Enteric glial cells exert neuroprotection from hyperglycemia-induced damage via Akt/GSK3β pathway.

Objective: Enteric glial cells (EGCs) can activate multiple pathways to inhibit the deleterious effects of acute and chronic insults. Our aim was to test the effect of EGCs on hyperglycemia-induced neuron damage and its underlying intracellular mechanisms.

Methods: A coculture model composed of EGCs and neuroblastoma cells (SH-SY5Y) was established to examine glial-mediated neuroprotection under high glucose conditions.

[Mechanism of Calculus Bovis Sativus in inhibiting hepatocyte lipid deposition based on serum pharmacology].

The aim of this paper was to investigate the molecular mechanism of Calculus Bovis Sativus( CBS) in alleviating lipid accumulation in vitro by serum pharmacology. The CBS-containing serum of mice was obtained by serum pharmacology method to evaluate its effect on the proliferation of LO2 hepatocytes. The lipid reducing effects of CBS-containing serum through Nrf2 was evaluated by fructose-induced LO2 hepatocyte steatosis model,nuclear factor erythroid 2 related factor 2( Nrf2) agonist oltipraz combined intervention,cell oil red O staining and intracellular triglyceride( TG) content.

A Retrospective Analysis on 1330 Adverse Event Reports of Qingkailing in China: Further Perception of Its Risks and Rational Use.

Qingkailing (QKL) is a modern preparation exploited according to the traditional Chinese medicine theory. It becomes the second leading cause of adverse drug events (ADEs) in all traditional Chinese medicine injections. The safety evaluation and rational use of QKL are of special importance.

Protective Effects of Ginsenosides on 17[Formula: see text]-Ethynyelstradiol-Induced Intrahepatic Cholestasis via Anti-Oxidative and Anti-Inflammatory Mechanisms in Rats.

The present study was designed to assess the effects and potential mechanisms of ginsenosides on 17[Formula: see text]-ethynyelstradiol (EE)-induced intrahepatic cholestasis (IC). Ginsenoside at doses of 30, 100, 300[Formula: see text]mg/kg body weight was intragastrically (i.g.

Stem cells in cancer therapy: opportunities and challenges.

Metastatic cancer cells generally cannot be eradicated using traditional surgical or chemoradiotherapeutic strategies, and disease recurrence is extremely common following treatment. On the other hand, therapies employing stem cells are showing increasing promise in the treatment of cancer. Stem cells can function as novel delivery platforms by homing to and targeting both primary and metastatic tumor foci.

Baicalin may alleviate inflammatory infiltration in dextran sodium sulfate-induced chronic ulcerative colitis via inhibiting IL-33 expression.

Aims: To investigate the therapeutic effect of baicalin treatment in chronic ulcerative colitis (UC), and explore the potential anti-inflammation mechanism(s) via IL-33 pathway.

Main Methods: UC model were established by giving three cycles of 5-day 2% dextran sodium sulfate (DSS) with two intervals of 14-day recovery in mice, totaling 43days. At the 13th day of the UC modeling, mice received baicalin at doses of 50, 100, or 150mg/kg, respectively.

Upregulation of PDZK1 by May Play an Important Role in Restoring Biliary Transport Function in Intrahepatic Cholestasis.

Intrahepatic cholestasis is a main cause of hepatic accumulation of bile acids leading to liver injury, fibrosis, and liver failure. Our previous studies proved that (CBS) can restore biliary transport function through upregulating the multidrug resistance-associated protein 2 (MRP2) and breast cancer resistance protein (BCRP) in 17-ethynylestradiol- (EE-) induced intrahepatic cholestasis rats. The regulation mechanism of CBS on these transporters, however, remains unclear.

Intestinal injury in the rat model of 17α-ethynylestradiol-induced intrahepatic cholestasis.

Objective: Although the intimate relationship between liver and gut has been previously reported under physiological and pathological conditions, intestinal involvement in the process of intrahepatic cholestasis of pregnancy remains unclear. The aim of this study was to investigate intestinal changes in 17α-ethynylestradiol (EE)-induced cholestatic rat model.

Methods: Liver injury was assessed by HE stain and serum biochemical parameters were measured.

[Design and implementation of a long wavelength near infrared spectrometer based on MEMS scanning mirror].

Long Wavelength Near InfraRed (LW-NIR) spectrometer has wide applications. Miniaturization and low-cost are two major goals of the development of LW-NIR spectrometer in the industrial or research community. Under the background that having a trend of spectrometer miniaturization and integration, method and main problems involved in miniaturization of LW-NIR spectrometer through MEMS scanning mirror, such as the design strategy of the light-splitting optical system, selection considerations of the MEMS scanning mirror, design method of the preamplifier circuit, etc, have been presented in detail.

Biodentine induces human dental pulp stem cell differentiation through mitogen-activated protein kinase and calcium-/calmodulin-dependent protein kinase II pathways.

Introduction: Biodentine (Septodont, Saint-Maur-des-Fossès, France), a new tricalcium silicate cement formulation, has been introduced as a bioactive dentine substitute to be used in direct contact with pulp tissue. The aim of this study was to investigate the response of human dental pulp stem cells (hDPSCs) to the material and whether mitogen-activated protein kinase (MAPK), nuclear factor-kappa B (NF-κB), and calcium-/calmodulin-dependent protein kinase II (CaMKII) signal pathways played a regulatory role in Biodentine-induced odontoblast differentiation.

Methods: hDPCs obtained from impacted third molars were incubated with Biodentine.

Effect of Biodentine™ on the proliferation, migration and adhesion of human dental pulp stem cells.

Objectives: To investigate the proliferative, migratory and adhesion effect of Biodentine™, a new tricalcium silicate cement formulation, on the human dental pulp stem cells (hDPSCs).

Methods: The cell cultures of hDPSCs obtained from impacted third molars were treated with Biodentine™ extract at four different concentrations: Biodentine™ 0.02mg/ml (BD 0.

[Study of cbfalpha1 on the expression of extracellular matrix proteins in dental papilla cells induced by BMP-2 in vitro].

Purpose: To evaluate the function of cbfalpha1 on BMP-2 signaling to extracellular matrix proteins in dental papilla cells in vitro.

Methods: RT-PCR and Western blot were performed to detect the expression of ALP, OC, ON, OPN, BSP, DMP-1 and DSPP in cultured dental papilla cells induced by 200ng/mL BMP-2 and/or down-regulated by cbfalpha1 antisense technology, the results were analysed with SPSS 11.0 software package.

[Transcriptional regulation of dentin sialophosphoprotein by c-Jun/c-Fos].

Objective: To investigate the role of c-Jun and c-Fos as transcriptional factors in regulation of dentin sialophosphoprotein (DSPP) gene by a promoter-luciferase reporter gene construct in odontoblast cell line MDPC-23.

Methods: Endogenous c-Jun or c-Fos protein was determined by immunocytochemistry. The role of c-Jun or c-Fos in transcription of DSPP was investigated in co-transfection experiments using promoter-luciferase reporter gene construct containing the sequence between -791 bp and +54 bp of mouse DSPP gene.

Smad protein mediated transforming growth factor beta1 induction of apoptosis in the MDPC-23 odontoblast-like cell line.

Objective: The function of apoptosis and its regulation in odontoblasts remain unclear. In this study, we characterize the possible role of transforming growth factor (TGF)-beta 1 in the induction of apoptosis and the molecular mechanisms that mediate TGF-beta1-induced apoptosis in odontoblasts.

Methods: Annexin V/propidium iodide staining, cell Death Detection ELISA and DNA ladder were used to examine the effect of TGF-beta1 on apoptosis in a mouse odontoblast-like cell line, MDPC-23.

[Role of Smad signaling in transcription of Smad7 gene mediated by TGF-beta1 in odontoblast cell line MDPC-23].

Purpose: To investigate the role of Smad signaling in transcription of Smad7 gene mediated by TGF-beta1 in odontoblast cell line MDPC-23, and to explore the molecular mechanism of Smad7 gene expression mediated by TGF-beta1 at the transcriptional level.

Methods: Smad function and its role in transcription of Smad7 were investigated in cotransfection experiments using Smad7 promoter-luciferase reporter construct containing the sequence between -408 bp and +112 bp of mouse Smad7 gene. The data were analysed by one-way ANOVA.

[Bone morphogenetic protein-2-induced alpha 2 (I) collagen expression in odontoblastic MDPC-23 cells mediated by Smad proteins].

Objective: To characterize the role of Smads proteins in alpha 2 (I) collagen (COL1A2) gene expression induced by bone morphogenetic protein-2 (BMP-2) in odontoblast cell line MDPC-23.

Methods: Endogenous Smad protein expression was determined by immunocytochemistry. Smads function and their role in COL1A2 gene expression were investigated in cotransfection experiments using promoter-luciferase reporter gene construct.

TGF-beta activated Smad signalling leads to a Smad3-mediated down-regulation of DSPP in an odontoblast cell line.

Objective: Transforming growth factor-beta (TGF-beta) regulates odontoblast differentiation and stimulates dentine extracellular matrix synthesis. However, until recently, the molecular mechanisms of action of TGF-beta have been unknown. Smad proteins have recently been identified as intracellular signalling mediators of TGF-beta.