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Ru Q.,Jianghan University | Ru Q.,Hanjea Wuhan Biological Technology Co. | Tian X.,Jianghan University | Tian X.,Hanjea Wuhan Biological Technology Co. | And 11 more authors.
International Journal of Oncology | Year: 2015

Accumulating evidence has proved that potassium channels (K+ channels) are involved in regulating cell proliferation, cell cycle progression and apoptosis of tumor cells. However, the precise cellular mechanisms are still unknown. In the present study, we investigated the effect and mechanisms of quinidine, a commonly used voltage-gated K+ channel blocker, on cell proliferation and apoptosis of human glioma U87-MG cells. We found that quinidine significantly inhibited the proliferation of U87-MG cells and induced apoptosis in a dose-dependent manner. The results of caspase colorimetric assay showed that the mitochondrial pathway was the main mode involved in the quinidine-induced apoptotic process. Furthermore, the concentration range of quinidine, which inhibited voltage-gated K+ channel currents in electrophysiological assay, was consistent with that of quinidine inhibiting cell proliferation and inducing cell apoptosis. In U87-MG cells treated with quinidine (100 μmol/l), 11 of 2, 042 human microRNA s (miRNA s) were upregulated and 16 were downregulated as detected with the miRNA array analysis. The upregulation of miR- 149-3p and downregulation of miR- 424-5p by quinidine treatment were further verified by using quantitative real-time PCR. In addition, using miRNA target prediction program, putative target genes related to cell proliferation and apoptosis for two differentially expressed miRNA s were predicted. Taken together, these data suggested that the anti-proliferative and pro-apoptosis effect of voltage-gated K+ channel blocker quinidine in human glioma cells was mediated at least partly through regulating expression of miRNA s, and provided further support for the mechanisms of voltage-gated K+ channels in mediating cell proliferation and apoptosis.

Xiong Q.,Jianghan University | Xiong Q.,Hanjea Wuhan Biological Technology Co. | Ru Q.,Jianghan University | Ru Q.,Hanjea Wuhan Biological Technology Co. | And 17 more authors.
Journal of Toxicology and Environmental Health - Part A: Current Issues | Year: 2015

Alveolar macrophages (AM) are the predominant lung cells responsible for both ingestion and clearance of inhaled particulate matter (PM). The aims of this study were (1) to examine effects of fine PM on rat NR8383 cell line apoptosis, and (2) to determine whether NR8383 cell functions are further affected when exposed to fine PM in the presence of inflammation induced by lipopolysaccharide (LPS). Standard Reference Material 2786 (SRM 2786) for fine PM was used to measure the following parameters: cytotoxicity, apoptotic rate, Bax/Bcl-2 expression, nitric oxide (NO) production, and reactive oxygen species (ROS) generation in NR8383 cells. Data showed that SRM 2786 alone induced damage and apoptosis in NR8383 cells in a concentration-dependent manner as demonstrated by significant decrease in expression of Bcl-2 and increase in expression of Bax, suggesting fine PM might trigger apoptosis involving a mitochondria-mediated apoptotic pathway. In addition, there was elevated production of free radicals, such as NO and ROS, suggesting oxidative stress plays a role in the observed apoptotic responses. Further, LPS pretreatment enhanced apoptosis of NR8383 cells induced by SRM 2786. Consequently, data indicate that SRM 2786 triggered cell apoptosis in NR8383 cells, probably by mechanisms involving oxidative stress, as evidenced by elevated NO and ROS levels, while the degree of apoptosis was further aggravated by inflammation. Copyright © Taylor & Francis Group, LLC.

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