Mccannhauser5509
Results revealed that
,
, and
displayed promising inhibition in cisplatin-resistant cell lines in comparison to parent cells in terms of both resistance factor (RF) and IC
values. Moreover,
proved to be most active compound in both parent and resistant cell lines with IC
values 15.57 µM and 11.52 µM respectively. Our docking studies demonstrated that compounds
,
, and
exhibited significant binding affinity with multiple protein targets of the signaling cascade.
Anticancer activities of compounds
,
, and
in cisplatin-resistant cell lines suggested that these ligands may contribute as lead compounds for the development of new anticancer drugs.
Anticancer activities of compounds S3c, S5b, and S6c in cisplatin-resistant cell lines suggested that these ligands may contribute as lead compounds for the development of new anticancer drugs.
White tip silver needle, a slightly fermented white tea, is abundant in flavonoids, and it has great significance in terms of D-galactose/lipopolysaccharide-induced aging in mice.
We analyzed the antioxidant capacity of white tip silver needle flavonoids (WTSNF) in vitro, assessed the effects of WTSNF on organ indexes, pathological changes, liver function indexes, biochemical indicators, molecular biological indicators, and genes related to oxidation and inflammation.
Ultra-high performance liquid chromatography-tandem mass spectrometry results showed that WTSNF contained baicalin, kaempferol, kaempferide, quercetin, isorhamnetin, lespenephryl, and rutin. WTSNF showed strong scavenging ability for both 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) free radicals. click here Pathological analysis results showed that WTSNF reduced liver, kidney, and lung damage in mice with induced aging. In the serum and liver tissue, WTSNF effectively increasα, IFN-γ, inducible nitric oxide synthase, cyclooxygenase-2, and nuclear factor kappa-light chain-enhancer of activated B cells (NF-κB).
WTSNF is a high-quality natural product with antioxidative and anti-inflammatory properties that can inhibits D-galactose/lipopolysaccharide-induced aging in mice.
WTSNF is a high-quality natural product with antioxidative and anti-inflammatory properties that can inhibits D-galactose/lipopolysaccharide-induced aging in mice.
Understanding raw material variability and its impact on product quality are crucial for developing robust pharmaceutical processes. This work aimed to study the effects of spray drying conditions on properties of the spray dried
saponin (PNS) powders as well as the subsequent intra-batch dissolution variability of PNS hydrophilic matrix tablets.
The Plackett-Burman design was applied to screen the critical process parameters (CPPs). Then, the Box-Behnken design was used to investigate the relationship between the CPPs and the physiochemical properties of spray dried PNS powders. The PNS hydrophilic matrix tablets containing 57% spray dried PNS powders were directly compressed. The partial least squares (PLS) regression was used to uncover the hidden multivariate relationships among the CPPs, intermediate powder properties, and tablet quality attributes.
The identified CPPs were the feed concentration, the inlet air temperature, and the atomization pressure. It was found that the CPPs exerted little impact on chemical properties of spray dried PNS powders, but had significant impact on physical properties, such as particle size, specific surface area, bulk density, hygroscopicity, and inter-particle porosity, etc. Latent variable modeling results revealed that the high inlet air temperature of spray drying process could produce PNS powders with low moisture content and high hygroscopicity, which were beneficial to reduce the intra-batch dissolution variability of PNS hydrophilic matrix tablets. Finally, a design space of the spray drying process was built in order to ensure the dissolution consistency.
Our research provided a reference for improving the spray drying conditions in order to ensure the dissolution consistency of the PNS hydrophilic matrix tablet.
Our research provided a reference for improving the spray drying conditions in order to ensure the dissolution consistency of the PNS hydrophilic matrix tablet.[This corrects the article DOI 10.2147/DDDT.S288859.].
To investigate the neuroprotective effect of edaravone on excessive-dose propofol-induced neurotoxicity in the hippocampus of newborn rats and HT22 cells.
Cell proliferation was investigated by assessing ki67 expression in the neural stem of the hippocampus of newborn rats and by cell counting kit-8 (CCK8) assay in HT22 cells. Cell apoptosis was assessed in vivo by caspase 3 detection in Western blots and measurement of apoptosis in neurons and glial cells by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Apoptosis was analyzed by flow cytometry in HT22 cells. The Morris water maze was used to evaluate the long-term learning and memory ability of rats. Inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA). The expression of mBDNF/TrkB/PI3K pathway-related proteins was detected by Western blot and quantitative reverse transcription-polymerase chain reaction (q-RT PCR).
In neonatal rat hippocampus and HT22 cells, edaravone increased cell proliferation and decreased cell apoptosis after excessive propofol-induced neurotoxicity. In addition, the levels of proinflammatory factors interleukin (IL)-6 and tumor necrosis factor (TNF)-α were reduced by edaravone pretreatment. The use of the tropomyosin receptor kinase B (TrkB) antagonist ANA-12 and TrkB agonist 7,8DHF with propofol groups showed that edaravone mitigated excessive propofol-induced neurotoxicity through the mature brain-derived neurotrophic factor (mBDNF)/TrkB/phosphoinositide 3-kinase (PI3K) pathway. However, the current dose of propofol did not significantly affect long-term learning and memory in rats.
Edaravone pretreatment ameliorated propofol-induced proliferation inhibition, neuroapoptosis, and neural inflammation by activating the mBDNF/TrkB/PI3K pathway.
Edaravone pretreatment ameliorated propofol-induced proliferation inhibition, neuroapoptosis, and neural inflammation by activating the mBDNF/TrkB/PI3K pathway.
