Yam Code
Sign up
Login
New paste
Home
Trending
Archive
English
English
Tiếng Việt
भारत
Sign up
Login
New Paste
Browse
nclusions.Sennoside A (SA) is a bioactive component of Rheum officinale Baill. with an activity of irritant laxative, which has been reported to possess therapeutic potential in various diseases or conditions including obesity, insulin resistance, liver steatosis, prostate cancer and pancreatic cancer progression. However, whether SA has therapeutic potential in hepatocellular carcinoma (HCC) treatment remains elusive. In this study, we treated two HCC cell lines, HepG2 and SMMC-7721 with SA and found that SA selectively inhibited the growth of HCC cells by proliferation assay. SA has a good inhibitory effect on proliferation of HepG2 cells in a concentration dependent manner, but there was no effect on SMMC-7721 cells. Then we conducted transwell assays and transcriptome analysis in HCC cells and examined the effects of SA on HCC in vivo. The results showed that SA significantly inhibited the migration and invasion of HCC. Comparison of RNA-seq transcriptome profiles from control groups and SA-treated groups identified 171 and 264 differentially expressed genes (DEGs) in HepG2 and SMMC-7721 cells respectively, in which includes 2 overlapping up-regulated DEGs and 12 overlapping down-regulated DEGs between HepG2 and SMMC-7721 cells. The qPCR were applied to investigate the transcriptional level of 9 overlapping down-regulated DEGs related to cancer metastasis, and the results were consistent with RNA-seq data. The dominate pathways including Wnt signaling pathway, TNF signaling pathway, VEGF signaling pathway, and NF-κB signaling pathway were strongly inhibited by SA, which are involved in regulating cancer metastasis. Finally, we confirmed that the downregulation of KRT7 and KRT81 could inhibit HCC metastasis. This study has provided new insight into the understanding of the inhibitory effects and potential targets of SA on the metastasis of HCC.Alzheimer's disease (AD) is the most common type of neurodegenerative diseases. There are over 44 million people living with the disease worldwide. While there are currently no effective treatments for AD, induced pluripotent stem cell-derived brain organoids have the potential to provide a better understanding of Alzheimer's pathogenesis. Nevertheless, developing brain organoid models is expensive, time consuming and often does not reflect disease progression. Using accurate and inexpensive computer simulations of human brain organoids can overcome the current limitations. Induced whole brain organoids (aiWBO) will greatly expand our ability to model AD and can guide wet lab research. In this study, we have successfully developed and validated artificially induced a whole brain organoid platform (NEUBOrg) using our previously validated machine learning platform, DeepNEU (v6.1). Using NEUBorg platform, we have generated aiWBO simulations of AD and provided a novel approach to test genetic risk factors associated with AD progression and pathogenesis.The pathogenesis of Alzheimer's disease (AD) involves activation of many NLRP3 inflammatory bodies, which may be related to amyloid β peptide and aggregation of misfolded proteins. Autophagy is an important regulator of inflammatory bodies. However, autophagy shows dynamic changes in the development of AD, and its role in inflammation remains controversial. In this study, the key link between autophagic disorders and the NLRP3 inflammasome in AD was investigated. APP/PS1 double transgenic mice and C57 mice with Aβ25-35 injected into the lateral ventricle were used as two animal models of AD. Immunofluorescence staining and Western blot analysis showed that NLRP3 inflammasome-related proteins and inflammatory cytokines, such as IL-1α, IL-1β, IL-6, IL-12, and TNF-α, were increased and microglia were activated in the brains of both AD animal models. Endogenous overexpression of the APPswe gene and exogenous addition of Aβ25-35 increased the expression of NLRP3 inflammasome-related proteins, while exogenous Aβ25-35 intervention more significantly activated inflammation. Furthermore, LC3 was increased in the AD animal and cell models, and the level of Lamp1 decreased. https://www.selleckchem.com/products/sc-43.html After overexpression of the primary regulator of lysosomal biogenesis, TFEB, the lysosome protein Lamp1 was increased, and LC3 and inflammatory protein expression were decreased. These results suggest that the NLRP3 inflammasome-mediated inflammatory response is activated in AD animal and cell models, which may be related to the decline in autolysosome function. Overexpression of the TFEB protein can reduce the inflammatory response by improving autolysosome function in AD model cells.Perineuronal nets (PNNs) are specialized, reticular structures of the extracellular matrix (ECM) that can be found covering the soma and proximal dendrites of a neuronal subpopulation. Recent studies have shown that PNNs can highly influence synaptic plasticity and are disrupted in different neuropsychiatric disorders like schizophrenia. Interestingly, there is a growing evidence that microglia can promote the loss of PNNs and contribute to neuropsychiatric disorders. Based on this knowledge, we analyzed the impact of activated microglia on hippocampal neuronal networks in vitro. Therefore, primary cortical microglia were cultured and stimulated via polyinosinic-polycytidylic acid (Poly IC; 50 μg/ml) administration. The Poly IC treatment induced the expression and secretion of different cytokines belonging to the CCL- and CXCL-motif chemokine family as well as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). In addition, the expression of matrix metalloproteinases (MMPs) could be verified via RT-PCR g the ECM.A 56-year-old woman with a history of cerebral amyloid angiopathy (CAA) complicated by prior intracranial hemorrhage (ICH) was evaluated for an asymptomatic ischemic stroke discovered on screening brain MRI. On echocardiogram, she was found to have a mass on her mitral valve and strongly positive antiphospholipid antibodies. She was diagnosed with nonbacterial thrombotic (Libman-Sacks) endocarditis associated with the primary antiphospholipid syndrome (APS). The treatment decision was complicated by the history of CAA with ICH within the last year with very high risk for bleeding complications if on anticoagulation. A multidisciplinary decision was made to initiate a trial of warfarin for 3 months. She fared well and warfarin was continued. She has not had any further bleeding or ischemic events over the subsequent 1.5 years and remains on warfarin for her APS.
Paste Settings
Paste Title :
[Optional]
Paste Folder :
[Optional]
Select
Syntax Highlighting :
[Optional]
Select
Markup
CSS
JavaScript
Bash
C
C#
C++
Java
JSON
Lua
Plaintext
C-like
ABAP
ActionScript
Ada
Apache Configuration
APL
AppleScript
Arduino
ARFF
AsciiDoc
6502 Assembly
ASP.NET (C#)
AutoHotKey
AutoIt
Basic
Batch
Bison
Brainfuck
Bro
CoffeeScript
Clojure
Crystal
Content-Security-Policy
CSS Extras
D
Dart
Diff
Django/Jinja2
Docker
Eiffel
Elixir
Elm
ERB
Erlang
F#
Flow
Fortran
GEDCOM
Gherkin
Git
GLSL
GameMaker Language
Go
GraphQL
Groovy
Haml
Handlebars
Haskell
Haxe
HTTP
HTTP Public-Key-Pins
HTTP Strict-Transport-Security
IchigoJam
Icon
Inform 7
INI
IO
J
Jolie
Julia
Keyman
Kotlin
LaTeX
Less
Liquid
Lisp
LiveScript
LOLCODE
Makefile
Markdown
Markup templating
MATLAB
MEL
Mizar
Monkey
N4JS
NASM
nginx
Nim
Nix
NSIS
Objective-C
OCaml
OpenCL
Oz
PARI/GP
Parser
Pascal
Perl
PHP
PHP Extras
PL/SQL
PowerShell
Processing
Prolog
.properties
Protocol Buffers
Pug
Puppet
Pure
Python
Q (kdb+ database)
Qore
R
React JSX
React TSX
Ren'py
Reason
reST (reStructuredText)
Rip
Roboconf
Ruby
Rust
SAS
Sass (Sass)
Sass (Scss)
Scala
Scheme
Smalltalk
Smarty
SQL
Soy (Closure Template)
Stylus
Swift
TAP
Tcl
Textile
Template Toolkit 2
Twig
TypeScript
VB.Net
Velocity
Verilog
VHDL
vim
Visual Basic
WebAssembly
Wiki markup
Xeora
Xojo (REALbasic)
XQuery
YAML
HTML
Paste Expiration :
[Optional]
Never
Self Destroy
10 Minutes
1 Hour
1 Day
1 Week
2 Weeks
1 Month
6 Months
1 Year
Paste Status :
[Optional]
Public
Unlisted
Private (members only)
Password :
[Optional]
Description:
[Optional]
Tags:
[Optional]
Encrypt Paste
(
?
)
Create New Paste
You are currently not logged in, this means you can not edit or delete anything you paste.
Sign Up
or
Login
Site Languages
×
English
Tiếng Việt
भारत