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Adult Sprague (adult + sprague)
Selected AbstractsProtective effect of melatonin against hippocampal injury of rats with intermittent hypoxiaJOURNAL OF PINEAL RESEARCH, Issue 2 2008Ming-Wai Hung Abstract:, Obstructive sleep apnea (OSA) patients suffer from intermittent hypoxia (IH) and neuropsychologic impairments. Oxidative stress is involved in the pathogenesis of OSA, so the application of an antioxidant may be useful. We evaluated the hypothesis that melatonin would reduce IH-induced hippocampal injury via an increased expression of antioxidant enzymes. Adult Sprague,Dawley rats that had received a daily injection of melatonin or vehicle were exposed to IH for 8 hr/day for 7 or 14 days. The serum and hippocampus were harvested for the measurement of malondialdehyde (MDA). Apoptotic cell death was studied histologically in hippocampal sections. The mRNA expression of inflammatory mediators including tumor necrosis factor-alpha, inducible nitric oxide synthase, cyclooxygenase-2 and antioxidant enzymes including glutathione peroxidase, catalase and copper/zinc superoxide dismutase were examined in the hippocampus by RT-PCR. The results show significant increases in levels of serum and hippocampal MDA, apoptotic cell death and mRNA levels of inflammatory mediators in hypoxic rats when compared with the normoxic controls. Also, mRNA levels of the antioxidant enzymes were decreased in hypoxic animals. In the melatonin-treated hypoxic rats, serum MDA levels were comparable with those in normoxic control rats. Also, melatonin treatment significantly reduced hippocampal MDA levels and totally prevented apoptosis. Moreover, there were a decreased expression of the inflammatory mediators and an elevated expression of antioxidant enzymes in the melatonin injected rats when compared with vehicle-treated animals. These results indicate that melatonin mitigates oxidative stress and the pathogenesis of IH-induced hippocampal injury via its antioxidant and anti-inflammatory properties which includes stimulation of transcriptional regulation of antioxidant enzymes. [source] Regulation of GADD153 induced by mechanical stress in cardiomyocytesEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 11 2009W. P. Cheng Abstract Background, Growth arrest and DNA damage-inducible gene 153 (GADD153), an apoptosis regulated gene, increased during endoplasmic reticulum stress. However, the expression of GADD153 in cardiomyocytes under mechanical stress is little known. We aimed to investigate the regulation mechanism of GADD153 expression and apoptosis induced by mechanical stress in cardiomyocytes. Materials and methods, Aorta-caval shunt was performed in adult Sprague,Dawley rats to induce volume overload. Rat neonatal cardiomyocytes grown on a flexible membrane base were stretched by vacuum to 20% of maximum elongation, at 60 cycles min,1. Results, The increased ventricular dimension measured using echocardiography in the shunt group (n = 8) was reversed to normal by treatment with chaperon 4-phenylbutyric acid (PBA) (n = 8) at 500 mg kg,1 day,1 orally for 3 days. GADD153 protein and mRNA were up-regulated in the shunt group when compared with sham group (n = 8). Treatment with PBA reversed the protein of GADD153 to the baseline values. The TUNEL assay showed that PBA reduced the apoptosis induced by volume overload. Cyclic stretch significantly increased GADD153 protein and mRNA expression after 14 h of stretch. Addition of c-jun N-terminal kinase (JNK) inhibitor SP600125, JNK small interfering RNA and tumour necrosis factor-, (TNF-,) antibody 30 min before stretch, reduced the induction of GADD153 protein. Stretch increased, while GADD153-Mut plasmid, SP600125 and TNF-, antibody abolished the GADD153 promoter activity induced by stretch. GADD153 mediated apoptosis induced by stretch was reversed by GADD153 siRNA, GADD153-Mut plasmid and PBA. Conclusions, Mechanical stress enhanced apoptosis and GADD153 expression in cardiomyocytes. Treatment with PBA reversed both GADD153 expression and apoptosis induced by mechanical stress in cardiomyocytes. [source] NMDA receptor-mediated metaplasticity during the induction of long-term depression by low-frequency stimulationEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2002Bruce Mockett Abstract Metaplasticity refers to the activity-dependent modification of the ability of synapses to undergo subsequent synaptic plasticity. Here, we have addressed the question of whether metaplasticity contributes to the induction of long-term depression (LTD) by low-frequency stimulation (LFS). The experiments were conducted using standard extracellular recording techniques in stratum radiatum of area CA1 in hippocampal slices made from adult Sprague,Dawley rats. The degree of LTD induction was found to be a nonlinear function of the number of pulses during a 1-Hz LFS. Little LTD was observed following 600 or 900 pulses, but a significant LTD occurred following 1200 pulses of LFS, whether delivered in one episode, or in two bouts of 600 pulses given 10 min apart. A similar pattern was observed for 3 Hz LFS. The data support the suggestion that pulses occurring early in the LFS train prime synapses for LTD induction, as triggered by later occurring stimuli. The priming effect lasted at least 120 min, when tested by giving two bouts of 1 Hz LFS (600 pulses each) at different intervals. Neither heterosynaptic nor homosynaptic stimulation by itself was sufficient to prime LTD. However, a combination of the stimuli, induced by increased stimulus strength during the LFS, appeared necessary for inducing the effect. An N -methyl- d -aspartate (NMDA) receptor antagonist markedly reduced total LTD induction, regardless of whether it was administered during the first or second LFS in a protocol employing two bouts of 600 pulse LFS, 30 min apart. These findings strongly support the hypothesis that NMDA receptor-dependent metaplasticity processes contribute to the induction of LTD during standard LFS protocols. [source] Expression of the RNA-binding protein Musashi1 in adult liver stem-like cellsHEPATOLOGY RESEARCH, Issue 4 2010Etsuko Hattori Aim:, Musashi1 is an RNA-binding protein that regulates the Notch signaling pathway in stem cells. Our previous study revealed that Musashi1 is expressed in early hepatocytes during liver development in the mouse. However, whether this unique protein is expressed with Notch signaling markers in adult liver stem-like cells remains unknown. Methods:, Established hepatic stem-like cells (HSLC), which were derived from adult Sprague,Dawley rats, were used for experiments in vitro. HSLC were differentiated into mature cells in terms of producing albumin when co-cultured with epidermal growth factor (EGF). The mRNA expression of Musashi1, Notch family (Notch1 and Notch2), Jagged1 and Hes1 was examined in HSLC before and after cell differentiation using polymerase chain reaction-based techniques. Protein expression of Musashi1 was examined in the HSLC and normal mature hepatocytes by immunofluorescence staining. Results:, The mRNA expression of Musashi1, Notch1, Jagged1 and Hes1 was detected in the original HSLC before culturing with EGF but not in primary cultured mature hepatocytes. The mRNA expression of Musashi1 and Hes1 was found to be downregulated in differentiated HSLC that produce albumin. Protein expression of Musashi1 was detectable in the original HSLC but not in both differentiated HSLC and mature hepatocytes. Conclusion:, These findings demonstrate that the RNA-binding protein Musashi1 is expressed with Notch signaling markers in adult liver stem-like cells. [source] Connections of the zona incerta to the reticular nucleus of the thalamus in the ratJOURNAL OF ANATOMY, Issue 2 2006Safiye Çavdar Abstract This study demonstrated that there is a pathway from the zona incerta to the thalamic reticular nucleus. Injections of horseradish peroxidase or Fluorogold were made, using stereotaxic coordinates, into the rostral, intermediate or caudal regions of the thalamic reticular nucleus of adult Sprague,Dawley rats. The results show that the different regions of the thalamic reticular nucleus have distinct patterns of connections with the sectors of the zona incerta. In terms of the relative strength of the connections, injections made into the rostral regions of the thalamic reticular nucleus showed the highest number of labelled cells within the rostral and ventral sectors of the zona incerta; injections made into the intermediate regions of the thalamic reticular nucleus showed labelled cells in the dorsal and ventral sectors; while injections to the caudal regions of the thalamic reticular nucleus showed only a few labelled cells in the caudal sector of the zona incerta. Previous studies have shown that the zona incerta projects to the higher order thalamic nuclei but not first order thalamic nuclei. The labelling observed in the present study may represent collaterals of zona incerta to higher order thalamic nuclei projections. [source] Tissue-specific expression of the tight junction proteins claudins and occludin in the rat salivary glandsJOURNAL OF ANATOMY, Issue 4 2004M. Peppi Abstract Tight junctions (TJs) are essential features of endothelial barrier membranes and of fluid-secreting epithelial cells, such as in the salivary glands. Novel integral membrane proteins have been identified as components of TJs, namely claudins and occludin. The aim of the present study was to determine the distribution of occludin and claudins in the large salivary glands of the rat. The parotid, submandibular and sublingual salivary glands were harvested from adult Sprague,Dawley rats and cryostat sections were stained using immunoperoxidase and immunofluorescence methods. Claudin-1 was expressed in endothelial cells of microvessels and in short selected segments of the duct system. Claudin-3 was expressed principally in the acinar cells and intercalated ducts, while claudin-4 was principally expressed by the striated and interlobular ducts. Claudin-5 was specific to endothelial cells of microvessels. Occludin was ubiquitously detected in the duct system. Double labelling and confocal microscopy showed some co-localization of claudin-3 with claudin-4, and minimal co-localization of occludin with claudin-4, in the striated ducts. Claudin 2 was not detected in any of the salivary glands. The results indicate specificity of the chemical composition of tight junctions in the rat salivary glands, and may reflect different physiological roles for TJs in the glandular and duct epithelial cells, and in endothelial cells of salivary gland microvessels. [source] Antifibrogenic effects of tamoxifen in a rat model of periportal hepatic fibrosisLIVER INTERNATIONAL, Issue 2 2009Soo Hyung Ryu Abstract Backgrounds/Aims: It has been reported that tamoxifen may affect hepatoma cell growth in vitro by suppressing transforming growth factor ,-1 (TGF-,1) expression, suggesting that tamoxifen might also retard fibrogenesis. Thus, we examined whether tamoxifen might suppress TGF-,1 expression and consequently inhibit the process of hepatic fibrosis in vivo. Methods: To induce periportal hepatic fibrosis, 50 male adult Sprague,Dawley rats were injected with 0.62 mmol/kg of allyl alcohol, intraperitoneally, twice a week for 8 weeks. Hepatic fibrosis scores, intrahepatic collagen levels and plasma TGF-,1 expression levels were evaluated in three groups of 10 rats orally administered tamoxifen at 1, 5 and 10 mg/kg, respectively, and in 20 controls. Messenger RNAs (mRNAs) encoding TGF-,1 and TGF-, receptors in liver tissue were semiquantified using reverse transcriptase polymerase chain reaction. Results: Hepatic fibrosis scores decreased progressively as the dose of tamoxifen increased, resulting in a significant change in rats treated with tamoxifen at 10 mg/kg compared with controls (P=0.018). Intrahepatic collagen content was significantly less in the group treated with tamoxifen at 10 mg/kg compared with the control (P=0.045). Plasma TGF-,1 levels were also significantly lower in rats treated with tamoxifen at 10 mg/kg compared with controls (P=0.007). All three concentrations of tamoxifen tested decreased the expression levels of hepatic TGF-,1 mRNA and type I TGF-, receptor (TGF-, RI) mRNA to similar extents. Conclusions: Tamoxifen seems to inhibit the process of hepatic fibrosis dose-dependently by suppressing the transcription of TGF-,1 and TGF-, RI in an experimental model of periportal hepatic fibrosis. [source] | |||||||||||||