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مجله پزشکی ارومیه، جلد ۲۸، شماره ۸، صفحات ۴۸-۵۴

عنوان فارسی Effect of betaine supplement on isoprenaline induced myocardial infarction and serum cathepsin G level in rat model
چکیده فارسی مقاله
Background & Aims: Myocardial infarction is one of the most common life threatening diseases in worldwide. Betaine is a safe and well tolerated compound that shows beneficial antioxidant and anti-inflammatory properties. Previous studies demonstrated, betaine reduce cardiovascular diseases but molecular mechanism of action did not known completely. Cathepsin G play pivotal role in tissue injury and inflammation. Hence, we hypothesized betaine protective effects mediated by cathepsin G enzyme.
Materials & Methods: To examine this hypothesis, an animal model of 48 Albino rats weighing 200 ± 10 g was used. Light – dark cycle, temperature, humidity of cage were controlled. Rats divided into G1, G2, and G3 Groups and received betaine in dosage 50, 150 and 250 mg/kg via gavage respectively. Deionized water administrated for control group in same conditions. After 60 days treatment, isoproterenol (100 mg/kg) used for induction of myocardial infarction and then anesthesia and sampling performed. Serum level of cardiac troponin I and cathepsin G were measured via ELISA test. Serum homocysteine level measured by auto analyzer. Statistical analyses were done using SPSS 23.
Results: Our results shows, homocysteine level in control, G1, G2, and G3 are 9.98 ± 3.27, 7.29 ± 1.79, 6.69 ± 2.55 and 2.88 ± 1.4 µmol/L respectively that reduced dose dependently. Betaine protect heart against isoproterenol induced myocardial infraction. Cardiac troponin level in control, G1, G2, and G3 are 285.59 ± 49.87, 159.4 ± 66.94, 199.15 ± 78.33 and 209.31 ± 86.66 respectively. Cathepsin G level did not changed significantly between groups.
Conclusion: These results demonstrated betaine have protective effects on isoprenaline-induced myocardial infraction but cathepsin G is not underlay molecular mechanism.
کلیدواژه‌های فارسی مقاله betaine، isoprenaline، myocardial infarction، cathepsin G، rat

عنوان انگلیسی Effect of betaine supplement on isoprenaline induced myocardial infarction and serum cathepsin G level in rat model
چکیده انگلیسی مقاله Background & Aims: Myocardial infarction is one of the most common life threatening diseases in worldwide. Betaine is a safe and well tolerated compound that shows beneficial antioxidant and anti-inflammatory properties. Previous studies demonstrated, betaine reduce cardiovascular diseases but molecular mechanism of action did not known completely. Cathepsin G play pivotal role in tissue injury and inflammation. Hence, we hypothesized betaine protective effects mediated by cathepsin G enzyme.
Materials & Methods: To examine this hypothesis, an animal model of 48 Albino rats weighing 200 ± 10 g was used. Light – dark cycle, temperature, humidity of cage were controlled. Rats divided into G1, G2, and G3 Groups and received betaine in dosage 50, 150 and 250 mg/kg via gavage respectively. Deionized water administrated for control group in same conditions. After 60 days treatment, isoproterenol (100 mg/kg) used for induction of myocardial infarction and then anesthesia and sampling performed. Serum level of cardiac troponin I and cathepsin G were measured via ELISA test. Serum homocysteine level measured by auto analyzer. Statistical analyses were done using SPSS 23.
Results: Our results shows, homocysteine level in control, G1, G2, and G3 are 9.98 ± 3.27, 7.29 ± 1.79, 6.69 ± 2.55 and 2.88 ± 1.4 µmol/L respectively that reduced dose dependently. Betaine protect heart against isoproterenol induced myocardial infraction. Cardiac troponin level in control, G1, G2, and G3 are 285.59 ± 49.87, 159.4 ± 66.94, 199.15 ± 78.33 and 209.31 ± 86.66 respectively. Cathepsin G level did not changed significantly between groups.
Conclusion: These results demonstrated betaine have protective effects on isoprenaline-induced myocardial infraction but cathepsin G is not underlay molecular mechanism.
کلیدواژه‌های انگلیسی مقاله

نویسندگان مقاله سروش قدرتی زاده | soroush ghodratizadeh
department of biochemistry, faculty of medicine, urmia university of medical sciences, urmia, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی ارومیه (Urmia university of medical sciences)

یوسف رسمی | yousef rasmi
department of biochemistry, faculty of medicine, urmia university of medical sciences, urmia, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی ارومیه (Urmia university of medical sciences)

mohammad hassan خادم انصاری | mohammad hassan khadem khadem ansari
department of biochemistry, faculty of medicine, urmia university of medical sciences, urmia, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی ارومیه (Urmia university of medical sciences)


نشانی اینترنتی http://umj.umsu.ac.ir/browse.php?a_code=A-10-3405-1&slc_lang=en&sid=fa
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زبان مقاله منتشر شده fa
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نوع مقاله منتشر شده پژوهشی(توصیفی- تحلیلی)
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