scholarly journals Analysis of the elotinib-regulated transcriptome in a rat model of diethylnitrosamine (DEN)-induced liver cirrhosis

Author(s):  
BC Fuchs
Keyword(s):  
Bone ◽  
2010 ◽  
Vol 46 ◽  
pp. S74-S75
Author(s):  
Xing Ma ◽  
Xiangdong Ma ◽  
Shengchun Wang ◽  
Jun Wang ◽  
Xiaoming Wu ◽  
...  

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Shereen Helmy ◽  
Doaa I Mohamed ◽  
Wesam Elbakly ◽  
Lobna F Abd Elaziz ◽  
Eman Khairy ◽  
...  

Abstract Background Liver cirrhosis is considered the terminal stage of many hepatic diseases of different etiologies. Liver cirrhosis was associated with increased incidence rates of some extrahepatic manifestations such as osteoporosis. Regardless of the liver disease etiology, the presence of cirrhosis implies a twofold risk of bone fractures higher than non-cirrhotic patients. The liver is the main storage depot for iron and is the primary organ that is responsible for clearing excess iron in conditions of iron overload. When the iron storage and antioxidant capacity of the liver is overwhelmed, iron overload can lead to marked oxidantmediated liver and bone injury and iron overload was a risk factor for osteoporosis via affecting osteoblast survival. Aim of the work to examine the possible protective effect of Deferoxamine (DFO) on liver cirrhosis rat model induced osteoporosis. Material and Method rats was divided into 4 groups Animal Groups: Naïve control, DFO-treated group, TAA-treated group received Thioacetamide (TAA) ip (200 mg/kg/rat) twice weekly for 12 weeks, TAA+DFO treated group received TAA intra-peritoneal in addition to DFO intraperitoneal injections (300 mg/kg/3 times/week, for the last 4 weeks of TAA injections. Results and Conclusion Deferoxamine produced significant improvement in bone mineralization alongside its significant effect on liver function test in a rat model of liver cirrhosis induced osteoporosis.


2010 ◽  
Vol 4 (1) ◽  
pp. 57-67 ◽  
Author(s):  
Shakir Ali ◽  
Ram Prasad ◽  
Mohammed Naime ◽  
Hina Zafar ◽  
Amena Mahmood ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Guolin Ma ◽  
Rongjie Bai ◽  
Huijie Jiang ◽  
Xuejia Hao ◽  
Zaisheng Ling ◽  
...  

Rationale and Objectives. To develop an optimal scanning protocol for multislice spiral CT perfusion (CTP) imaging to evaluate hemodynamic changes in liver cirrhosis with diethylnitrosamine- (DEN-) induced precancerous lesions.Materials and Methods. Male Wistar rats were randomly divided into the control group (n=80) and the precancerous liver cirrhosis group (n=40). The control group received saline injection and the liver cirrhosis group received 50 mg/kg DENi.p.twice a week for 12 weeks. All animals underwent plain CT scanning, CTP, and contrast-enhanced CT scanning. Scanning parameters were optimized by adjusting the diatrizoate concentration, the flow rate, and the delivery time. The hemodynamics of both groups was further compared using optimized multislice spiral CTP imaging.Results. High-quality CTP images were obtained with following parameters: 150 kV; 150 mAs; 5 mm thickness, 5 mm interval; pitch, 1; matrix,512×512; and FOV, 9.6 cm. Compared to the control group, the liver cirrhosis group had a significantly increased value of the hepatic arterial fraction and the hepatic artery perfusion (P<0.05) but significantly decreased hepatic portal perfusion and mean transit time (P<0.05).Conclusion. Multislice spiral CTP imaging can be used to evaluate the hemodynamic changes in the rat model of liver cirrhosis with precancerous lesions.


2011 ◽  
Vol 100 (2) ◽  
pp. 775-783 ◽  
Author(s):  
Kazuaki Taguchi ◽  
Mayumi Miyasato ◽  
Hiroshi Watanabe ◽  
Hiromi Sakai ◽  
Eishun Tsuchida ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Se Ho Kim ◽  
Jae Yeon Kim ◽  
Soo Young Park ◽  
Won Tae Jeong ◽  
Jin Man Kim ◽  
...  

Abstract Background Cholesterol accumulation and calcium depletion induce hepatic injury via the endoplasmic reticulum (ER) stress response. ER stress regulates the calcium imbalance between the ER and mitochondria. We previously reported that phosphatase of regenerating liver-1 (PRL-1)-overexpressing placenta-derived mesenchymal stem cells (PD-MSCsPRL−1) promoted liver regeneration via mitochondrial dynamics in a cirrhotic rat model. However, the role of PRL-1 in ER stress-dependent calcium is not clear. Therefore, we demonstrated that PD-MSCsPRL−1 improved hepatic functions by regulating ER stress and calcium channels in a rat model of bile duct ligation (BDL). Methods Liver cirrhosis was induced in Sprague–Dawley (SD) rats using surgically induced BDL for 10 days. PD-MSCs and PD-MSCsPRL−1 (2 × 106 cells) were intravenously administered to animals, and their therapeutic effects were analyzed. WB-F344 cells exposed to thapsigargin (TG) were cocultured with PD-MSCs or PD-MSCsPRL−1. Results ER stress markers, e.g., eukaryotic translation initiation factor 2α (eIF2α), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP), were increased in the nontransplantation group (NTx) compared to the control group. PD-MSCsPRL−1 significantly decreased ER stress markers compared to NTx and induced dynamic changes in calcium channel markers, e.g., sarco/endoplasmic reticulum Ca2+ -ATPase 2b (SERCA2b), inositol 1,4,5-trisphosphate receptor (IP3R), mitochondrial calcium uniporter (MCU), and voltage-dependent anion channel 1 (VDAC1) (*p < 0.05). Cocultivation of TG-treated WB-F344 cells with PD-MSCsPRL−1 decreased cytosolic calmodulin (CaM) expression and cytosolic and mitochondrial Ca2+ concentrations. However, the ER Ca2+ concentration was increased compared to PD-MSCs (*p  < 0.05). PRL-1 activated phosphatidylinositol-3-kinase (PI3K) signaling via epidermal growth factor receptor (EGFR), which resulted in calcium increase via CaM expression. Conclusions These findings suggest that PD-MSCsPRL−1 improved hepatic functions via calcium changes and attenuated ER stress in a BDL-injured rat model. Therefore, these results provide useful data for the development of next-generation MSC-based stem cell therapy for regenerative medicine in chronic liver disease.


2019 ◽  
Vol 97 (3) ◽  
pp. 423-434 ◽  
Author(s):  
Liangshuo Hu ◽  
Lin Su ◽  
Zhixia Dong ◽  
Yunhua Wu ◽  
Yi Lv ◽  
...  

2010 ◽  
Vol 4 (1) ◽  
pp. 57-67
Author(s):  
Shakir Ali ◽  
Ram Prasad ◽  
Mohammed Naime ◽  
Hina Zafar ◽  
Amena Mahmood ◽  
...  

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