Cell Activation and Function Alteration in Rat Livers Induced by Repeated Aluminum Oxide Nanoparticles Exposure

2012 ◽  
Vol 486 ◽  
pp. 75-79
Author(s):  
Xiao Bo Li ◽  
Hao Zheng ◽  
Ran Liu ◽  
Ge Yu Liang
Keyword(s):  
Aluminum Oxide ◽  
Cell Activation ◽  
Control Group ◽  
Oxide Nanoparticles ◽  
Sprague Dawley ◽  
Aluminum Oxide Nanoparticles ◽  
Liver Macrophages ◽  
Sprague Dawley Rats ◽  
And Function ◽  
And Control

Liver is a major target of nanoparticles accumulation. Here we have analyzed the liver function and activation of liver macrophages, which are sensitive to alteration of liver internal environment after repeated exposure to aluminum oxide nanoparticles. Sprague-Dawley rats where intraperitoneally injected very two days for 60 dyas with aluminum oxide nanoparticles (50mg/kg), non-nanoaluminum oxide (50mg/kg) and saline. After 60 days exposure, the concentrations of alanine aminotransferase and aspartic transaminase in plasma were significantly higher in nanoaluminum oxide group than non-nanoaluminum oxide and control groups. The number of ED-1+and GFAP+cells in liver of nanoaluminum oxide and non-nanoaluminum oxide groups increased significantly than control group. Compared with non-nanoaluminum oxide, aluminum oxide nanoparticles display potential adverse effects on the hypatocytes and biliary tract of rat liver and less stimulus to macrophages in liver than non-nanoaluminum oxide. It is suggested that part aluminum oxide nanoparticles avoided from phagocytosis by liver macrophages. The effects of aluminum oxide nanoparticles exposure should be assessed for its potential hepatic toxicology.

scholarly journals Twenty-Eight-Day Repeated Inhalation Toxicity Study of Aluminum Oxide Nanoparticles in Male Sprague-Dawley Rats

2018 ◽  
Vol 34 (4) ◽  
pp. 343-354 ◽  
Author(s):  
Yong-Soon Kim ◽  
Yong-Hyun Chung ◽  
Dong-Seok Seo ◽  
Hyun-Sung Choi ◽  
Cheol-Hong Lim
Keyword(s):  
Aluminum Oxide ◽  
Toxicity Study ◽  
Oxide Nanoparticles ◽  
Inhalation Toxicity ◽  
Sprague Dawley ◽  
Aluminum Oxide Nanoparticles ◽  
Sprague Dawley Rats

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.

scholarly journals Experimental Study of the Effects of Hypoxia Simulator on Osteointegration of Titanium Prosthesis in Osteoporotic Rats

2021 ◽  
Author(s):  
Jiangfeng Liu ◽  
Huijun Kang ◽  
Jiangfeng Lu ◽  
Yike Dai ◽  
Fei Wang
Keyword(s):  
Control Group ◽  
Osteoporotic Bone ◽  
Mrna Levels ◽  
Micro Ct ◽  
Sprague Dawley ◽  
Pull Out ◽  
Sprague Dawley Rats ◽  
Bone To Implant Contact ◽  
Polymerase Chain ◽  
And Control

Abstract Purpose: Poor osseointegration is the key reason for implant failure after arthroplasty, whether in osteoporotic or normal bone conditions. To date, osseointegration remains a major challenge. Recent studies have shown that deferoxamine(DFO) can accelerate osteogenesis by activation of the hypoxia signal pathway. The purpose of this study is to test the following hypothesis: after knee replacement, intra-articular injection of DFO will promote osteogenesis and osseointegration with titanium prosthesis in the bones of osteoporotic rats.Materials and Methods: 90 female sprague-dawley rats were used for the experiment. Ovariectomy and knee arthroplasty were performed. Then, the rats were randomly divided into DFO and control group(n=40 per group). The two groups were treated by intraarticular injection of DFO and saline respectively. After 2 weeks, polymerase chain reaction(PCR) and immunohistochemistry were used to evaluate the levels of HIF-1a, VEGF and CD31. After 12 weeks, the specimens were examined by micro CT, biomechanics and histopathology to evaluate osteogenesis and osseointegration.Results: The results of PCR showed mRNA levels of VEGF and CD31 in DFO group were significantly higher than those in control group. The immunohistochemistry results indicated positive cell expressions of HIF-1a, VEGF and CD31 in DFO group were also higher. Compared to control group, the microCT parameters of BMD, BV/TV, TB.N, TB.Th were significantly higher. The maximal pull-out force and the bone-to-implant contact (BIC) value were also higher . Conclusions: The local administration of DFO which is used to activate HIF-1a signaling pathway can promote osteogenesis and osseointegration with the prosthesis in osteoporotic bone.

scholarly journals Curcumin Improves Pulmonary Hypertension Rats by Regulating Mitochondrial Function

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Jing Chen ◽  
Wen Jiang ◽  
Fei Zhu ◽  
Qiong Wang ◽  
Haiyan Yang ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Mitochondrial Function ◽  
Vascular Remodeling ◽  
Control Group ◽  
Sprague Dawley ◽  
Pulmonary Vascular Remodeling ◽  
Sprague Dawley Rats ◽  
Pulmonary Arterial ◽  
Toxicological Mechanism ◽  
And Function

Objective. To investigate the role of curcumin in regulating pathogenesis of pulmonary arterial smooth muscle cells (PASMCs) derived from pulmonary arterial hypertension (PAH) model. Methods. Male Sprague Dawley rats were injected with monocrotaline (MCT) to establish the PAH experimental model. The rats were divided into control group, MCT group, and curcumin group. At the end of the study, hemodynamic data were measured to determine pulmonary hypertension. Proliferation ability of PASMCs, a remodeling indicator of pulmonary artery and right ventricle, was detected. In addition, the morphology and function of mitochondria, antiglycolysis and antiproliferation pathways, and genes were also analyzed. Results. Curcumin may function by reversing MCT-mediated pulmonary vascular remodeling in rats. Curcumin effectively improved pulmonary vascular remodeling, promoted PASMC apoptosis, and protected mitochondrial function. In addition, curcumin treatment suppressed the PI3K/AKT pathway in PASMCs and regulated the expression of antiproliferative genes. Conclusion. Curcumin can improve energy metabolism and reverse the process of PAHS. However, there were side effects of curcumin in MCT-induced rats, suggesting that the dosage should be treated with caution and its toxicological mechanism should be further studied and evaluated.

scholarly journals The Effects of L-Arginine on Liver Damage in Experimental Acute Cholestasis an Immunohistochemical Study

HPB Surgery ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Yucel Ozsoy ◽  
Mustafa Ozsoy ◽  
Teoman Coskun ◽  
Kemal Namlı ◽  
Ahmet Var ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Damage ◽  
Biliary Obstruction ◽  
Hepatic Tissue ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Duct Ligation ◽  
And Control ◽  
Acute Cholestasis

Obstructive jaundice damages critical functions in the liver. Nitric oxide modulation would influence liver damage induced by biliary obstruction, and little is known about it Acute cholestasis was induced by bile duct ligation (BDL) in two groups of male Sprague-Dawley rats. L-Arginine or serum physiologic was administered to treatment and control group. Histopathological and immunohistochemical iNOS expression was investigated in hepatic tissue. Plasma enzyme activities were increased in acute cholestasis, and that L-arginine treatment partially but significantly prevented the elevation of these markers of liver damage (P< .05). Also histopathology scoring showed that the liver injury was prevented and immunohistochemical iNOS activity was increased significantly in L-arginine group (P< .05). This study shows that, after 7 days of biliary obstruction, liver damage is well established and exogenous L-arginine treatment partially but significantly prevented the liver injury in acute cholestasis.

scholarly journals Possible Association Between DHEA and PKCε in Hepatic Encephalopathy Amelioration: A Pilot Study

2021 ◽  
Vol 8 ◽  
Author(s):  
Alessandro Di Cerbo ◽  
Luca Roncati ◽  
Carlotta Marini ◽  
Gianluca Carnevale ◽  
Manuela Zavatti ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Neuroprotective Effect ◽  
Brain Area ◽  
Control Group ◽  
Sprague Dawley ◽  
Kinase C ◽  
Sprague Dawley Rats ◽  
Protein Kinase C Epsilon ◽  
Neuronal Functions ◽  
And Control

Objective: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome caused by liver failure and by an impaired neurotransmission and neurological function caused by hyperammonemia (HA). HE, in turn, decreases the phosphorylation of protein kinase C epsilon (PKCε), contributing to the impairment of neuronal functions. Dehydroepiandrosterone (DHEA) exerts a neuroprotective effect by increasing the GABAergic tone through GABAA receptor stimulation. Therefore, we investigated the protective effect of DHEA in an animal model of HE, and the possible modulation of PKCε expression in different brain area.Methods: Fulminant hepatic failure was induced in 18 male, Sprague–Dawley rats by i.p. administration of 3 g/kg D-galactosamine, and after 30 min, a group of animals received a subcutaneous injection of 25 mg/kg (DHEA) repeated twice a day (3 days). Exploratory behavior and general activity were evaluated 24 h and 48 h after the treatments by the open field test. Then, brain cortex and cerebellum were used for immunoblotting analysis of PKCε level.Results: DHEA administration showed a significant improvement of locomotor activity both 24 and 48 h after D-galactosamine treatment (****p &lt; 0.0001) but did not ameliorate liver parenchymal degeneration. Western blot analysis revealed a reduced immunoreactivity of PKCε (*p &lt; 0.05) following D-galactosamine treatment in rat cortex and cerebellum. After the addition of DHEA, PKCε increased in the cortex in comparison with the D-galactosamine-treated (***p &lt; 0.001) and control group (*p &lt; 0.05), but decreased in the cerebellum (*p &lt; 0.05) with respect to the control group. PKCε decreased after treatment with NH4Cl alone and in combination with DHEA in both cerebellum and cortex (****p &lt; 0.0001). MTS assay demonstrated the synergistic neurotoxic action of NH4Cl and glutamate pretreatment in cerebellum and cortex along with an increased cell survival after DHEA pretreatment, which was significant only in the cerebellum (*p &lt; 0.05).Conclusion: An association between the DHEA-mediated increase of PKCε expression and the improvement of comatose symptoms was observed. PKCε activation and expression in the brain could inhibit GABA-ergic tone counteracting HE symptoms. In addition, DHEA seemed to ameliorate the symptoms of HE and to increase the expression of PKCε in cortex and cerebellum.

scholarly journals Supplementation with Fermented Rice Bran Attenuates Muscle Atrophy in a Diabetic Rat Model

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2409 ◽  
Author(s):  
Tubagus Bahtiar Rusbana ◽  
Afifah Zahra Agista ◽  
Wahyu Dwi Saputra ◽  
Yusuke Ohsaki ◽  
Kouichi Watanabe ◽  
...  
Keyword(s):  
Muscle Atrophy ◽  
Rice Bran ◽  
Rat Model ◽  
Muscle Size ◽  
Diabetic Rat ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
And Control ◽  
Diabetic Rat Model

Fermented rice bran (FRB), a prospective supplement, has been proven to ameliorate certain medical conditions. However, its nutraceutical effect on muscle atrophy has never been investigated. The present study aimed to evaluate the effect of FRB on muscle atrophy in a streptozotocin (STZ)-induced diabetic rat model. Three groups of Sprague-Dawley rats, namely the control, STZ, and FRB groups, were treated as follows. The diabetic groups (STZ and FRB) were injected intraperitoneally with STZ (40 mg/kg BW), whereas the control group was injected with the vehicle. The STZ and control groups were fed the AIN93M diet, and the FRB group was fed 10% of FRB based on the AIN93M diet. The diabetic groups had reduced muscle size compared to the control group; however, these changes were alleviated in the FRB group. Moreover, the FRB group had a significantly lower expression of FBXO32/Atrogin-1 and TRIM63/MuRF1 (p < 0.05) due to blocked NF-κB activation. In conclusion, the anti-inflammatory effect of FRB may be beneficial for ameliorating muscle atrophy in diabetic conditions.

Tetrahydroxystilbene glucoside improves the learning and memory of amyloid-β1–42-injected rats and may be connected to synaptic changes in the hippocampus

2012 ◽  
Vol 90 (11) ◽  
pp. 1446-1455 ◽  
Author(s):  
Lin Zhou ◽  
Ying Hou ◽  
Qidong Yang ◽  
Xiaoping Du ◽  
Min Li ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Treated Group ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Polygonum Multiflorum ◽  
Synaptic Structure ◽  
Sprague Dawley Rats ◽  
And Function ◽  
Synaptic Structures ◽  
And Control

The aim of this study was to evaluate the protective effects of 2,3,5,4′-tetrahydroxystilbene-2-O-β-d-glucoside (TSG), an active component extracted from Polygonum multiflorum, on learning/memory deficits in Alzheimer’s disease (AD). We randomly divided 24 male Sprague–Dawley rats among 4 groups: (i) the sham-operated group (control); (ii) sham-operated group also treated with TSG (sham+TSG); (iii) beta amyloid treated group (Aβ); and (iv) Aβ treatment group also treated with TSG (Aβ+TSG). Rats in the Aβ and Aβ+TSG groups were treated with Aβ1–42 intracerebroventricularly, whereas the control and sham+TSG groups were given phosphate-buffered saline. Rats in the sham+TSG and Aβ+TSG groups were then treated intragastrically with TSG (50 mg·(kg body mass)–1·day–1) for 4 weeks, and rats in the Aβ and control groups were treated with saline. The results from Morris water maze tests, electron microscopy, real-time polymerase chain reaction, and Western blotting demonstrated that Aβ1–42 induced impairment in learning and memory, degeneration in synaptic structures, and downregulation of Src and NR2B at the gene and protein level, respectively. These alterations were reversed by the administration of TSG, suggesting that TSG exerts anti-AD properties by protecting synaptic structure and function. TSG-induced upregulation of Src and NR2B may be responsible for this process.

scholarly journals Effect of Different Doses of Nitrate Supplements on hepatocellular Damage Markers in Male Sprague Dawley Rats Following One Session of Exercise

2020 ◽  
pp. 119-133
Keyword(s):  
Body Weight ◽  
Low Dose ◽  
Male Rats ◽  
Control Group ◽  
High Dose ◽  
Sprague Dawley ◽  
Hepatocellular Damage ◽  
Sprague Dawley Rats ◽  
And Control ◽  
Different Doses

Background: Hepatocellular damage caused by physical activity or the use of supplements is one of the serious problems facing athletes in various fields. This study aimed to evaluate the effect of different doses of nitric oxide supplements on AST and ALT liver enzymes and the ratio of AST to ALT following a session of eccentric exercise in Sprague Dawley male rats. Materials and Methods: In this study, 36 Sprague Dawley male rats (two months old) were divided into three groups of control, low dose (4.8 mg/kg body weight), and high dose of NO supplements (15.4 mg/kg body weight). Supplements were given to rats for seven days. Subsequently, all three groups of rats were forced to run on a treadmill for 45 min with a speed of 20 m/min, and a slope of -15 degrees. Blood samples were taken directly from cardiac puncture of rats 24 h after the running exercise. Blood serum variables of the study were measured afterward. Results: Low dose of nitrate supplements did not change AST and ALT indices, while the high dose of nitrate supplements increased ALT serum level and decreased AST to ALT ratio, compared to a low dose of NO supplements and control group. Conclusion: Based on the obtained results, the consumption of a low dose of NO supplements does not change hepatocellular damage markers, while the high dose of NO supplements causes degeneration of hepatic cells in athletes.

scholarly journals Effect of Experimentally Induced Hepatic and Renal Failure on the Pharmacokinetics of Topiramate in Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Kamal M. Matar ◽  
Yasin I. Tayem
Keyword(s):  
Renal Failure ◽  
Pharmacokinetic Profile ◽  
Treated Group ◽  
Time Profile ◽  
Control Group ◽  
Sprague Dawley ◽  
Elimination Phase ◽  
Sprague Dawley Rats ◽  
And Control ◽  
Control Plasma

We aimed to investigate the effect of induced hepatic and renal failure on the pharmacokinetics of topiramate (TPM) in rats. Twenty-four Sprague-Dawley rats were used in this study. Renal or hepatic failure was induced by a single i.p. dose of 7.5 mg/kg cisplatin (n=8) or 0.5 mL/kg carbon tetrachloride (CCl4) (n=8), respectively. Three days after cisplatin dose or 24 h after CCl4dose, the rats were administered a single oral dose of 20 mg/kg TPM. The plasma samples were quantified by LC-MS/MS method. Compared to control, plasma concentration-time profile in CCl4-treated and, to a lesser extent, in cisplatin-treated rats decreased more slowly particularly in the elimination phase. TPM oral clearance (CL/F) in CCl4-treated group was significantly lower than that in control (P<0.001), whereasAUC0−∞, T1/2, and Vd/F were significantly higher in CCl4-treated rats compared to the control (P<0.01). The CL/F was not significantly different between cisplatin-treated rats and control (P>0.05). However, in cisplatin-treated rats, the T1/2 and Vd/F were significantly higher than that in the control group (P<0.01). Both conditions failed to cause a significant effect onCmaxorTmax. The present findings suggest that induced hepatic or renal failure could modify the pharmacokinetic profile of TPM in the rat.

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