Biomedical subjects

Sayuri Kato

Publications and source records attributed to Sayuri Kato.

3 recordsLinked to original sources

PubMed2006

Specific type IV phosphodiesterase inhibitor ameliorates cerulein-induced pancreatitis in rats.

BACKGROUND AND AIMS: Type IV phosphodiesterase is a key enzyme to metabolize intracellular adenosine 3',5'-cyclic monophosphate (cAMP) expressed in inflammatory cells. The specific type IV phosphodiesterase inhibitor that increases intracellular cAMP is known to be potent suppressor of proinflammatory cytokines. However, the effect of phosphodiesterase inhibitors on the development of pancreatitis has not been well understood. In the present study, we examined the effect of a specific type IV phosphodiesterase inhibitor on experimentally induced pancreatitis. METHODS: Severity of cerulein-induced pancreatitis and pancreatic proinflammatory cytokine levels were studied with or without pretreatment with a specific type IV phosphodiesterase inhibitor (rolipram) in Sprague-Dawley rats. RESULTS: Administration of rolipram clearly ameliorated severity of pancreatitis evaluated by edema, serum amylase (P<0.05), and lipase levels (P<0.05) in rats. Also, the level of pancreatic proinflammatory cytokine (interleukin-1beta (IL-1beta)) was significantly reduced when rats were treated with rolipram prior cerulein injection (P<0.05). CONCLUSIONS: Our results demonstrated that intracellular cAMP and pancreatic proinflammatory cytokine level, which are regulated by type IV phosphodiesterase, might play an important role in the pathogenesis of acute pancreatitis.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed2006

Systemic stress increases serum leptin level.

BACKGROUND AND AIM: Leptin, the product of the obese (ob) gene, is a circulating peptide mainly synthesized by adipocytes. Leptin inhibits food intake and decreases body weight. A recent report has suggested that the gastric mucosa is also the source of leptin, and that the stomach leptin also contributes to the regulation of the serum leptin level. The aim of the present study was to investigate the effect of water-immersion stress on serum, stomach and adipose tissue leptin levels to understand the relationship between stress and eating behavior. METHODS: Male Sprague-Dawley rats were used in this experiment. The leptin level in the serum, gastric mucosa and adipose tissue was measured using ELISA system before and after the initiation of water-immersion stress. RESULTS: The serum leptin level was significantly increased by water-immersion stress. The peak was observed 9 h after the initiation of the stress (P < 0.01). However, the gastric leptin level significantly decreased 6 and 9 h after the stress. The adipose tissue leptin level significantly increased 3 h after the stress. CONCLUSIONS: The results suggest that changes in serum leptin levels could be associated with stimulation of leptin secretion from the gastric mucosa and leptin production in the adipose tissue by systemic stress and that leptin might be regulated by stress-related events.

Adipocytes↗

PubMed2002

Induction of a 72-kDa heat-shock protein in cultured rat gastric mucosal cells and rat gastric mucosa by zinc L-carnosine.

An antiulcer drug, zinc L-carnosine (polaprezinc), provides gastric mucosal protection against various irritants. In this study, we evaluated the effects of zinc L-carnosine on expression of 72-kDa heat shock protein (HSP72, stress inducible HSP70), which is known as an endogenous cytoprotectant in a wide variety of cells, including rat gastric mucosa in vitro and in vivo. Expression of HSP72 after exposure to zinc L-carnosine, zinc sulfate, or L-carnosine (1-300 microM) in rat gastric mucosal cells (RGM1) and intragastric administration of zinc L-carnosine, zinc sulfate (30 or 100 mg/kg) and L-carnosine (76 mg/kg) was investigated by western blotting and densitometric analysis. Exposure to zinc L-carnosine and zinc sulfate increased the expression of HSP72 significantly in RGM1 cells. Intragastric administration of zinc L-carnosine and zinc sulfate showed significant increment in HSP72 in rat gastric mucosa also in vivo. The ability to induce HSP72 is significantly higher in zinc L-carnosine compared with zinc sulfate based on molecular concentration in vivo. However, L-carnosine did not increase the expression of HSP72 in vitro and in vivo. Zinc derivatives, especially zinc L-carnosine, could be a strong HSP72 (chaperon) inducer, which has been known to enhance mucosal protective ability.

Animals↗