BACKGROUND AND OBJECTIVES: Amiodarone (AM), one of the most commonly prescribed antiarrhythmics, is frequently associated with thyroid dysfunction. Green tea extract (GTE) supplementation would attenuate oxidative stress and activate progenitor cells. However, the potential toxicity of GTE on various organs when administered at high doses has not been completely investigated. The present study aimed at investigating the possible relation between endogenous stem cells and GTE in overconsumption and AM induced thyroid damage in albino rat. METHODS AND RESULTS: Twenty four male albino rats were divided into control group, GTE group (rats given 50 mg/kg), Overconsumption group (rats given 1,000 mg/kg GTE), AM group (rats given 30 mg/kg) and combined AM, GTE therapy group. AM and GTE were administered orally 5 days/week for 8 weeks. Serological tests were performed. Thyroid sections were exposed to histological, immunohistochemical and morphometric studies. In overconsumption group, multiple distorted follicles with cellular debris in the lumen and multiple follicles devoid of colloid were found. In AM group, multiple follicles exhibiting crescent of colloid and few follicles devoid of colloid were detected. In combined therapy group, multiple follicles were filled with colloid. Significant decrease in area of colloid and significant increase in the area% of collagen were recorded in overconsumption and AM groups. Area% of CD 105 +ve cells denoted significant increase in combined therapy group. Serological tests were confirmative. CONCLUSIONS: Endogenous SCs activation was proved in AM and GTE combined therapy group with regression of AM induced morphological, morphometric and serological changes. However, overconsumption of GTE recruited endogenous SCs suppression.
Amiodarone* ; Animals ; Collagen ; Colloids ; Humans ; Male ; Mesenchymal Stromal Cells ; Oxidative Stress ; Rats* ; Serologic Tests ; Stem Cells* ; Tea* ; Thyroid Gland*

BACKGROUND AND OBJECTIVES: The myocyte death that follows intestinal ischemia reperfusion (I/R) injury is a major factor contributing to high mortality and morbidity in ischemic heart disease. The purpose of stem cell (SC) therapy for myocardial infarction is to improve clinical outcomes. The present study aimed at investigating the possible therapeutic effect of intravenous human cord blood mesenchymal stem cells (HCBMSCs) on intestinal ischemia reperfusion induced cardiac muscle injury in albino rat. METHODS AND RESULTS: Thirty male albino rats were divided equally into control (Sham-operated) group, I/R group where rats were exposed to superior mesenteric artery ligation for 1 hour followed by 1 hour reperfusion. In SC therapy group, the rats were injected with HCBMSCs into the tail vein. The rats were sacrificed four weeks following therapy. Cardiac muscle sections were exposed to histological, histochemical, immunohistochemical and morphometric studies. In I/R group, multiple fibers exhibited deeply acidophilic sarcoplasm with lost striations and multiple fibroblasts appeared among the muscle fibers. In SC therapy group, few fibers appeared with deeply acidophilic sarcoplasm and lost striations. Mean area of muscle fibers with deeply acidophilic sarcoplasm and mean area% of fibroblasts were significantly decreased compared to I/R group. Prussion blue and CD105 positive cells were found in SC therapy group among the muscle fibers, inside and near blood vessels. CONCLUSIONS: Intestinal I/R induced cardiac muscle degenerative changes. These changes were ameliorated following HCBMSC therapy. A reciprocal relation was recorded between the extent of regeneration and the existence of undifferentiated mesenchymal stem cells.
Animals ; Blood Vessels ; Fetal Blood ; Fibroblasts ; Humans ; Ischemia* ; Ligation ; Male ; Mesenchymal Stromal Cells ; Mesenteric Artery, Superior ; Mortality ; Muscle Cells ; Muscles ; Myocardial Infarction ; Myocardial Ischemia ; Myocardium ; Rats ; Regeneration ; Reperfusion* ; Stem Cells* ; Veins