Previous studies have reported that Met might be related to gefitinib resistance in non-small cell lung cancer (NSCLC). The present study aims to explore the mechanism of hepatocyte growth factor (HGF)-induced gefitinib resistance in different gene types of sensitive NSCLC in vitro.

To investigate the effects of heat injured keratinocytes (KC) supernatant on the expressions of collagen type I, collagen type III, and matrix metalloproteinase 1 (MMP-1) of dermal fibroblasts (Fb).

To investigate the effect of sunitinib malate (SU11284) on proliferation of nasopharyngeal carcinoma cell line CNE-2 and explore its mechanism.

To observe the effects of Qufengtongluo Recipe (QFTLR) on the expressions of cell cycle regulatory proteins in rat mesangial cells (MCs) in vitro and investigate the mechanism by which QFTLR inhibits MC proliferation.

To explore the antitumor activities of galactosylated artemisinin in vitro and the related mechanisms.

To study the feasibility of adenovirus-based nuclear factor-κB (NF-κB) reporter as a model to screen the upstream signal regulators of NF-κB.

To investigate the effects of arsenic trioxide (As(2);O(3);) on human hepatocellular carcinoma SMMC-7721 cells' migration and invasion and the underlying molecular mechanism.

To study the effect of calcitonin gene-related peptide (CGRP) receptor on the expression of nuclear factor-kappa b (NF-kappa b) in rat lung after ischemia reperfusion injury.

To determine the potential of the high mobility group box-1 protein 1 (HMGB1) to activate Toll-like receptor 4 (TLR4) signaling in hepatic stellate cells (HSCs) and investigate the subsequent transition of HSC towards the inflammatory phenotype. Three immortalized mouse HSC cell lines, wild-type (JS1), TLR4-/- (JS2) and MyD88-/- (JS3), were subcultured in plates and divided into groups of normal control (untreated), postive control (lipopolysaccaride, LPS treatment), and experimental (HMGB1 treatment). All groups were transfected with luciferase reporter plasmids carrying responsive elements for either the nuclear factor-kappa B (NF-kB) or activator protein-1 AP-1 transcription factors. Following stimulation with normal saline, LPS (100 ng/mL) or HMGB1 (100 ng/mL), the activation of NF-kB or AP-1 was detected by a dual-luciferase reporter assay system. The induction of monocyte chemotactic protein-1 (MCP-1) transcription was determined by measuring the mRNA levels using real time quantitative reverse transcription PCR (qRT-PCR). The secreted protein levels of MCP-1 were determined by enzyme-linked immunosorbent assay (ELISA) of the culture supernatants. Activation of NF-kB- and AP-1-responsive reporters was significantly up-regulated in JS1 cells treated with HMGB1 or LPS, and the activation was coincident with markedly up-regulated transcription and secretion of MCP-1. However, HMGB1 and LPS treatment produced no responsive of the NF-kB and AP-1 reporters, and no increase in expression or secretion of MCP-1, in JS2 or JS3 cells. As an endogeous ligand of TLR4, HMGB1 may activate TLR4 signaling and the TLR4-mediated inflammatory response of HSC.

To study the effect of resveratol on ischemia reperfusion-induced cardiocyte apoptosis and its relationship with PI3K-Akt signaling pathway.

It has been proven that cancer cell autophagy can be induced by hypoxia. In addition, autophagy was correlated with radiosensitivity. Thus, regulating the autophagy signaling pathway is a potential treatment strategy. The aim of this study is to investigate the effects of combined autophagy inhibitor 3-methyladenine (3-MA) on the radiosensitivity of human adenocarcinoma A549 cells in hypoxia condition.

The study is to report the investigation of the effects of isorhamnetin on CYP3A4 and herb-drug interaction. A reporter gene assay is used to test pregnane X receptor transactivation action, qRT-PCR and a luminescence-based assay were applied to determine mRNA induction and enzyme activity of CYP3A4 after isorhamnetin treatment. The interaction of irinotecan and isorhamnetin was assessed by inhibition assay of cell proliferation. Isorhamnetin at 1, 10 and 25 micromol x L(-1) transactivated the CYP3A4 reporter construct and upregulated CYP3A4 mRNA as well in a dose-dependent manner. However, isorhamnetin had no effect on enzyme activity of CYP3A4 and irinotecan HepG2 cytotoxicity. In conclusion, activation of PXR by isorhamnetin played a role in the upregulation of CYP3A4 mRNA. Moreover, joint action of isorhamnetin with other drugs may not be associated with the herb-drug interaction.

To explore the effects of curcumin on paclitaxel resistance reversal of SKOV3-TR30 cell line and its mechanism.

To study the effect of Panax notoginseng saponins (PNS) on expression of alpha-aecretase mRNA in the brains of senescence-accelerated SAMP8 mice.

To investigate whether inhaled sevoflurane is capable of producing delayed cardioprotection effect in rats and its underlying mechanisms.

To construct an expression plasmid for NY-ESO-1 gene and identify the expression of recombinant protein NY-ESO-1/GST in E.coli.

To obtain fetal mesenchymal stem cells isolated from human placental tissue (hfPMSCs) and study the effects of IFN-γ on immunomodulatory property of hfPMSCs in vitro.

To observe the effects of total flavonoids of tartary buckwheat on NO synthesis in EA.hy926 cells induced by palmitic acid.

To investigate the effect of co-stimulation of mimic viral infection [polyinosinic: polycytidylic acid, poly(I:C)] and endotoxin (lipopolysaccharide, LPS) on chemotactic factors production of human bronchial epithelial cells and explore its related mechanism.