Clinical study of lung-supplementing and stasis-dissolving decoction (Bufei Huayu Tang) combined with gefitnib for treatment of advanced non-small cell lung cancer.

To investigate the clinical efficacy and drug safety of Lung-Supplementing and Stasis-Dissolving Decoction (Bufei Huayu Tang) combined with gefitnib for treatment of advanced non-small cell lung cancer (NSCLC). Then, 80 patients with advanced NSCLC hospitalized in Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine were included, and were double-blindly randomized into 4 groups: control group (gefitinib alone 250mg, once daily), low-dose group (100mL/day), middle-dose group (150mL/day) and high-dose group (200mL/day) treated with different doses of Bufei Huayu Tang besides gefitinib. Clinical efficacy, life quality change before and after treatment, ECOG score, survival time and incidence of adverse drug reaction were compared.

Picroside II protects myocardium from ischemia/reperfusion-induced injury through inhibition of the inflammatory response.

The inflammatory response is important in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Picroside II, the primary active constituent of Picrorhizae, has been reported to protect the myocardium from I/R-induced injury, however, the exact mechanism underlying these protective effects remains unclear. The aim of the present study was to investigate the mechanism underlying the protective effects of picroside II on I/R-induced myocardial injury.

TRIM11, a direct target of miR-24-3p, promotes cell proliferation and inhibits apoptosis in colon cancer.

TRIM11 (tripartite motif-containing protein 11) is an E3 ubiquitin ligase recently identified as an oncogene in malignant glioma and lung cancer. In the present study, we report that expression of TRIM11 was increased in colon cancer (CC) tissue relative to paired normal tissues and that higher TRIM11 levels predicted poor overall survival (OS) and disease-free survival (DFS) in CC patients. Mechanistically, we showed that miR-24-3p downregulation contributes to TRIM11 upregulation in CC.

Biological significance of PinX1 telomerase inhibitor in esophageal carcinoma treatment.

In the present study, to investigate the expression of PinX1 gene and its functional effects in human esophageal carcinoma (Eca)-109 cell line, expression vectors of human PinX1 (pEGFP-C3-PinX1) and its small interfering RNA (PinX1-FAM-siRNA) were constructed and transfected into Eca-109 cells using Lipofectamine 2000. Firstly, the mRNA expression level of PinX1 was examined using reverse transcription-polymerase chain reaction (RT-PCR). Once successful transfection was achieved, the effects on the mRNA level of human telomerase reverse transcriptase (hTERT), telomerase activity, cell proliferation and apoptosis were examined by semi-quantitative RT-PCR, stretch PCR, MTT assay and flow cytometry, respectively.

Paeoniflorin inhibits doxorubicin-induced cardiomyocyte apoptosis by downregulating microRNA-1 expression.

Doxorubicin (DOX) is an effective anthracycline anti-tumor antibiotic. Because of its cardiotoxicity, the clinical application of DOX is limited. Paeoniflorin (PEF), a monoterpene glucoside extracted from the dry root of Paeonia, is reported to exert multiple beneficial effects on the cardiovascular system.

Therapeutic effect and apoptosis mechanism of lung-tonifying and expectorant decoction on lung cancer rats with Qi deficiency and blood stasis.

Objective: To explore the effect and specific mechanism of lung-tonifying and expectorant decoction on lung cancer rats with Qi deficiency and blood stasis, and aim to provide a new idea on treating the disease with traditional Chinese medicine based on syndrome differentiation.

Methods: A total of 60 C57BL/6J male rats were included in the study. The model of Qi deficiency and blood stasis was established in 60 rats by using multiple-factor stimulation.

Picroside Ⅱ inhibits hypoxia/reoxygenation-induced cardiomyocyte apoptosis by ameliorating mitochondrial function through a mechanism involving a decrease in reactive oxygen species production.

Reactive oxygen species (ROS)‑induced mitochondrial dysfunction plays an important role in cardiomyocyte apoptosis during myocardial ischemia/reperfusion (I/R) injury. Picroside Ⅱ, isolated from Picrorhiza scrophulariiflora Pennell (Scrophulariaceae), has been reported to protect cardiomyocytes from hypoxia/reoxygenation (H/R)‑induced apoptosis, but the exact mechanism is not fully clear. The aim of the present study was to explore the protective effects of picroside Ⅱ on H/R‑induced cardiomyocyte apoptosis and the underlying mechanism.

Anticancer effect of salidroside on A549 lung cancer cells through inhibition of oxidative stress and phospho-p38 expression.

Oxidative stress is important in carcinogenesis and metastasis. Salidroside, a phenylpropanoid glycoside isolated from L., shows potent antioxidant properties.

Inhibitory effects of paeoniflorin on lysophosphatidylcholine-induced inflammatory factor production in human umbilical vein endothelial cells.

Lysophosphatidylcholine (LPC) plays an important role in atherosclerosis through initiation of endothelial inflammation response. Paeoniflorin (PEF), isolated from the dry root of Paeonia, has been reported to exert an anti-inflammatory effect, but the exact mechanism is not fully understood. The aim of this study was to investigate the inhibitory effects of PEF on LPC-induced inflammatory factor production and the underlying mechanisms.

Paeoniflorin protects myocardial cell from doxorubicin-induced apoptosis through inhibition of NADPH oxidase.

Increased intracellular reactive oxygen species (ROS) are involved in doxorubicin (DOX)-induced myocardial cell apoptosis, and paeoniflorin (PEF) has been shown to exert an antioxidant effect. The aim of the present study was to explore the protective effect of PEF on DOX-induced myocardial cell apoptosis and the underlying mechanisms. In cultured H9c2 cells, different concentrations (1, 10, or 100 μmol/L) of PEF was added for 2 h prior to exposure to DOX (5 μmol/L) for 24 h.

Reversal of isoprenaline-induced cardiac remodeling by rutaecarpine via stimulation of calcitonin gene-related peptide production.

Dysfunction of capsaicin-sensitive sensory nerves is involved in cardiac remodeling, and rutaecarpine has been shown to exert a beneficial effect on cardiac function through activating the sensory nerves. This study was conducted to explore the potential inhibitory effect of rutaecarpine on cardiac remodeling and the underlying mechanisms. A rat cardiac remodeling model was established by injection of isoprenaline (5 mg/kg per day, s.