Browse
Submit Data
Databases
API
Help

Dataset Information

22 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Albizia julibrissin Ameliorates Memory Loss Induced by Insomnia in Drosophila.

ABSTRACT: In clinical practice in Taiwan, Albizia julibrissin is the most prescribed Chinese herbal medicine for insomnia. Short-term insomnia and hypnotic use both attenuate cognitive functions, especially learning memory. In previous studies, A. julibrissin exhibits sedative activity, antidepressant-like effects, and protection of learning and memory against amnesia. However, whether A. julibrissin ameliorates memory loss caused by short-term sleep deprivation is not clear. We utilized the sleep-deprived Drosophila model and olfactory associative learning-memory assay to test the effects of A. julibrissin on sleep-deprivation induced memory loss. We found that A. julibrissin ameliorated 3-hour memory but not 1-hour memory or instant learning. The findings might be applied to an anticipated short-term sleep disturbance.

SUBMITTER: Chang JS

PROVIDER: S-EPMC6463593 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Albizia julibrissin Ameliorates Memory Loss Induced by Insomnia in Drosophila.

Chang Jui-Shu JS Liu Hsin-Ping HP Cheng Jack J Chen Chao-Jung CJ Hwang Su-Lun SL Tseng Chi-Chuan CC Hsu Lee-Fen LF Lin Wei-Yong WY

Evidence-based complementary and alternative medicine : eCAM 20190401

In clinical practice in Taiwan, Albizia julibrissin is the most prescribed Chinese herbal medicine for insomnia. Short-term insomnia and hypnotic use both attenuate cognitive functions, especially learning memory. In previous studies, A. julibrissin exhibits sedative activity, antidepressant-like effects, and protection of learning and memory against amnesia. However, whether A. julibrissin ameliorates memory loss caused by short-term sleep deprivation is not clear. We utili ...[more]

PMID: 31057652

Similar Datasets

Albizia julibrissin isolate:Albizia julibrissin

Project description:Albizia julibrissin isolate:Albizia julibrissin Genome sequencing and assembly

| PRJNA786450 | ENA

Albizia julibrissin

Project description:Albizia julibrissin Genome sequencing and assembly

| PRJNA1005079 | ENA

Albizia julibrissin

Project description:Albizia julibrissin chloroplast Genome sequencing and assembly

| PRJNA734110 | ENA

Albizia julibrissin

Project description:Albizia julibrissin overview

| PRJNA772861 | ENA

Two Lignan Glycosides from Albizia julibrissin Durazz. Noncompetitively Inhibit Serotonin Transporter.

Project description:Albizia julibrissin Durazz. is one of the most common herbs used for depression and anxiety treatment, but its molecular basis and mechanism of action as an antidepressant or anxiolytic drug are not understood. In this study, we separated and identified two lignan glycosides that inhibit serotonin transporter (SERT) noncompetitively by decreasing Vmax with little change in Km for its fluorescence substrate. In addition, treatment with lignan glycosides did not alter total and cell surface expression levels of the transporter protein. The two compounds decreased the accessibility of a cysteine residue placed in the extracellular substrate permeation pathway by inducing a conformational shift toward an outward-closed state of SERT. These results are consistent with molecular docking for the association of the lignan glycosides to the allosteric site in SERT. The present work supports the proposal that these compounds act on SERT by a novel underlying mechanism of action different from that of conventional antidepressant drugs.

| S-EPMC8954383 | biostudies-literature

Commodity risk assessment of Albizia julibrissin plants from Israel.

Project description:The EFSA Panel on Plant Health was requested to prepare and deliver risk assessments for commodities listed in the relevant Implementing Acts as 'High risk plants, plant products and other objects' [Commission Implementing Regulation (EU) 2018/2019 establishing a provisional list of high-risk plants, plant products or other objects, within the meaning of Article 42 of Regulation (EU) 2016/2031]. The current Scientific Opinion covers all plant health risks posed by Albizia julibrissin imported from Israel, taking into account the available scientific information, including the technical information provided by Israel. The relevance of an EU-regulated pest for this opinion was based on evidence that: (i) the pest is present in Israel; (ii) A. julibrissin is a host of the pest and (iii) the pest can be associated with the commodity. The relevance of this opinion for other non EU-regulated pests was based on evidence that (i) the pest is present in Israel; (ii) the pest is absent in the EU; (iii) A. julibrissin is a host of the pest; (iv) the pest can be associated with the commodity and (v) the pest may have an impact and can pose a potential risk for the EU territory. Three pests (two insects, Aonidiella orientalis and Euwallacea fornicatus; one fungus, Fusarium euwallaceae) that fulfilled all criteria were selected for further evaluation. For the three selected pests, the risk mitigation measures proposed in the technical dossier were evaluated. Limiting factors on the effectiveness of the measures were documented. For the selected pests, an expert judgement on the likelihood of pest freedom is given taking into consideration the risk mitigation measures acting on the pest, including uncertainties associated with the assessment. The Panel is 95% sure that 9,950 or more units per 10,000 will be pest free from these three pests.

| S-EPMC7008799 | biostudies-literature

Mechanisms of Mixed Th1/Th2 Responses in Mice Induced by Albizia julibrissin Saponin Active Fraction by in Silico Analysis.

Project description:The purified active fraction of Albizia julibrissin saponin (AJSAF) is an ideal adjuvant candidate that improves antigen-specific both cellular and humoral immune responses and elicits mixed Th1/Th2 responses, but its mechanisms remain unclear. The key features of action of AJSAF were investigated in mice immunized with Newcastle disease virus-based recombinant influenza vaccine (rL-H5) and AJSAF at the same leg (AJSAF+rL-H5) or different legs (AJSAF/rL-H5). The adjuvant activity of AJSAF on rL-H5 is strictly dependent on their spatial colocalization. Serum H5 antigen (H5Ag)-specific IgG, IgG1, IgG2a, and IgG2b antibody titers in AJSAF+rL-H5 group were significantly higher than those in AJSAF/rL-H5 group. The mechanisms of selectivity of Th1 or Th2 in mice induced by AJSAF was explored by the transcriptomic and proteomic profiles of H5Ag-stimulated splenocytes from the immunized mice using gene microarray and two-dimensional difference gel electrophoresis coupled with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Compared to rL-H5 alone, AJSAF/rL-H5 induced more differentially expressed genes (DEGs) than AJSAF+rL-H5, whereas AJSAF+rL-H5 upregulated higher mRNA expression of Th1 (T-bet, IFN-γ, TNF-α, IL-12β, and IL-12Rβ1) and Th2 (IL-10 and AICDA) immune response genes. The neutrophil response and its derived S100A8 and S100A9 might be involved in the AJSAF-mediated Th1 response. Meanwhile, AJSAF might induce the adaptive immune responses by improving a local innate immune microenvironment. These findings expanded the current knowledge on the mechanisms of action of saponin-based adjuvants, and provided new insights into how adjuvants shape adaptive immune responses.

| S-EPMC7158666 | biostudies-literature

Bee venom ameliorates lipopolysaccharide-induced memory loss by preventing NF-kappaB pathway.

Project description:BackgroundAccumulation of beta-amyloid and neuroinflammation trigger Alzheimer's disease. We previously found that lipopolysaccharide (LPS) caused neuroinflammation with concomitant accumulation of beta-amyloid peptides leading to memory loss. A variety of anti-inflammatory compounds inhibiting nuclear factor kappaB (NF-κB) activation have showed efficacy to hinder neuroinflammation and amyloidogenesis. We also found that bee venom (BV) inhibits NF-κB.MethodsA mouse model of LPS-induced memory loss used administration of BV (0.8 and 1.6 μg/kg/day, i.p.) to ICR mice for 7 days before injection of LPS (2.5 mg/kg/day, i.p.). Memory loss was assessed using a Morris water maze test and passive avoidance test. For in vitro study, we treated BV (0.5, 1, and 2 μg/mL) to astrocytes and microglial BV-2 cells with LPS (1 μg/mL).ResultsWe found that BV inhibited LPS-induced memory loss determined by behavioral tests as well as cell death. BV also inhibited LPS-induced increases in the level of beta-amyloid (Aβ), β-and γ-secretases activities, NF-κB and its DNA-binding activity and expression of APP, and BACE1 and neuroinflammation proteins (COX-2, iNOS, GFAP and IBA-1) in the brain and cultured cells. In addition, pull-down assay and molecular modeling showed that BV binds to NF-κB.ConclusionsBV attenuates LPS-induced amyloidogenesis, neuroinflammation, and therefore memory loss via inhibiting NF-κB signaling pathway. Thus, BV could be useful for treatment of Alzheimer's disease.

| S-EPMC4501073 | biostudies-literature

Loss of Polo ameliorates APP-induced Alzheimer's disease-like symptoms in Drosophila.

Project description:The amyloid precursor protein (APP) has been implicated in the pathogenesis of Alzheimer's disease (AD). Despite extensive studies, little is known about the regulation of APP's functions in vivo. Here we report that expression of human APP in Drosophila, in the same temporal-spatial pattern as its homolog APPL, induced morphological defects in wings and larval NMJ, larva and adult locomotion dysfunctions, male choice disorder and lifespan shortening. To identify additional genes that modulate APP functions, we performed a genetic screen and found that loss of Polo, a key regulator of cell cycle, partially suppressed APP-induced morphological and behavioral defects in larval and adult stages. Finally, we showed that eye-specific expression of APP induced retina degeneration and cell cycle re-entry, both phenotypes were mildly ameliorated by loss of Polo. These results suggest Polo is an important in vivo regulator of the pathological functions of APP, and provide insight into the role of cell cycle re-entry in AD pathogenesis.

| S-EPMC4657023 | biostudies-literature

Quick and improved immune responses to inactivated H9N2 avian influenza vaccine by purified active fraction of Albizia julibrissin saponins.

Project description:BackgroundH9N2 Low pathogenic avian influenza virus (LPAIV) raises public health concerns and its eradication in poultry becomes even more important in preventing influenza. AJSAF is a purified active saponin fraction from the stem bark of Albizzia julibrissin. In this study, AJSAF was evaluated for the adjuvant potentials on immune responses to inactivated H9N2 avian influenza virus vaccine (IH9V) in mice and chicken in comparison with commercially oil-adjuvant.ResultsAJSAF significantly induced faster and higher H9 subtype avian influenza virus antigen (H9-Ag)-specific IgG, IgG1, IgG2a and IgG2b antibody titers in mice and haemagglutination inhibition (HI) and IgY antibody levels in chicken immunized with IH9V. AJSAF also markedly promoted Con A-, LPS- and H9-Ag-stimulated splenocyte proliferation and natural killer cell activity. Furthermore, AJSAF significantly induced the production of both Th1 (IL-2 and IFN-γ) and Th2 (IL-10) cytokines, and up-regulated the mRNA expression levels of Th1 and Th2 cytokines and transcription factors in splenocytes from the IH9V-immunized mice. Although oil-formulated inactivated H9N2 avian influenza vaccine (CH9V) also elicited higher H9-Ag-specific IgG and IgG1 in mice and HI antibody titer in chicken, this robust humoral response was later produced. Moreover, serum IgG2a and IgG2b antibody titers in CH9V-immunized mice were significantly lower than those of IH9V alone group.ConclusionsAJSAF could improve antigen-specific humoral and cellular immune responses, and simultaneously trigger a Th1/Th2 response to IH9V. AJSAF might be a safe and efficacious adjuvant candidate for H9N2 avian influenza vaccine.

| S-EPMC7648552 | biostudies-literature