Sponsored by chinese phrmacological socity
ISSN 1001-1978 CN 34-1086/R
12 issues per year
Discipline(s): Medical Science
Current Issue: Issue 02, 2019
Chinese Pharmacological Bulletin is supervised by China Association for Science and Technology and sponsored by Chinese Pharmacological Society. The journal mainly publishes the original research reports and reviews on pharmacology. The readers of Chinese Pharmacological Bulletin mainly include research workers in pharmacological, medical and other related areas, clinical physicians, pharmacists and pharmaceutical industry technical personnel at different levels. The columns cover chiefly on original articles, reviews and lectures, experimental methodologies, research bulletins and short monographs. The journal is included in CA, JST and CSCD.
Sodium selenite induced human lung cancer A549 cells apoptosis through Keap1/Nrf2/ARE signaling pathway
Vol 35,No. 02
Aim To study the efficacy of sodium selenite in inducing apoptosis of human lung cancer A549 cells and its mechanisms. Methods A549 cells were exposed to different concentrations of sodium selenite for 24 h. MTT assay was applied to determine A549 cell proliferation. Inverted fluorescence microscope was used to investigate the morphological changes in A549 cells. Flow cytometry analysis was applied to assess the apoptotic rates of A549 cells. Laser confocal microscope was employed to measure the reactive oxygen species (ROS) fluorescence intensity. A multi-detection reader was used to determine the antioxidant parameter. Western blot was utilized to detect the expression of Keap1, Nrf2, HO-1 and Nrf2 in cytoplasm and nucleus. Results MTT results showed that sodium selenite inhibited the proliferation of A549 cells in a concentration-dependent manner. After treatment with sodium selenite for 24 h, the apoptotic rate of A549 cells was markedly increased after Hoechst 33342 staining by flow cytometry. Sodium selenite significantly up-regulated ROS and malondialdehyde (MDA) contents and down-regulated the levels of superoxide dismutase (SOD) and glutathione (GSH). Meanwhile, sodium selenite also reduced the expressions of Keap1, Nrf2 and HO-1 at protein levels and inhibited Nrf2 protein nuclear translocation in A549 cells. Conclusions Sodium selenite promotes apoptosis of human lung adenocarcinoma A549 cells by inhibiting their proliferation, inducing apoptosis, regulating oxidative stress in cells, and regulating Keap1/Nrf2/ARE antioxidant signaling pathway.
miR-27a-3p inhibited synthesis of Col Ⅰ and Col Ⅲ in pulmonary fibroblasts through Wnt3a/β-catenin signaling pathway
Vol 35,No. 02
Aim To explore the effects of microRNA-27a-3p (miR-27a-3p) on collagen type Ⅰ (Col Ⅰ) and collagen type Ⅲ (Col Ⅲ) synthesis in pulmonary fibroblasts and the underlying mechanisms. Methods Human pulmonary fibroblasts MRC-5 were cultured and then transfected with miR-27a-3p mimic or its inhibitor. qPCR and Western blot were used to detect miR-27a-3p level and nuclear β-catenin content, respectively. The expression levels of Col Ⅰ, Col Ⅲ and Wnt3a were measured using qPCR and Western blot. Bioinformatics was adopted to predict the potential of miR-27a-3p bound to a 3′-untranslated region (3′-UTR) of Wnt3a. Dual luciferase reporter gene assay was conducted to analyze the effects of miR-27a-3p mimic transfection on luciferase activity of wild type and mutant Wnt3a 3′-UTR. MRC-5 cells were treated with the Wnt3a/β-catenin signaling pathway inhibitor Dkk1, followed by transfection with miR-27a-3p mimic or its inhibitor. Col Ⅰ and Col Ⅲ expression levels were detected by qPCR and Western blot. Results miR-27a-3p mimic markedly increased miR-27a-3p level and decreased Col Ⅰ, Col Ⅲ, Wnt3a and β-catenin expression ( P < 0.01), while an opposite effect was observed in response to miR-27a-3p inhibitor ( P < 0.01). Bioinformatics prediction showed a binding site of miR-27a-3p in the 3′-UTR of Wnt3a. Importantly, miR-27a-3p mimic reduced luciferase activity of wild type Wnt3a 3′-UTR, but the miR-27a-3p inhibitor exerted the opposite effects. Compared with the control group, the difference was statistically significant ( P < 0.01). There was a binding site for miR-27a-3p in Wnt3a 3′-UTR. miR-27a-3p overexpression reduced wild type Wnt3a 3′-UTR luciferase activity ( P < 0.01), but the luciferase activity of its mutant was not affected ( P > 0.05). Dkk1 pretreatment almost completely reversed the induction of Col I and Col III by miR-27a-3p inhibitor ( P < 0.05). Conclusions miR-27a-3p inhibits the biosynthesis of Col Ⅰ and Col Ⅲ in pulmonary fibroblasts, which is attributed to inactivated Wnt3a/β-catenin signaling pathway.
Vol 35,No. 02
Aim To investigate the functional influences of saponins from Anemarrhena asphdeloids Bge (SAaB) on lipopolysaccharide (LPS) -induced RAW264.7 cells and the regulation of SAaB on NF-κB-iNOS-NO signaling pathway. Methods The inflammatory model in vitro was induced by LPS in RAW264.7 cells, and the levels of NO, iNOS, TNF-α and IL-6 in inflammatory RAW264.7 cells affected by SAaB were analyzed using Griess and ELISA method, respectively. The protein expression level of NF-κB p65 was measured by Western blot. Results Compared with control group, LPS (10 mg·L −1) -induced RAW264.7 cells expressed a significant increase in the levels of NO, iNOS, TNF-α, IL-6 and NF-κB p65 protein. SAaB (0.3, 3, and 30 mg·L −1) obviously reduced the contents of these inflammatory factors ( P < 0.01) and the expression of NF-κB p65 protein ( P < 0.01) in LPS-induced RAW264.7 cells. Conclusion SAaB can inhibit the functions of LPS-induced RAW264.7 cells by modulating NF-κB-iNOS-NO signaling pathway.