NF-κB activation in organs from STZ-treated rats

2011 ◽  
Vol 36 (1) ◽  
pp. 121-127 ◽  
Author(s):  
Marius Locke ◽  
Jocelyn Anderson
Keyword(s):  
Subunit Composition ◽  
Sprague Dawley ◽  
Mobility Shift ◽  
Diabetic State ◽  
Sprague Dawley Rats ◽  
Inflammatory State ◽  
Mobility Shift Assay ◽  
Related Proteins ◽  
And Control ◽  
Insight Into

Nuclear factor kappa B (NF-κB) is a ubiquitously expressed transcription factor comprised of various subunits (p50 (NF-κB1), p52 (NF-κB2), p65 (RelA), RelB, and c-Rel). Activation of certain NF-κB subunits appears to foster an inflammatory state that may promote the development of disease. Thus characterizing the specific NF-κB subunits may provide insight into the pathogenesis of certain diseases. The purpose of this study was to determine if 1 month of a diabetic state, induced by streptozotocin (STZ) treatment, alters the constitutive level of NF-κB activation, its subunit composition, or the content of NF-κB-related proteins in rodent liver, kidney, spleen, and heart. Diabetes was induced in male Sprague–Dawley rats by a single tail vein injection of STZ (55 mg·kg–1 body weight). After 30 days, the heart, liver, spleen, and kidney were assessed for NF-κB activation and subunit composition with electrophoretic mobility shift assay (EMSA), and p50 and p65 subunit content was assessed with Western blotting. In diabetic animals, the constitutive level of NF-κB activation was reduced in liver, but was unchanged in kidney, spleen, and heart. EMSA supershifts showed the predominant subunit in the activated NF-κB complexes from both diabetic and control animals to be p50, although the p65 subunit was detected in NF-κB complexes from diabetic hearts. The content of p50 was unaltered in all diabetic tissues examined, whereas the content of p65 was increased only in hearts from diabetic animals. These findings support the idea that a diabetic state may induce specific changes in NF-κB subunit composition in certain tissues.

Heat shock treatment suppresses angiotensin II-induced activation of NF-κB pathway and heart inflammation: a role for IKK depletion by heat shock?

2004 ◽  
Vol 287 (3) ◽  
pp. H1104-H1114 ◽  
Author(s):  
Yu Chen ◽  
André-Patrick Arrigo ◽  
R. William Currie
Keyword(s):  
Angiotensin Ii ◽  
Heat Shock ◽  
Nuclear Translocation ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Mobility Shift ◽  
Iκb Kinase ◽  
Sprague Dawley Rats ◽  
Mobility Shift Assay ◽  
High Level

Heat shock (HS) proteins (Hsps) function in tissue protection through their chaperone activity and by interacting with cell signaling pathways to suppress apoptosis. Here, we investigated the effect of HS treatment on the nuclear factor (NF)-κB signaling pathway in the angiotensin II (ANG II) model of inflammation. Male Sprague-Dawley rats were divided into sham and HS-, ANG II-, and HS + ANG II-treated groups. HS treatment was administered 24 h before the initiation of ANG II infusion. HS treatment (42°C for 15 min) decreased 7-day ANG II-induced hypertension from 191 ± 4 to 147 ± 3 mmHg ( P < 0.01). Histological staining of hearts showed that HS treatment reduced ANG II-induced leukocyte infiltration, perivascular and interstitial inflammation, and fibrosis. Heart NF-κB nuclear translocation and activity, examined by Western blot analysis and electrophoretic mobility shift assay, was suppressed by HS treatment. HS treatment depleted IκB kinase-α (IKK-α) and phosphorylated IKK-α and suppressed the depletion of IκB-α and the accumulation of phosphorylated IκB-α. HS treatment blocked ANG II induced expression of IL-6 and ICAM-1 in the heart. ANG II and HS treatment induced high-level expression of Hsp27 and Hsp70 and their phosphorylation. Phosphorylated isoforms of Hsp27 and Hsp70 may play an important role in protecting the heart against ANG II-induced inflammation.

EFFECT OF EXPERIMENTALLY INDUCED THYROIDITIS ON BIOSYNTHESIS OF THYROXINE IN RATS

1969 ◽  
Vol 62 (1) ◽  
pp. 11-20 ◽  
Author(s):  
Colum A. Gorman ◽  
James W. Anderson ◽  
Eunice V. Flock ◽  
Charles A. Owen ◽  
Khalil G. Wakim
Keyword(s):  
Intravenous Administration ◽  
Hashimoto's Thyroiditis ◽  
Sprague Dawley ◽  
Thyroid Extract ◽  
Histologic Appearance ◽  
Gland Weight ◽  
Sprague Dawley Rats ◽  
Thyroid Glands ◽  
And Control ◽  
Experimentally Induced

ABSTRACT Thyroiditis was induced in Sprague-Dawley rats by repeated immunization with thyroid extract and Freund's adjuvant. Immunized and control animals were killed at intervals up to 6 hours after intravenous administration of 131I as iodide at 5, 8 and 10 weeks after the first injection. Radioiodinated compounds in the thyroid glands were identified chromatographically. Evidence of moderate thyroiditis was present (histologic appearance, gland weight, and protein-bound iodine-butanol-extractable iodine difference) but the rate of incorporation of radioiodide into thyroxine, the percentage of radioactivity in the gland as iodide, and the MIT/DIT ratio were not significantly different in immunized and control animals. The MIT/DIT ratio was found to vary with time after 131I administration in both immunized and control animals. These studies did not uncover a defect in organification of iodide in experimental thyroiditis similar to that described by others in humans with Hashimoto's thyroiditis.

scholarly journals Lodenafil treatment in the monocrotaline model of pulmonary hypertension in rats

2014 ◽  
Vol 40 (4) ◽  
pp. 421-424 ◽  
Author(s):  
Igor Bastos Polonio ◽  
Milena Marques Pagliareli Acencio ◽  
Rogério Pazetti ◽  
Francine Maria de Almeida ◽  
Bárbara Soares da Silva ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Experimental Model ◽  
Ventricular Hypertrophy ◽  
Right Heart Catheterization ◽  
Heart Catheterization ◽  
Sprague Dawley ◽  
Control Groups ◽  
Right Heart ◽  
Sprague Dawley Rats ◽  
And Control

We assessed the effects of lodenafil on hemodynamics and inflammation in the rat model of monocrotaline-induced pulmonary hypertension (PH). Thirty male Sprague-Dawley rats were randomly divided into three groups: control; monocrotaline (experimental model); and lodenafil (experimental model followed by lodenafil treatment, p.o., 5 mg/kg daily for 28 days) Mean pulmonary artery pressure (mPAP) was obtained by right heart catheterization. We investigated right ventricular hypertrophy (RVH) and IL-1 levels in lung fragments. The number of cases of RVH was significantly higher in the monocrotaline group than in the lodenafil and control groups, as were mPAP and IL-1 levels. We conclude that lodenafil can prevent monocrotaline-induced PH, RVH, and inflammation.

scholarly journals Synergistic suppression of pre-perfusion of donor livers with recipient serum and cobra venom factor treatment on hyperacute rejection following liver xenotransplantation

2012 ◽  
Vol 27 (5) ◽  
pp. 301-305 ◽  
Author(s):  
Baohua Zhu ◽  
Chuanming Tong ◽  
Weitao Guo ◽  
Rong Pu ◽  
Guoping Zhang ◽  
...  
Keyword(s):  
Survival Time ◽  
Hyperacute Rejection ◽  
Cobra Venom ◽  
Control Group ◽  
Sprague Dawley ◽  
Donor Liver ◽  
Cobra Venom Factor ◽  
Sd Rats ◽  
Sprague Dawley Rats ◽  
And Control

PURPOSE: To investigate synergistic suppression of donor liver pre-perfusion with recipient serum (RS) and cobra venom factor (CVF) treatment on hyperacute rejection (HAR) following liver xenotransplantation. METHODS: Guinea-pigs (GP, n=24) and Sprague-Dawley rats (SD, n=24) were recruited. Before transplantation, serum was collected from SD rats and used for preparation of inactivated complements. GP and SD rats were randomly assigned into four groups (n=6), respectively: RS group, CVF group, RS+CVF group and control group. Orthotopic liver xenotransplantation was performed with modified two-cuff technique. The survival time and liver function of recipients, morphological and pathological changes in rat livers were investigated. RESULTS: There was no piebald like change in the recipient livers in all experiment groups. The survival time of recipients in all experiment groups was longer than that in control group (p<0.05). Moreover, the survival time in the RS+CVF group was markedly longer than that in the RS group (p<0.01) and CVF group (p<0.05). The serum ALT level in all experiment groups were lower than that in the control group (p<0.05). Furthermore, the ALT level in the RS+CVF group was significantly lower than that in the CVF group (p<0.05) and RS group (p<0.01). The histological damages were significantly improved when compared with the control group, and the histological damages in the RS+CVF group were milder than those in the remaining groups (p<0.05) CONCLUSION: Pre-perfusion of donor liver with recipient serum and cobra venom factor treatment can exert synergistic suppressive effects on the hyperacute rejection following liver xenotransplantation.

Changes in total body calcium balance with exercise in the rat

1983 ◽  
Vol 55 (1) ◽  
pp. 201-204 ◽  
Author(s):  
A. D. LeBlanc ◽  
H. J. Evans ◽  
P. C. Johnson ◽  
S. Jhingran
Keyword(s):  
Least Squares ◽  
Voluntary Exercise ◽  
Calcium Balance ◽  
Sprague Dawley ◽  
Total Body Calcium ◽  
Sprague Dawley Rats ◽  
Least Squares Fit ◽  
Significant Change ◽  
Total Body ◽  
And Control

The purpose of this study was to evaluate the effect of deconditioning on the total body calcium in rats. Two separate experiments were performed using female Sprague-Dawley rats, 187-266 days of age. Total body calcium was measured in experimental and control rats during and following several weeks of voluntary exercise. The slope from the least-squares fit of total body calcium with time was used to obtain an average calcium balance for each animal during each study period. In both groups the exercised rats had a significantly decreased calcium balance after cessation of exercise, whereas no significant change was seen in nonexercised controls. In both groups, the exercised animals gained calcium at a significantly greater rate than controls. Our findings indicate that while exercised rats may gain calcium at a faster rate compared with nonexercising controls, the rate of gain following cessation of exercise is less than the controls.

scholarly journals TRANSFERSOME GEL FORMULATION OF AN ETHANOL EXTRACT OF APPLES (MALUS DOMESTICA MILL) CONTAINING ANTIOXIDANTS AND IN VITRO PENETRATION TESTING USING FRANZ DIFFUSION CELLS

2017 ◽  
Vol 9 ◽  
pp. 32 ◽  
Author(s):  
Nurarita Fadila Zesiorani ◽  
Effionora Anwar
Keyword(s):  
Ethanol Extract ◽  
Sprague Dawley ◽  
Diffusion Cells ◽  
Sprague Dawley Rats ◽  
Apple Peel ◽  
Franz Diffusion Cells ◽  
Drug Efficiency ◽  
And Control ◽  
Peel Extract

Objective: This study aims to formulate and characterize a transfersome apple peel extract, formulate it into a gel, and compare it with a control gelmade without transfersome.Methods: Both gels were evaluated, stability tested, and penetration tested using Franz diffusion cells on the skin of female Sprague-Dawley rats. Thetransfersome preparations were formulated with different concentrations of the active substance, quercetin: 0.5% (F1); 0.7% (F2), and 1.0% (F3).Results: Based on the characterization results, F1 was selected as the optimum gel formulation because it had spherical morphology, a Dmean volume of106.44±2.70 nm, a polydispersity index of 0.078±0.01, a zeta potential of −49.96±2.05 mV, and a drug efficiency entrapment percentage of 78.78±0.46%.The cumulative amount of quercetin that was penetrated with the transfersome gel was 1514.41±26.31 μg/cm2, whereas the penetration with thecontrol gel extract was 1133.62±18.96 μg/cm2. The cumulative percentages of the penetrated gel transfersome and gel extract were 78.40±1.89%and 49.89±0.88%, respectively. The fluxes of transfersome gel and control gel extract were 52.33±0.11 μg/cm²/hrs and 40.89±0.68 μg/cm²/hrs,respectively.Conclusions: Based on these results, it can be concluded that the gel with transfersome exhibited better penetration than the gel extract alone.

Lung Cancer Incidence After Exposure of Rats to Low Doses of Radon: Influence of Dose Rate

1994 ◽  
Vol 56 (1-4) ◽  
pp. 93-97 ◽  
Author(s):  
J.P. Morlier ◽  
M. Morin ◽  
G. Monchaux ◽  
P. Fritsch ◽  
J.F. Pineau ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dose Rate ◽  
Cancer Incidence ◽  
Lung Cancer Incidence ◽  
Sprague Dawley ◽  
Survival Times ◽  
Radon Exposure ◽  
Sprague Dawley Rats ◽  
Low Levels ◽  
And Control

Abstract To study the effect on lung cancer incidence of a long exposure to low levels of radon, 500 male 3-month-old Sprague-Dawley rats, were exposed to a cumulative dose of 25 WLM of radon and its daughters, 6 hours a day, 5 days a week, during 18 months. Exposure conditions were controlled in order to maintain a defined PAEC: 42 x 10-6 J.m-3 (2 WL), in the range of domestic and environmental exposures. Animals were kept until they died or given euthanasia when moribund. Mean survival times were similar in both irradiated and control groups: 828 days (SD = 169) and 830 days (SD = 137), as well as lung cancer incidence, 0.60% at 25 WLM and 0.63% for controls. The incidence of lung lesions was compared statistically with controls and those previously obtained at cumulative exposures of 25 and 50 WLM delivered over a 4-6 month period, inducing a significant increase of lung cancer, 2.2% and 3.8% respectively. Such a comparison showed a decreased lung cancer incidence related to a decrease in the dose rate for low levels of radon exposure.

scholarly journals Chronic Microcystin-LR Exposure Induces Hepatocarcinogenesis via Increased Gankyrin in Vitro and in Vivo

2018 ◽  
Vol 49 (4) ◽  
pp. 1420-1430 ◽  
Author(s):  
Lixiong He ◽  
Yujing Huang ◽  
Qiaonan Guo ◽  
Hui Zeng ◽  
Chuanfen Zheng ◽  
...  
Keyword(s):  
Low Dose ◽  
Soft Agar ◽  
Tumor Formation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
L02 Cells ◽  
Insight Into

Background/Aims: Our recent study indicated that the serum microcystin-LR (MC-LR) level is positively linked to the risk of human hepatocellular carcinoma (HCC). Gankyrin is over-expressed in cancers and mediates oncogenesis; however, whether MC-LR induces tumor formation and the role of gankyrin in this process is unclear. Methods: We induced malignant transformation of L02 liver cells via 35 passages with exposure to 1, 10, or 100 nM MC-LR. Wound healing, plate and soft agar colony counts, and nude mice tumor formation were used to evaluate the tumorigenic phenotype of MC-LR-treated cells. Silencing gankyrin was used to confirm its function. We established a 35-week MC-LR exposure rat model by twice weekly intraperitoneal injection with 10 μg/kg body weight. In addition, 96 HCC patients were tested for tumor tissue gankyrin expression and serum MC-LR levels. Results: Chronic low-dose MC-LR exposure increased proliferation, mobility, clone and tumor formation abilities of L02 cells as a result of gankyrin activation, while silencing gankyrin inhibited the carcinogenic phenotype of MC-LR-treated cells. MC-LR also induced neoplastic liver lesions in Sprague-Dawley rats due to up-regulated gankyrin. Furthermore, a trend of increased gankyrin was observed in humans exposed to MC-LR. Conclusion: These results suggest that MC-LR induces hepatocarcinogenesis in vitro and in vivo by increasing gankyrin levels, providing new insight into MC-LR carcinogenicity studies.

scholarly journals Mumefural Improves Blood Flow in a Rat Model of FeCl3-Induced Arterial Thrombosis

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3795
Author(s):  
Jihye Bang ◽  
Won Kyung Jeon
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Rat Model ◽  
Arterial Thrombosis ◽  
Thrombus Formation ◽  
Sprague Dawley ◽  
Fiber Damage ◽  
Sprague Dawley Rats ◽  
Related Proteins

Mumefural (MF), a bioactive component of the processed fruit of Prunus mume Sieb. et Zucc, is known to inhibit platelet aggregation induced by agonists in vitro. In this study, we investigated the anti-thrombotic effects of MF using a rat model of FeCl3-induced arterial thrombosis. Sprague–Dawley rats were intraperitoneally injected with MF (0.1, 1, or 10 mg/kg) 30 min before 35% FeCl3 treatment to measure the time to occlusion using a laser Doppler flowmeter and to assess the weight of the blood vessels containing thrombus. MF treatment significantly improved blood flow by inhibiting occlusion and thrombus formation. MF also prevented collagen fiber damage in injured vessels and inhibited the expression of the platelet activation-related proteins P-selectin and E-selectin. Moreover, MF significantly reduced the increased inflammatory signal of nuclear factor (NF)-κB, toll-like receptor 4 (TLR4), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 in blood vessels. After administration, MF was detected in the plasma samples of rats with a bioavailability of 36.95%. Therefore, we suggest that MF may improve blood flow as a candidate component in dietary supplements for improving blood flow and preventing blood circulation disorders.

scholarly journals Antiapoptosis and Antifibrosis Effects of Qishen Granules on Heart Failure Rats via Hippo Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Jian Zhang ◽  
Junjie Liu ◽  
Sheng Gao ◽  
Weili Lin ◽  
Pengrong Gao ◽  
...  
Keyword(s):  
Heart Failure ◽  
Hippo Pathway ◽  
Underlying Mechanism ◽  
Sprague Dawley ◽  
Artery Ligation ◽  
Regulatory Pathways ◽  
Sprague Dawley Rats ◽  
The Hippo Pathway ◽  
Related Proteins ◽  
P 53

Qishen granules (QSG) are a famous formula with cardioprotective properties to heart failure (HF). The aim of this study was to investigate the underlying mechanism of QSG on apoptosis and fibrosis in the treatment of HF. HF model was induced by left anterior descending artery ligation on Sprague-Dawley rats. Transcriptome analysis was used to investigate the regulatory pathways of QSG on HF. Interestingly, downregulated genes of QSG were significantly enriched in Hippo pathway which plays a crucial role in regulating cell apoptosis and proliferation. We found that QSG inhibited the expressions of proapoptotic key proteins P-53 and fibrosis-related proteins TGF-β1, SMAD3, and CTGF. Further, we conducted research on the key proteins in the Hippo pathway upstream of CTGF and P-53. The results showed that MST1, P-MST1, P-LATS1, and RASSF1A that exert proapoptotic function were downregulated after QSG intervention. Similarly, P-YAP and P-TAZ, mediating self-degradation and apoptosis, were both observably decreased after QSG administration. Taken together, QSG are shown to be likely to exert cardioprotective effects by inhibiting the progression of apoptosis and fibrosis through Hippo pathway.

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