement of autophagic flux was responsible for the protective effects of DNLA on axonal degeneration. CONCLUSIONS: DNLA prevents Aß25-35 -induced axonal degeneration via activation of autophagy process and could be a novel therapeutic target.

Formation of Curvature Subunit of Carbon in Combustion.

Curvature prevalently exists in the world of carbon materials (e.g., fullerenes, buckyl bowls, carbon nanotubes, and onions), but traditional C2-addition mechanisms fail to elucidate the mechanism responsible for the formation of carbon curvature starting from a pentagonal carbon ring in currently available chemical-physical processes such as combustion. Here, we show a complete series of nascent pentagon-incorporating C5-C18 that are online produced in the flame of acetylene-cyclopentadiene-oxygen and in situ captured by C60 or trapped as polycyclic aromatic hydrocarbons for clarifying the growth of the curved subunit of C20H10. A mechanism regarding C1-substitution and C2-addition has been proposed for understanding the formation of curvature in carbon materials, as exemplified by the typical curved molecule containing a single pentagon completely surrounded by five hexagons. The present mechanism, supported by the intermediates characterized by X-ray crystallography as well as NMR, has been experimentally validated for the rational synthesis of curved molecule in the commercially useful combustion process.

Icariin is a PPARα activator inducing lipid metabolic gene expression in mice.

Icariin is effective in the treatment of hyperlipidemia. To understand the effect of icariin on lipid metabolism, effects of icariin on PPARα and its target genes were investigated. Mice were treated orally with icariin at doses of 0, 100, 200, and 400 mg/kg, or clofibrate (500 mg/kg) for five days. Liver total RNA was isolated and the expressions of PPARα and lipid metabolism genes were examined. PPARα and its marker genes Cyp4a10 and Cyp4a14 were induced 2-4 fold by icariin, and 4-8 fold by clofibrate. The fatty acid (FA) binding and co-activator proteins Fabp1, Fabp4 and Acsl1 were increased 2-fold. The mRNAs of mitochondrial FA ß-oxidation enzymes (Cpt1a, Acat1, Acad1 and Hmgcs2) were increased 2-3 fold. The mRNAs of proximal ß-oxidation enzymes (Acox1, Ech1, and Ehhadh) were also increased by icariin and clofibrate. The expression of mRNAs for sterol regulatory element-binding factor-1 (Srebf1) and FA synthetase (Fasn) were unaltered by icariin. The lipid lysis genes Lipe and Pnpla2 were increased by icariin and clofibrate. These results indicate that icariin is a novel PPARα agonist, activates lipid metabolism gene expressions in liver, which could be a basis for its lipid-lowering effects and its beneficial effects against diabetes.

Light-triggered covalent assembly of gold nanoparticles in aqueous solution.

UV light irradiation triggers Au NPs that are respectively functionalized on the surface by o-nitrobenzyl alcohol and benzylamine to proceed with a covalent ligation reaction, which leads to assembling of Au NPs into anisotropic one-dimensional (1D) arrays in aqueous solution via indazolone linkages.

Light-responsive nanogated ensemble based on polymer grafted mesoporous silica hybrid nanoparticles.

Mesoporous silica nanoparticles grafted with light-responsive polymer on the outer surface were developed as novel nanogated ensembles, which allow encapsulation and release of drug and biological molecules under light irradiation.