11 research outputs found
Effects of evodiamine (EVO) on the cell cycle distribution and apoptosis rate of the H446 and H1688 SCLC cells.
<p>Cell cycle was detected by PI assay. Apoptosis was detected using an Annexin V/PI double staining assay. The H446 cells stained with Annexin V/PI were observed under an inverted fluorescence microscope. Each experiment was repeated 3 times. Data presented as mean ± standard deviation (n = 3). *<i>P</i><0.05 as compared to corresponding control group. Untreated H446 or H1688 cells were used as a negative control group.</p
Additional file 3 of Genomic profiles and transcriptomic microenvironments in 2 patients with synchronous lung adenocarcinoma and lung squamous cell carcinoma: a case report
Additional file 3: Table S1. Non-synonymous mutations of P1 and P2. Table S2. Gene expressions (FPKM) of P1
Additional file 2 of Genomic profiles and transcriptomic microenvironments in 2 patients with synchronous lung adenocarcinoma and lung squamous cell carcinoma: a case report
Additional file 2: Figure S2. Immunohistology of CD8+ and CD4+ T cells in P1 (X400). (A) CD8+ T cells of P1A. (B) CD8+ T cells of P1S. (C) CD4+ T cells of P1A. (D) CD4+ T cells of P1S
Additional file 1 of Genomic profiles and transcriptomic microenvironments in 2 patients with synchronous lung adenocarcinoma and lung squamous cell carcinoma: a case report
Additional file 1: Figure S1. Mutational spectra of four tumor samples. The mutational type proportion for each substitution in a trinucleotide context is shown (total 96 contexts)
Effects of evodiamine (EVO) on the protein expression of Cyt C, caspase-12, -8, -9 and -3, Fas and Trail in the H446 and H1688 SCLC cells.
<p>Cell lysates were analyzed by Western blot. Each experiment was repeated 3 times. Data presented as mean ± standard deviation (n = 3). Untreated H446 or H1688 cells were used as a negative control group. *<i>P</i><0.05 as compared to corresponding control group. Fas: factor associated suicide; Trail: tumor necrosis factor-related apoptosis inducing ligand; Cyt C: cytochrome C.</p
Evodiamine (EVO) induces apoptosis through two intrinsic caspase-dependent pathways, but not through an extrinsic caspase-dependent pathway.
<p>Evodiamine (EVO) induces apoptosis through two intrinsic caspase-dependent pathways, but not through an extrinsic caspase-dependent pathway.</p
Effects of evodiamine (EVO) on the activities of caspase-8 (A), -9 (B) and -3 (C) in H446 cells.
<p>Cell lysates were analyzed by a colorimetric assay of Ac-DEVD-pNA. Each experiment was repeated 3 times. Data presented as mean ± standard deviation (n = 3). Caspase activities were given as arbitrary units (AU) per milligram of protein. Untreated H446 cells were used as a negative control group. *<i>P</i><0.05 as compared to the corresponding control group. <sup>#</sup><i>P</i><0.05 as compared to corresponding EVO treated group at 24 h. <sup></sup><i>P</i><0.05 as compared to corresponding EVO treated group at 48 h.</p
Effects of evodiamine (EVO) on the mRNA expression of Bax and Bcl-2 in H446 and H1688 cells.
<p>Cell lysates were analyzed by RT-PCR. Each experiment was repeated 3 times. Data presented as mean ± standard deviation (n = 3). Untreated H446 or H1688 cells were used as a negative control group. *<i>P</i><0.05 as compared to the control group. <sup>#</sup><i>P</i><0.05 as compared to corresponding EVO treated group at 24 h. <sup></sup><i>P</i><0.05 as compared to corresponding EVO treated group at 48 h.</p
Effects of evodiamine (EVO) on the levels of ROS, Ca<sup>2+</sup> and ψ<sub>m</sub> in H446 and H1688 SCLC cells.
<p>ROS, Ca<sup>2+</sup> and ψ<sub>m</sub> were separately detected by DCF-DA, Fluo-3/AM and JC-1 assays. Each experiment was repeated 3 times. Data presented as mean ± standard deviation (n = 3). Untreated H446 or H1688 cells were used as a negative control group. *<i>P</i><0.05 as compared to corresponding control group.</p
Nanosomal Microassemblies for Highly Efficient and Safe Delivery of Therapeutic Enzymes
Enzyme
therapy has unique advantages over traditional chemotherapies
for the treatment of hyperuricemia, but overcoming the delivery obstacles
of therapeutic enzymes is still a significant challenge. Here, we
report a novel and superior system to effectively and safely deliver
therapeutic enzymes. Nanosomal microassemblies loaded with uricase
(NSU-MAs) are assembled with many individual nanosomes. Each nanosome
contains uricase within the alkaline environment, which is beneficial
for its catalytic reactions and keeps the uricase separate from the
bloodstream to retain its high activity. Compared to free uricase,
NSU-MAs exhibited much higher catalytic activity under physiological
conditions and when subjected to different temperatures, pH values
and trypsin. NSU-MAs displayed increased circulation time, improved
bioavailability, and enhanced uric acid-lowering efficacy, while decreasing
the immunogenicity. We also described the possible favorable conformational
changes occurring in NSU-MAs that result in favorable outcomes. Thus,
nanosomal microassemblies could serve as a valuable tool in constructing
delivery systems for therapeutic enzymes that treat various diseases
