Hot temperature Pushes Topoisomerase Mediated Chromosomal Crack Restoration Process Choice

1 and a potential of about 40 mV, showed a good serum stability. The polypeptide material had no obvious cytotoxicity. The miR-16/polypeptide nanoparticles could be efficiently absorbed by human ovarian cancer cells and were distributed in the cytoplasm. The nanoparticles significantly increased the intracellular expression level of miR-16 (
< 0.001) and decreased the expression of Bcl-2 and Chk-1 proteins in ovarian cancer cells, thus enabling miR-16 to promote apoptosis and enhance cisplatin sensitivity of the cells.
We successfully prepared a miR-16/polypeptide nano-delivery system for targeted delivery of miR-16 to ovarian cancer cells for enhancing cisplatin sensitivity of the cancer cells.
We successfully prepared a miR-16/polypeptide nano-delivery system for targeted delivery of miR-16 to ovarian cancer cells for enhancing cisplatin sensitivity of the cancer cells.
To investigate the protective effect of luteolin against cadmium (Cd)-induced injury in human lung epithelial Beas-2B cells.
Beas-2B cells were treated with different concentrations of luteolin (0-160 μmol/L) or Cd (0-40 μmol/L) for 24 h, and the cell viability was examined using MTT assay. After treatment with luteolin (0.25, 0.5 and 0.75 μmol/L) with or without Cd (5 μmol/L) for 24 h, the cells were examined for viability, lactate dehydrogenase (LDH) activity and morphological changes of the cell nuclei using Hoechst fluorescent staining. The levels of ROS, SOD, GSH and MDA in the treated cells were detected, and the expression levels of Akt, p-Akt and nuclear factor E2-related factor 2 (Nrf2) proteins were determined using Western blotting.
Luteolin within the concentration range of 0-80 μmol/L did not significantly affect the survival rate of Beas-2B cells (
>0.05), but Cd at 5 μmol/L significantly decreased the cell viability (
< 0.05) with an IC
of 24.6 μmol/L. In Cd-treated cells, treatment with luteolin significantly mitigated the decrease of cell viability, reduced LDH release and cell apoptosis, enhanced SOD activity and GSH content, and inhibited the production of MDA and ROS (all
< 0.05). Luteolin also significantly up-regulated the expression levels of p-Akt and Nrf2 protein in Cd-treated Beas-2B cells (
< 0.05).
Luteolin has a significant protective effect against Cd-induced injury in Beas-2B cells, and the effects are probably mediated, at least in part, by promoting the activation of Akt and Nrf2.
Luteolin has a significant protective effect against Cd-induced injury in Beas-2B cells, and the effects are probably mediated, at least in part, by promoting the activation of Akt and Nrf2.
To investigate the effect of curcumin on cell cycle and apoptosis of human lens epithelial cells and the possible molecular mechanism.
Cultured human lens epithelial cell line HLEC-SRA01/04 was treated with 20, 40 and 60 μmol/L curcumin for 24 or 48 h. The cell proliferation inhibition rate was determined using MTT assay, and the changes in cell cycle, mitochondrial membrane potential and apoptosis rate were analyzed with flow cytometry. Western blotting was used to detect the expression levels of caspase-9, caspase-3, Bcl-2, Bax, cyclin B1, CDK1, β-catenin, c-myc, and cyclin D1 in the cells.
Curcumin concentration- and time-dependently inhibited the proliferation of in HLEC-SRA01/04 cells as compared with the control cells (
< .05). selleck Flow cytometric analysis showed that curcumin significantly increased apoptosis rate and cell percentage in G2/M phase and lowered mitochondrial membrane potential of HLEC-SRA01/04 cells in a concentrationdependent manner (
< 0.05). The results of Western blotting showed that curcumin also concentration-dependently increased the cellular expressions of caspase-3, caspase-9 and Bax and lowered the expressions of Bcl-2, cyclin B1, CDK1 and β-catenin along with the downstream proteins cyclin D1 and c-myc in the Wnt/β-catenin signaling pathway (
< 0.05).
Curcumin inhibits the proliferation of HLEC-SRA01/04 cells possibly by inhibiting the Wnt/β-catenin signaling pathway and causing cell cycle arrest to induce cell apoptosis.
Curcumin inhibits the proliferation of HLEC-SRA01/04 cells possibly by inhibiting the Wnt/β-catenin signaling pathway and causing cell cycle arrest to induce cell apoptosis.
To investigate whether aryl hydrocarbon receptor (AhR) modulates cockroach allergen (CRE)-induced asthma by regulating Th17/Treg differentiation.
Mouse models of CRE-induced asthma established by sensitizing and challenging the mice with CRE were randomized into asthma model group, AhR agonist group treated with TCDD (10 μg/ kg), and AhR antagonist group treated with TCDD and CH223191 (10 mg/kg) (
=5), with 5 mice without CRE challenge as the control group. The expressions of AhR, Cyp1a1 and Cyp1b1 mRNA in the lung tissues of the mice were detected using RT-PCR, and pulmonary inflammation was evaluated with immumohistochemical staining. The expressions of inflammatory cytokines in the lungs were detected using ELISA, and the expression of Treg in the lung tissues and pulmonary lymph nodes was analyzed with flow cytometry.
Both TCDD and CH223191 were capable of modulating pulmonary expressions of AhR and its downstream genes Cyp1a1 and Cyp1b1 in asthmatic mice (
< 0.002). TCDD treatment significant;0.05).
AhR activation modulates airway inflammation in mice with CRE-induced asthma by modulating the differentiation of Th17/Treg.
AhR activation modulates airway inflammation in mice with CRE-induced asthma by modulating the differentiation of Th17/Treg.
To investigate serum levels of von Willebrand factor lytic protease (ADAMTS13) and thrombospondin-1 (TSP1) in patients with different types of acute coronary syndrome (ACS) and their correlation with the patients' clinical prognosis.
According to their disease history, results of angiography and clinical biochemical tests, a total of 405 patients undergoing coronary angiography, were divided into unstable angina (UAP) group (
=215), acute myocardial infarction (AMI) group (
=96), and angiographically normal group (
=94). Serum ADAMTS13 and TSP1 levels were detected in all the patients, who were followed up for 15 months to evaluate the occurrence of long-term major cardiac adverse events (MACE).
Serum ADAMTS13 level was significantly lower and TSP1 level was significantly higher in AMI group and UAP group than in the normal group (
< 0.001). Serum ADAMTS13 and TSP1 levels were negative correlated in ACS patients (
=-0.577,
< 0.001). The patients experiencing MACE had significantly different serum TSP1 level from those without MACE (
< 0.