Parisa Habibi

Transplantation of interscapular brown adipose tissue in rats

Background: the activity of brown adipose tissue (BAT) – a highly metabolic tissue – has a magnificent role in the management of metabolic diseases such as obesity and diabetes and numerous researchers have attempted to increase BAT via different methods including transplantation of BAT in animal models. Aims: to describe the protocol of the BAT transplantation in rats, as an animal model for studies about elevated BAT. Methods: twenty female Wistar rats were randomly divided in two groups (donor and recipient). Interscapular BAT (iBAT) were carefully removed from donors and transplanted into the interscapular region of the recipient rats, subcutaneously. To approve the successfulness of the operation, expression of the UCP1 mRNA and histological changes were evaluated in the grafts two months after surgery. Results: all operated rats have survived and fifty percent of the operations were successful. Conclusion: transplantation of BAT following this procedure in rats could be used as an acceptable animal model to investigate multiple aspects of elevated BAT.

Apoptosis and Histopathology of the Heart after Renal Ischemia-Reperfusion in Male Rat Running title: Ischemia-Reperfusion Injury

Ischemia-reperfusion injury was seen in strokes, myocardial infarctions, acute kidney injury, mesenteric ischemia, liver and systemic shock. Renal ischemia-reperfusion is more importance in the setting of kidney transplantation that affects distant organs. In this study forty Male Albino Wistar rats (200-250g) were randomly divided in four group (n=10) including control, sham operation group, nephrectomy and IRI group. All rats anesthetized with intraperitoneal injection of ketamine (50 mg/kg) and xylazine (10 mg/kg) and maintained the core body temperature at approximately 37°C. For inducing IRI group, it was performed right nephrectomy, and in continuing, the left kidney pedicle occluded to 45 min via nontraumatic microvascular clamp for making ischemia that followed 24 hours reperfusion. TUNEL assay was used to detect the cardiac apoptotic cells. Hematoxylin-Eosin staining and periodic acid-Schiff (PAS) procedure was used to histopathological assessment and glycogen accumulation respectively. There was more heart damage at 24 h reperfusion in IRI group. Renal IRI group showed myocardial degeneration, necrosis and increasing connective tissue in myofibril. There were apparent hypertrophy and swelling of myofibril, fragmentation and vacuolization of sarcoplasm. In addition, it was shown elevated apoptotic cell at 24 hours reperfusion in renal IRI group than sham group. There were increases of glycogen accumulation in cardimyocyte of renal IRI group. Our findings suggest that renal IRI-induced cardiac damage, accompanied by an accumulation of glycogen granules, induced apoptosis and histological changes in cardiomyocytes.

Fibrotic and apoptotic markers alteration in ovariectomised rats: addition of swimming training preserves lung architecture

Abstract Context: The important role of exercise in pulmonary function during menopause is not well known. Oestrogen deficiency in ageing female mice is accompanied by increase in apoptotic markers such as caspase3 in the lung. Objective: The present study was designed to investigate whether swimming training will ameliorate fibrosis and apoptosis resolution in the ovariectomy-induced lung injury rats. Material and method: Thirty female rats were assigned to three groups (n = 10 in each group): sham; rats underwent bilateral laparotomy without ovariectomy, OVX; rats underwent bilateral ovariectomy, OVX.Exe; ovariectomised rats that underwent swimming training for eight weeks. At the end of eight weeks, the lungs were harvested and protein expressions in whole lung tissues were analysed by western blotting technique. Result: Analysis of proteins expression in the lung showed significant differences between exercise and ovariectomised group (p < .05). Conclusion: The present study indicates strong potential of exercise in experimental oestrogen deficiency-induced lung damage.