Rosmarinic Acid Potently Detoxifies Amylin Amyloid and Ameliorates Diabetic Pathology in a Transgenic Rat Model of Type 2 Diabetes

2021 ◽  
Author(s):  
Ling Wu ◽  
Paul Velander ◽  
Anne M. Brown ◽  
Yao Wang ◽  
Dongmin Liu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Rat Model ◽  
Rosmarinic Acid ◽  
Transgenic Rat ◽  
Transgenic Rat Model

1045: Pioglitazone Ameliorates Penile Corpora Veno-Occlusive Dysfunction (CVOD) in a Rat Model of Type 2 Diabetes

2005 ◽  
Vol 173 (4S) ◽  
pp. 283-284
Author(s):  
Istvan Kovanecz ◽  
Monica G. Ferrini ◽  
Hugo H. Davila ◽  
Jacob Rajfer ◽  
Nestor F. Gonzalez-Cadavid
Keyword(s):  
Type 2 Diabetes ◽  
Rat Model

Riluzole Exhibits No Therapeutic Efficacy on a Transgenic Rat model of Amyotrophic Lateral Sclerosis

2020 ◽  
Vol 17 (3) ◽  
pp. 275-285 ◽  
Author(s):  
Si Chen ◽  
Qiao Liao ◽  
Ke Lu ◽  
Jinxia Zhou ◽  
Cao Huang ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Motor Neurons ◽  
Rat Model ◽  
Microglial Activation ◽  
Transgenic Rat ◽  
Intragastric Administration ◽  
Behavioral Deficits ◽  
Als Patients ◽  
Lateral Sclerosis ◽  
Transgenic Rat Model

Background: Amyotrophic lateral sclerosis (ALS) is a neurological disorder clinically characterized by motor system dysfunction, with intraneuronal accumulation of the TAR DNAbinding protein 43 (TDP-43) being a pathological hallmark. Riluzole is a primarily prescribed medicine for ALS patients, while its therapeutical efficacy appears limited. TDP-43 transgenic mice are existing animal models for mechanistic/translational research into ALS. Methods: We developed a transgenic rat model of ALS expressing a mutant human TDP-43 transgene (TDP-43M337V) and evaluated the therapeutic effect of Riluzole on this model. Relative to control, rats with TDP-43M337V expression promoted by the neurofilament heavy subunit (NEF) gene or specifically in motor neurons promoted by the choline acetyltransferase (ChAT) gene showed progressive worsening of mobility and grip strength, along with loss of motor neurons, microglial activation, and intraneuronal accumulation of TDP-43 and ubiquitin aggregations in the spinal cord. Results: Compared to vehicle control, intragastric administration of Riluzole (30 mg/kg/d) did not mitigate the behavioral deficits nor alter the neuropathologies in the transgenics. Conclusion: These findings indicate that transgenic rats recapitulate the basic neurological and neuropathological characteristics of human ALS, while Riluzole treatment can not halt the development of the behavioral and histopathological phenotypes in this new transgenic rodent model of ALS.

scholarly journals Role of TLR4/MyD88/NF-κB signaling in heart and liver-related complications in a rat model of type 2 diabetes mellitus

2021 ◽  
Vol 49 (3) ◽  
pp. 030006052199759
Author(s):  
Jiajia Tian ◽  
Yanyan Zhao ◽  
Lingling Wang ◽  
Lin Li
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Signaling Pathway ◽  
Rat Model ◽  
Fasting Blood Glucose ◽  
Diabetic Rats ◽  
Primary Response ◽  
Monocyte Chemoattractant Protein 1

Aims To analyze expression of members of the Toll-like receptor (TLR)4/myeloid differentiation primary response 88 (MyD88)/nuclear factor (NF)-κB signaling pathway in the heart and liver in a rat model of type 2 diabetes mellitus (T2DM). Our overall goal was to understand the underlying pathophysiological mechanisms. Methods We measured fasting blood glucose (FBG) and insulin (FINS) in a rat model of T2DM. Expression of members of the TLR4/MyD88/NF-κB signaling pathway as well as downstream cytokines was investigated. Levels of mRNA and protein were assessed using quantitative real-time polymerase chain reaction and western blotting, respectively. Protein content of tissue homogenates was assessed using enzyme-linked immunosorbent assays. Results Diabetic rats had lower body weights, higher FBG, higher FINS, and higher intraperitoneal glucose tolerance than normal rats. In addition, biochemical indicators related to heart and liver function were elevated in diabetic rats compared with normal rats. TLR4 and MyD88 were involved in the occurrence of T2DM as well as T2DM-related heart and liver complications. TLR4 caused T2DM-related heart and liver complications through activation of NF-κB. Conclusions TLR4/MyD88/NF-κB signaling induces production of tumor necrosis factor-α, interleukin-6, and monocyte chemoattractant protein-1, leading to the heart- and liver-related complications of T2DM.

The effects of apelin treatment on a rat model of type 2 diabetes

2015 ◽  
Vol 60 (1) ◽  
pp. 94-100 ◽  
Author(s):  
Raziye Akcılar ◽  
Sebahat Turgut ◽  
Vildan Caner ◽  
Aydın Akcılar ◽  
Ceylan Ayada ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Rat Model

P3-328: Dissection of physiological and pathological phosphorylation in Axon transgenic rat model of neurofibrillary pathology

2006 ◽  
Vol 2 ◽  
pp. S471-S471
Author(s):  
Miroslava Pevalova ◽  
Jozef Hanes ◽  
Norbert Zilka ◽  
Ludmila Cuninkova ◽  
Martin Cente ◽  
...  
Keyword(s):  
Rat Model ◽  
Transgenic Rat ◽  
Neurofibrillary Pathology ◽  
Transgenic Rat Model

scholarly journals Combined Effects of a Dietary Fiber Mixture and Wheat Albumin in a Rat Model of Type 2 Diabetes Mellitus

2016 ◽  
Vol 62 (6) ◽  
pp. 416-424
Author(s):  
Kazuhiro KUBO ◽  
Ayano KOIDO ◽  
Misako KITANO ◽  
Hirotaka YAMAMOTO ◽  
Morio SAITO
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Dietary Fiber ◽  
Rat Model ◽  
Combined Effects
Sign in / Sign up

Export Citation Format

Share Document