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Background and Objective: A brief and short duration episode of ischemia is recorded in ischemic preconditioning (IPC). This latter condition provides a status in which large region of heart is protected when prolonged ischemia occurred. Levothyroxine play a protective role in IPC induction, and simultaneously with stress oxidative. This study was conducted to determine the protective effect of levothyroxine with oxidative stress reduction mechanism in ischemic preconditioning model in rat heart.
Methods: This experimental study was performed on 30 male Wistar rats in three groups of 10, as follows. In the reperfusion ischaemia group (IR), the heart of the animal was placed in a Langendorff apparatus. In the ischemic preconditioning group (IPC), prior to major ischemia, was exposed to 4 periods of 5-minute ischemia with reperfusion. In the intraperitoneally administered group, levothyroxine at a dose of 25 microgram per 100 g of body weight, the heart was exposed to reperfusion ischemia. The area of infarct and the level of malondialdehyde in the heart tissue were measured.
Results: The volume of Infarcted region in IR and IPC groups was 26.55 and 11.11 respectively. The same index for the Levothyroxine receiver was 12.56. Based on these findings it was demonstrated that Levothyroxine injection reduced the Infarcted region significantly similar with IPC (P<0.05). The MDA Levels in IR and IPC were 1328 and 777, respectively and in Levothyroxine group it was determined as 762. The size of Infarcted region in both IPC and treated with Levothyroxine groups significantly reduced in compared to IR group (P<0.05).
Conclusion: Injection of levothyroxine with ischemic preconditioning reduced the effect of reperfusion maladaptive ischemia in rat heart.

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Background and Objective: Sodium levothyroxine is one of the common medicines used for treatment of hypothyroidism and thyroid cancer. The study was done to determine the effect of sodium levothyroxine on knee articular cartilage tidemark integrity, plateau tibia cartilage thickness (calcified and non-calcified) and liver enzymes in induced hypothyroidism rats.
Methods: In this experimental study, 50 adult female BALB/c mice, weighting 25-30 grams were randomly allocated into one control and four experimental groups. Animals in control did not receive any medicine. Animals in the second group were received different increasing doses of sodium levothyroxine daily for 8 weeks. Animals in the third group were received constantly high dose of levothyroxine daily for 8 weeks. In the fourth group, the animals became hypothyroid with propylthiouracil (PTU). In the fifth group, animals with hypothyroidism were received sodium levothyroxine by gavage same as group 2. After 8 weeks serum samples were taken to determine ALT, AST and ALP. The plateau tibia cartilage stained with hematoxylin-eosin. Histologic changes evaluated by light microscopy. Using a light microscope equipped with camera, the samples were photographed and using a computer equipped with axiovision software. Cartilage (calcified and non-calcified) thickness measured in micrometer. The integrity of tidemark line on hematoxylin-eosin staining also evaluated.
Results: The results of the present study showed separation, disruption and destruction in tidemark line in group 3 (the group with high dosage of sodium levothyroxine from the beginning of the treatment). The total cartilage and non-calcified part thickness in groups 3, 4, 5 were reduced and in group 3 showed significant reduction (P<0.05). Calcified cartilage thickness in all groups were reduced and in group 3 showed significant reduction (P<0.05). ALT level decreased in all groups compared to control group but only in the second and third groups, the decrease of ALT was significant (P<0.05). AST serum level in all groups significantly increased in compared to control group (P<0.05). ALP serum level in all groups increased compared to the control group, but this increase was significant only in the groups 4, 5.
Conclusion: Consumption of sodium levothyroxine with constantly high dose can cause severe alteration in knee joint cartilage in hypothyroidism rats.

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Background and Objective: Obesity is a well-known public health problem that affects people of all ages. It has myriad effects on several body tissues, including the thyroid, in both human and animal models. Some treatments, such as dietary modification and physical activity, may be effective or ineffective in reducing obesity. Accordingly, the present research investigated the effects of obesity on thyroid tissue and the impact of diet modification and aerobic exercises on histopathological and hormonal changes in the thyroid tissue of obese male rats.
Methods: In this experimental study, for obesity induction, 50 three-week-old male Wistar rats were exposed to a high-fat diet (including 40% fat, 40% protein, and 20% carbohydrate) for 12 weeks. Then, 25 rats were randomly divided into 5 groups: healthy control, obese + high-fat diet, obese + normal diet, obese + high-fat diet + aerobic, obese + normal diet + aerobic. After the induction of obesity, 2 groups were given a standard diet (including 20% fat, 10% protein, and 70% carbohydrates). Aerobic exercises for 8 weeks included 30 minutes per day, 8 m/min, and 5 days per week. After anesthesia, an autopsy was performed, and the thyroid tissue was sent to the laboratory for histopathological studies. Also, 5 cc of blood was taken to study TSH, T3, and T4 using a radioimmunoassay kit.
Results: The serum levels of TSH hormone increased slightly in the high-fat diet groups compared to the control group and the normal diet with/without aerobic activity group. Also, the amount of T3 hormone in the group receiving a normal diet along with aerobic activity was significantly lower than in the control, high-fat diet, and high-fat diet along with aerobic activity groups (P<0.05). The T4 hormone increased significantly in all obesity groups compared to the control group (P<0.05), and these values were at the level of the control group (P<0.05) only in the group receiving the normal diet along with aerobic activity. Regarding the histopathological results, many changes were found in the follicular, parafollicular, and follicle cells of the thyroid tissue in the obesity group continuing the high-fat diet; these changes were significantly reduced in the groups for which the diet was changed to the normal diet alone and with aerobic activity.
Conclusion: Induction of obesity causes significant structural and biochemical changes in the thyroid, and the combination of diet modification and aerobic activity is more effective in alleviating these changes.