scholarly journals Late Administration of a Palladium Lipoic Acid Complex (POLY-MVA) Modifies Cardiac Mitochondria but Not Functional or Structural Manifestations of Radiation-Induced Heart Disease in a Rat Model

2017 ◽  
Vol 187 (3) ◽  
pp. 361 ◽  
Author(s):  
Vijayalakshmi Sridharan ◽  
John W. Seawright ◽  
Francis J. Antonawich ◽  
Merrill Garnett ◽  
Maohua Cao ◽  
...  
Keyword(s):  
Heart Disease ◽  
Lipoic Acid ◽  
Rat Model ◽  
Cardiac Mitochondria ◽  
Acid Complex ◽  
Radiation Induced

scholarly journals Investigation of the Antihypertrophic and Antifibrotic Effects of Losartan in a Rat Model of Radiation-Induced Heart Disease

2021 ◽  
Vol 22 (23) ◽  
pp. 12963
Author(s):  
Mónika Gabriella Kovács ◽  
Zsuzsanna Z. A. Kovács ◽  
Zoltán Varga ◽  
Gergő Szűcs ◽  
Marah Freiwan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Growth Factor ◽  
Rat Model ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Left Ventricular ◽  
Tissue Growth ◽  
Sprague Dawley ◽  
Radiation Induced

Radiation-induced heart disease (RIHD) is a potential late side-effect of thoracic radiotherapy resulting in left ventricular hypertrophy (LVH) and fibrosis due to a complex pathomechanism leading to heart failure. Angiotensin-II receptor blockers (ARBs), including losartan, are frequently used to control heart failure of various etiologies. Preclinical evidence is lacking on the anti-remodeling effects of ARBs in RIHD, while the results of clinical studies are controversial. We aimed at investigating the effects of losartan in a rat model of RIHD. Male Sprague-Dawley rats were studied in three groups: (1) control, (2) radiotherapy (RT) only, (3) RT treated with losartan (per os 10 mg/kg/day), and were followed for 1, 3, or 15 weeks. At 15 weeks post-irradiation, losartan alleviated the echocardiographic and histological signs of LVH and fibrosis and reduced the overexpression of chymase, connective tissue growth factor, and transforming growth factor-beta in the myocardium measured by qPCR; likewise, the level of the SMAD2/3 protein determined by Western blot decreased. In both RT groups, the pro-survival phospho-AKT/AKT and the phospho-ERK1,2/ERK1,2 ratios were increased at week 15. The antiremodeling effects of losartan seem to be associated with the repression of chymase and several elements of the TGF-β/SMAD signaling pathway in our RIHD model.

SU-E-T-312: Development of a Rat Model of Radiation-Induced Heart Disease Using SACRTD

2011 ◽  
Vol 38 (6Part15) ◽  
pp. 3559-3559
Author(s):  
S Sharma ◽  
V Sridharan ◽  
M Boerma ◽  
P Corry ◽  
E Moros
Keyword(s):  
Heart Disease ◽  
Rat Model ◽  
Radiation Induced

scholarly journals Dexrazoxane ameliorates radiation-induced heart disease in a rat model

Aging ◽  
2021 ◽  
Author(s):  
Long Li ◽  
Xiaoqi Nie ◽  
Peng Zhang ◽  
Yongbiao Huang ◽  
Li Ma ◽  
...  
Keyword(s):  
Heart Disease ◽  
Rat Model ◽  
Radiation Induced

Mitigation of Radiation-induced Gastrointestinal System Injury using Resveratrol or Alpha-lipoic Acid: A Pilot Histopathological Study

2020 ◽  
Vol 19 (4) ◽  
pp. 413-424
Author(s):  
Bagher Farhood ◽  
Gholamreza Hassanzadeh ◽  
Peyman Amini ◽  
Dheyauldeen Shabeeb ◽  
Ahmed Eleojo Musa ◽  
...  
Keyword(s):  
Lipoic Acid ◽  
Gamma Ray ◽  
Morphological Changes ◽  
Gastrointestinal System ◽  
Alpha Tocopherol ◽  
Whole Body ◽  
Histopathological Study ◽  
Alpha Lipoic Acid ◽  
Pilot Investigation ◽  
Radiation Induced

Aim: In this study, we aimed to determine possible mitigation of radiationinduced toxicities in the duodenum, jejunum and colon using post-exposure treatment with resveratrol and alpha-lipoic acid. Background: After the bone marrow, gastrointestinal system toxicity is the second critical cause of death following whole-body exposure to radiation. Its side effects reduce the quality of life of patients who have undergone radiotherapy. Resveratrol has an antioxidant effect and stimulates DNA damage responses (DDRs). Alpha-lipoic acid neutralizes free radicals via the recycling of ascorbic acid and alpha-tocopherol. Objective: This study is a pilot investigation of the mitigation of enteritis using resveratrol and alpha-lipoic acid following histopathological study. Methods: 60 male mice were randomly assigned to six groups; control, resveratrol treatment, alpha-lipoic acid treatment, whole-body irradiation, irradiation plus resveratrol, and irradiation plus alpha-lipoic acid. The mice were irradiated with a single dose of 7 Gy from a cobalt-60 gamma-ray source. Treatment with resveratrol or alpha-lipoic acid started 24 h after irradiation and continued for 4 weeks. All mice were sacrificed after 30 days for histopathological evaluation of radiation-induced toxicities in the duodenum, jejunum and colon. Results and Conclusion: Exposure to radiation caused mild to severe damages to vessels, goblet cells and villous. It also led to significant infiltration of macrophages and leukocytes, especially in the colon. Both resveratrol and alpha-lipoic acid were able to mitigate morphological changes. However, they could not mitigate vascular injury. Conclusion: Resveratrol and alpha-lipoic acid could mitigate radiation-induced injuries in the small and large intestine. A comparison between these agents showed that resveratrol may be a more effective mitigator compared to alpha-lipoic acid.

scholarly journals P1692 The past returns after 20 years: a case report

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S Habjan ◽  
D Cantisani ◽  
I S Scarfo` ◽  
M C Guarneri ◽  
G Semeraro ◽  
...  
Keyword(s):  
Heart Disease ◽  
Coronary Artery ◽  
Aortic Valve ◽  
Aortic Stenosis ◽  
Valvular Heart Disease ◽  
Radiation Treatment ◽  
Severe Aortic Stenosis ◽  
Aortic Valve Area ◽  
Radiation Induced ◽  
Valve Area

Abstract Introduction Radiation therapy is one of the cornerstones of treatment for many types of cancer. These patients can later in life develop cardiovascular complications associated with radiation treatment. Late cardiovascular effects of radiation treatment include coronary artery disease (CAD), valvular heart disease, congestive heart failure, pericardial disease and sudden death. The most common sign of radiation-induced valvular heart disease is the calcification of the intervalvular fibrosa between the aortic and mitral valve. Case presentation A 71-year-old male patient with a history of Non-Hodgkin lymphoma treated with radiotherapy and chemotherapy 20 years ago, CAD, arterial hypertension, diabetes type II, dyslipidemia, obesity and currently smoking presented in the emergency room in our medical facility with acute pulmonary edema. The patient had unstable angina pectoris in 2018, the coronary angiography showed two-vessel disease with a non-significant stenosis of the left main coronary artery (LMCA) and 70% stenosis of the left anterior descending artery (LAD), for which he refused the percutaneous coronary intervention. At the same time, a transthoracic echocardiography (TTE) showed severe aortic stenosis and moderately severe mitral stenosis, at that time the patient refused the operation. After the initial treatment for pulmonary edema, TTE and transesophageal echocardiography (TEE) were performed and showed a tricuspid aortic valve with calcification of the cusps and a very severe aortic stenosis (planimetric aortic valve area 0.74 cm², functional aortic valve area 0.55 cm², indexed functional aortic valve area 0.25 cm²/m², mean gradient 61 mmHg, peak gradient 100 mmHg, stroke volume (SV) 69 ml, stroke volume index (SVI) 31 ml/m², flow rate 221 ml/s, aortic annulus 20x26 mm). The left ventricle was severely dilated (end diastolic volume 268 ml) with diffuse hypokinesia and severe systolic dysfunction (ejection fraction 32%). We appreciated a calcification of the mitral-aortic intervalvular fibrosa and the mitral annulus, without mitral stenosis but with moderate mitral regurgitation. The calcification of the intervalvular fibrosa suggested our final diagnosis of radiation-induced valvular heart disease with a severe aortic stenosis in low-flow conditions. The patient was successfully treated with transcatheter aortic valve implantation (TAVI). Conclusion Radiation-induced heart disease is a common reality and is destinated to raise due to the increasing number of cancer survivors. Effects are seen also many years after the radiation treatment. The exact primary mechanism of radiation injury to the heart is still unknown. The treatment of radiation-induced valve disease is the same as the treatment of valve disease in the general population. Abstract P1692 Figure. Radiation-induced valvular heart disease

Fucoidan from Undaria pinnatifida prevents vascular dysfunction through PI3K/Akt/eNOS-dependent mechanisms in the l-NAME-induced hypertensive rat model

2016 ◽  
Vol 7 (5) ◽  
pp. 2398-2408 ◽  
Author(s):  
Xiaofei Li ◽  
Jian Li ◽  
Zhike Li ◽  
Ying Sang ◽  
Yunhui Niu ◽  
...  
Keyword(s):  
Heart Disease ◽  
Rat Model ◽  
Undaria Pinnatifida ◽  
Vascular Dysfunction ◽  
Hypertensive Rat ◽  
Scientific Advances

Despite major scientific advances in its prevention, treatment and care, hypertension remains a serious condition that might lead to long-term complications such as heart disease and stroke.

“Second hit” of Tsc2 gene in radiation induced renal tumors of Eker rat model

2002 ◽  
Vol 1236 ◽  
pp. 163-174 ◽  
Author(s):  
Okio Hino ◽  
Hiroaki Mitani ◽  
Junko Sakaurai
Keyword(s):  
Rat Model ◽  
Renal Tumors ◽  
Tsc2 Gene ◽  
Second Hit ◽  
Eker Rat ◽  
Radiation Induced

Abstract 381: Prolonged Renal Failure Leads to Reduced Number of Active Cardiac Mitochondria in a Rat Model for Long Term Chronic Kidney Disease

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Einat A Hertzberg-Bigelman ◽  
Michal Entin-Meer ◽  
Genya Aharon-Hananel ◽  
Ann Saada ◽  
Ran Levy ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Mitochondrial Dna ◽  
Kidney Disease ◽  
Cardiac Function ◽  
Rat Model ◽  
Dna Content ◽  
Cardiac Mitochondria ◽  
Mitochondrial Content ◽  
Mitochondrial Dna Content

Objectives - Cardiorenal syndrome type 4 is characterized by primary chronic kidney disease (CKD) leading to an impairment of cardiac function. We recently showed a reduced expression of several cardiac mitochondrial genes in short-term CKD rat model. We aimed to evaluate whether cardiac mitochondrial structure and function is modified in long-term CKD and if so, to characterize the potential associated mechanisms. Methods - Lewis rats underwent 5/6 nephrectomy for induction of CKD. Upon necroscopy, eight months later, cardiac sections were analyzed by histology and electron microscopy (EM). Mitochondrial DNA content was determined by the mitochondrial gene, cytochrome B. Mitochondrial content was assessed by citrate synthase (CS) activity in tissue homogenate and respiratory chain function was determined by the activity of complexes I-IV in isolated mitochondria. The levels of PGC1a, a transcription factor for mitochondrial biogenesis, Angiotensin II type 1 receptor and cytosolic cytochrome C were assayed by western blot. Cytokine serum profile was determined by microarray. Results - Long-term CKD leads to cardiac hypertrophy and increased interstitial fibrosis. EM analysis revealed a massive spatial disarrangement accompanied by a considerably increased volume of swollen-damaged mitochondria in CKD hearts (32±3%, n=5, 48±6%, n=4; respectively; p<0.05). Total mitochondrial DNA content was decreased in cardiac tissue of CKD rats. Concomitantly, active mitochondrial content was significantly reduced. Conversely, no differences were observed in respiratory chain enzymes’ functions (complexes I-IV) in isolated active mitochondria. Moreover, inflammatory response and activation of Renin-Angiotensin-Aldosterone-System (RAAS) were detected in the CKD setting. Conclusion - CKD results in a marked reduction of active mitochondria in the heart. Inflammatory cytokines and RAAS, may set a deleterious environment to cardiac mitochondria, as suggested in non-CKD models. The data may represent a significant milestone in the personalized medicine strategy for treating CKD patients who present with normal cardiac function accompanied by positive biomarkers for cardiac mitochondria damage.

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