Mast cell activation and response to tolterodine in the rat urinary bladder in a chronic model of intravesical protamine sulfate and bacterial endotoxin-induced cystitis.

The aim of the present study was to use an animal model of interstitial cystitis (IC) in order to investigate the histology and function of the bladder, with a particular focus on mast cell degranulation and response to detrusor overactivity (DO) to tolterodine. A total of 18 female Sprague‑Dawley rats were used. In 12 rats, lipopolysaccharide (LPS) was intravesically instilled following the induction of IC by protamine sulfate (PS) and six rats were subjected to sham instillations.

Development and changes with age of detrusor overactivity in spontaneous hypertensive rats as observed by simultaneous registrations of intravesical and intraabdominal pressures.

Purpose: Overactive bladder is especially common in the elderly, although it is not regarded as a normal part of aging. Thus, we investigated how aging alters the cystometric and detrusor overactivity (DO) parameters and the density of nerve growth factor (NGF) in awake spontaneous hypertensive rats (SHRs) of different ages.

Methods: Three age groups of 12- (n=5), 17- (n=6), and 21- (n=6) week-old SHRs (Oriental Bio Inc.

Urodynamic findings in an awake chemical cystitis rat model observed by simultaneous registrations of intravesical and intraabdominal pressures.

Purpose: The aim of this study was to investigate the effect of urinary bladder inflammation on bladder function in a rat chemical cystitis model. We also histologically confirmed the effects of inflammation in the detrusor on chronically inflamed bladder in rats.

Materials And Methods: A total of 13 female Sprague-Dawley rats were used in this study.

Selection of a control rat for conscious spontaneous hypertensive rats in studies of detrusor overactivity on the basis of measurement of intra-abdominal pressures.

Aims: We investigated which animal model is appropriate as a control for the spontaneous hypertensive rat (SHR) in studies of detrusor overactivity (DO).

Methods: Age-matched SHRs (n = 10), Wistar-Kyoto (WKY) rats (n = 9), Wistar-ST (Wistar) rats (n = 10), and Sprague-Dawley (SD) rats (n = 10) were studied. A balloon-fitted catheter was positioned in the abdominal cavity to record intra-abdominal pressure (IAP).

A peroxisome-proliferator activated receptor-gamma ligand could regulate the expression of leptin receptor on human hepatic stellate cells.

Leptin is a peptide known to play a profibrogenic role in hepatic stellate cells (HSCs). Peroxisome-proliferator activated receptor (PPAR)-gamma ligands are suggested to have an anti-fibrogenic effect on HSCs. Since the association of these two factors in HSC activation has not been demonstrated, we hypothesized that PPAR-gamma ligands would suppress leptin-induced HSC activation and regulate leptin receptor expression.

Excessive nitric oxide attenuates leptin-mediated signal transducer and activator of transcription 3 activation.

The mechanisms of leptin resistance observed in most cases of human obesity are poorly understood. Therefore, we evaluated the effects of nitric oxide (NO) on the leptin-induced activation of Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathways and on the leptin receptor (LEPR) expression using SH-SY5Y cells. Here, we show that the NO donor spermine/NONOate inhibited leptin-induced activation of STAT3 in vitro.

Smad6 negatively regulates interleukin 1-receptor-Toll-like receptor signaling through direct interaction with the adaptor Pellino-1.

Transforming growth factor-beta1 (TGF-beta1) is a potent cytokine with pleiotropic effects, including anti-inflammatory activity. Here we show that the signaling protein Smad6 bound to Pellino-1, an adaptor protein of mammalian interleukin 1 receptor (IL-1R)-associated kinase 1 (IRAK1), and thereby promoted TGF-beta-mediated anti-inflammatory effects. Smad6-Pellino-1 interaction abrogated signaling mediated by a complex of IRAK1, Pellino-1 and adaptor protein TRAF6 that formed after stimulation by IL-1beta treatment.