scholarly journals Strain differences in cytochrome P450 mRNA and protein expression, and enzymatic activity among Sprague Dawley, Wistar, Brown Norway and Dark Agouti rats

2016 ◽  
Vol 78 (4) ◽  
pp. 675-680 ◽  
Author(s):  
Yoshihiro NISHIYAMA ◽  
Shouta M.M. NAKAYAMA ◽  
Kensuke P. WATANABE ◽  
Yusuke K. KAWAI ◽  
Marumi OHNO ◽  
...  
2021 ◽  
Author(s):  
Jianhua Chen ◽  
Ziqi Jing ◽  
Xue Wang ◽  
Chu Li ◽  
Yanyi Li ◽  
...  

Abstract Background: Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by insulin resistance and β-cell dysfunction, and accompanied by neuroendocrine disorders. Recently, Jiao-Tai-Wan (JTW) has been reported to exert hypoglycemic effects against diabetes. However, its mechanism has not been clarified. Therefore, we attempted to explore the effect of JTW on alleviating insulin resistance and lipid metabolism disorder in T2DM rats by regulating the level of neurotransmitters. Methods: Sprague-Dawley (SD) rats were treated with a high-fat diet/streptozotocin to induce T2DM and then gavaged with JTW for 4 weeks. Afterwards, endpoints including body weight, fasting blood glucose, glucose tolerance, serum insulin, and lipid index were determined, and we analyzed pathological changes in the liver and kidney. Meanwhile, the level of neurotransmitter neurotransmitters in the central nervous system and peripheral tissues was measured by UPLC-MS/MS. Furthermore, the expression of neurotransmitter transporter mRNA and protein levels in the brain and kidney of T2DM rats was analyzed by qRT-PCR and WB. Results: The results showed that JTW ameliorated glucose homeostasis, insulin resistance, and lipid metabolism in T2DM rats by regulating the disorder of neurotransmitter distribution in the brain, kidney, intestine, adrenal gland, blood, and urine of T2DM rats. Mechanically, JTW may improve neurotransmitter disturbance by reducing mRNA and protein expression of SERT, DAT, and GAT-1 and increasing mRNA and protein expression of NET in the brain and kidney of T2DM rats.Conclusion: Our findings confirm that JTW can play a hypoglycemic role by regulating the disorder level of neurotransmitter distribution in T2DM rats, which may have potential therapeutic implications for the treatment of T2DM.


2002 ◽  
Vol 93 (3) ◽  
pp. 974-983 ◽  
Author(s):  
Matthew R. Hodges ◽  
Hubert V. Forster ◽  
Paula E. Papanek ◽  
Melinda R. Dwinell ◽  
Genevieve E. Hogan

Our purpose in this study was to identify different ventilatory phenotypes among four different strains of rats. We examined 114 rats from three in-house, inbred strains and one outbred strain: Brown Norway (BN; n = 26), Dahl salt-sensitive ( n = 24), Fawn-hooded Hypertensive (FHH: n = 27), and outbred Sprague-Dawley rats (SD; n = 37). We measured eupneic (room air) breathing and the ventilatory responses to hypoxia (12% O2-88% N2), hypercapnia (7% CO2), and two levels of submaximal exercise. Primary strain differences were between BN and the other strains. BN rats had a relatively attenuated ventilatory response to CO2 ( P < 0.001), an accentuated ventilatory response to exercise ( P < 0.05), and an accentuated ventilatory roll-off during hypoxia ( P < 0.05). Ventilation during hypoxia was lower than other strains, but hyperventilation during hypoxia was equal to the other strains ( P > 0.05), indicating that the metabolic rate during hypoxia decreased more in BN rats than in other strains. Another strain difference was in the frequency and timing components of augmented breaths, where FHH rats frequently differed from the other strains, and the BN rats had the longest expiratory time of the augmented breaths (probably secondary to the blunted CO2 sensitivity). These strain differences not only provide insight into physiological mechanisms but also indicate traits (such as CO2 sensitivity) that are genetically regulated. Finally, the data establish a foundation for physiological genomic studies aimed at elucidating the genetics of these ventilatory control mechanisms.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Lingshuang Sun

Abstract Background and Aims My previous studies have found that Intestinal macrophages in the uremic rats are polarized towards a proinflammatory phenotype and had dysfunction of phagocytosis leading to aggravate microinflammation and assist bacterial translocation in uremia resulting in microinflammation. However, it is still unclear what kind of mechanism of action of intestinal bacteria activates intestinal macrophages and thus participates in the occurrence and development of microinflammation in uremia. Method Male Sprague-Dawley rats were randomly divided into two groups: sham, uremia. The macrophage ultrastructure was examined by transmission electron microscopy. Immunochemistry was used to analyze the expression of macrophage-inducible C-type lectin (Mincle). RT-PCR and western blot were employed to assess the mRNA and protein expression of toll-like receptor 4 (TLR4). Results Our RCT study found that the number of Lactobacilli in the intestines of patients with end-stage diabetic nephropathy was significantly higher than that in non-diabetic patients(Figure 1). The plasma levels of endotoxin, CRP, IL-6, and TNF-a in the uremia group were greater than those in the sham group (p&gt;0.05)(Table 1).Compared with the sham group, the uremic macrophages showed fewer cytoplasmic protrusions and pseudopodia(Figure 2) and the uremia group exhibited macrophages with higher staining intensities for Mincle and higher mRNA and protein expression of TLR4(Figure 3-5). Conclusion Studies have shown that Lactobacillus planta can directly activate Mincle. The relationship between Mincle and the activation of intestinal macrophages was verified. The solution to this scientific problem will not only clarify the molecular mechanism of intestinal bacteria in controlling the activation of intestinal macrophages, but also link the immune regulation of intestinal macrophages with the micro-inflammation of uremia so as to clarify the micro-inflammation state of uremia.


2006 ◽  
Vol 101 (4) ◽  
pp. 1097-1103 ◽  
Author(s):  
S. E. Davis ◽  
G. Solhied ◽  
M. Castillo ◽  
M. Dwinell ◽  
D. Brozoski ◽  
...  

Ventilatory sensitivity to CO2 in awake adult Brown Norway (BN) rats is 50–75% lower than in adult Sprague-Dawley (SD) and salt-sensitive Dahl S (SS) rats. The purpose of the present study was to test the hypothesis that this difference would be apparent during the development of CO2 sensitivity. Four litters of each strain were divided into four groups such that rats were exposed to 7% inspired CO2 for 5 min in a plethysmograph every third day from postnatal day (P) 0 to P21 and again on P29 and P30. From P0 to P14, CO2 exposure increased pulmonary ventilation (V̇e) by 25–50% in the BN and SD strains and between 25 to over 200% in the SS strain. In all strains beginning around P15, the response to CO2 increased progressively reaching a peak at P19–21 when V̇e during hypercapnia was 175–225% above eucapnia. There were minimal changes in CO2 sensitivity between P21 and P30, and at both ages there were minimal between-strain differences. At P30, the response to CO2 in the SS and SD strains was near the adult response, but the response in the BN rats was 100% greater at P30 than in adults. We conclude that 1) CO2-sensing mechanisms, and/or mechanisms downstream from the chemoreceptors, change dramatically at the age in rats when other physiological systems are also maturing (∼P15), and 2) there is a high degree of age-dependent plasticity in CO2 sensitivity in rats, which differs between strains.


2011 ◽  
Vol 43 (15) ◽  
pp. 930-941 ◽  
Author(s):  
Toshihiro Konno ◽  
Lea A. Rempel ◽  
M. A. Karim Rumi ◽  
Amanda R. Graham ◽  
Kazuo Asanoma ◽  
...  

The rat possesses a hemochorial form of placentation. Pronounced intrauterine trophoblast cell invasion and vascular remodeling characterize this type of placentation. Strain-specific patterns of placentation are evident in the rat. Some rat strains exhibit deep intrauterine trophoblast invasion and an expanded junctional zone [Holtzman Sprague-Dawley (HSD), Dahl salt sensitive (DSS)], whereas placentation sites of other rat strains are characterized by shallow invasion and a restricted junctional zone [Brown Norway (BN)]. In this report, we identified a quantitative trait that was used to distinguish strain-specific features of rat placentation. Junctional zone prolactin family 5, subfamily a, member 1 ( Prl5a1) transcript levels were significantly greater in BN rats than in HSD or DSS rats. Prl5a1 transcript levels were used as a quantitative trait to screen placentation sites from chromosome-substituted rat strains (BN chromosomes introgressed into the DSS inbred strain; DSS-BN panel). Litter size, placental weights, and fetal weights were not significantly different among the chromosome-substituted strains. Regulation of the junctional zone Prl5a1 transcript-level quantitative trait was multifactoral. Chromosome-substituted strains possessing BN chromosomes 14 or 17 introgressed into the DSS inbred rat strain displayed Prl5a1 transcript levels that were significantly different from the DSS pattern and more closely resembled the BN pattern. The in situ placental distribution of Prl5a1 mRNA and the structure of the junctional zone of DSS-BN17 rats mimicked that observed for the BN rat. Prl5a1 gene expression was also assessed in BN vs. HSD trophoblast stem cells and following reciprocal BN and HSD embryo transfer. Strain differences intrinsic to trophoblast and maternal environment were identified. In summary, we have identified chromosomes 14 and 17 as possessing regulatory information controlling a quantitative trait associated with rat placentation.


2018 ◽  
Vol 2018 ◽  
pp. 1-6
Author(s):  
Xiaomin Chen ◽  
Yue Wang ◽  
Fangfang Han ◽  
Min Ke

Purpose. Glaucoma is the leading cause of irreversible blindness throughout the world. The pathogenesis of glaucoma is complex, and neuroprotection is a crucial aspect of therapy. High concentrations of extracellular glutamate are toxic to the optic nerve. The glutamate-aspartate transporter (GLAST) in retinal Müller cells is involved in the development of glaucoma. Anthocyanin has been reported to protect retinal neurons. We hypothesize that cyanin chloride, a type of anthocyanin, can inhibit hyperbaric pressure-induced GLAST decreases in cultured rat retinal Müller cells and may serve as a potential neuroprotective agent in glaucoma treatment. Materials and Methods. Sprague Dawley rat Müller cells were cultured in a hyperbaric pressure device at 60 mmHg additional pressure and treated with cyanin chloride (10 μmol/L, 30 μmol/L, or 50 μmol/L) or vehicle for 2 hours. Cell survival rates (SRs) were evaluated by an MTT assay. GLAST mRNA and protein expression were determined by western blot and RT-PCR analyses, respectively. Results. Cell SR was significantly decreased in the 60 mmHg additional hyperbaric pressure group compared to the control group (P<0.01). Cyanin chloride treatment significantly improved SR under 60 mmHg additional pressure (P<0.01). GLAST mRNA and protein expression levels in Müller cells were significantly reduced in the 60 mmHg hyperbaric pressure group compared to the control group (P<0.01), but cyanin chloride significantly inhibited hyperbaric pressure-induced decreases in GLAST expression (P<0.01). Conclusion. Our results support our hypothesis and demonstrate that cyanin chloride can protect rat retinal Müller cells from hyperbaric pressure-induced decreases of GLAST.


2015 ◽  
Vol 51 (3) ◽  
pp. 673-679
Author(s):  
Fo-Quan Luo ◽  
Jun-Wu Liu ◽  
Shu-Xin Tang ◽  
Wei-Lu Zhao ◽  
Yan Hu ◽  
...  

This work aims to study the pathogenesis of learning and memory impairment in offspring rats resulting from maternal enflurane anesthesia by focusing on the expression of the N-methyl-d-aspartic acid receptor subunit 2B (NR2B) in the hippocampus of the offspring. Thirty female Sprague-Dawley rats were randomly divided into three groups: control (C group), 4 h enflurane exposure (E1 group), and 8 h enflurane exposure (E2 group) groups. Eight to ten days after the initiation of pregnancy, rats from the E1 and E2 groups were allowed to inhale 1.7% enflurane in 2 L/min oxygen for 4 h and 8 h, respectively. Rats from the C group were allowed to inhale 2 L/min of oxygen only. The Morris water maze was used to assay the learning and memory function of the offspring on postnatal days 20 and 30. RT-PCR and immunohistochemistry assays were then used to measure the mRNA levels and protein expression of NR2B, respectively. Relative to offspring rats from the C group, those from the E1 and E2 groups exhibited longer escape latencies, lesser number of crossings over the platform, and less time spent in the target quadrant in the spatial exploration test (P < 0.05). In addition, the mRNA and protein expression levels of NR2B in the hippocampus of offspring rats in the E1 and E2 groups were down-regulated (P < 0.05). No significant differences between the E1 and E2 groups were observed (P > 0.05) in terms of mRNA levels and protein expression of NR2B. The cognitive function of the offspring is impaired when maternal rats are exposed to enflurane during early pregnancy. A possible mechanism of this effect is related to the down-regulation of NR2B expression.


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