热应激可减轻链脲佐菌素诱导的糖尿病大鼠指长伸肌骨骼肌萎缩。

Kouji Nonaka, S. Une, J. Akiyama
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引用次数: 7

摘要

为了研究热应激是否能减轻链脲霉素诱导的糖尿病大鼠指长伸肌(EDL)骨骼肌萎缩,将12周龄雄性Wistar大鼠随机分为4组(每组n = 6):对照组(Con)、热应激组(HS)、糖尿病组(DM)和糖尿病/热应激组(DM + HS)。腹腔注射链脲佐菌素(50 mg/kg)诱导糖尿病。HS组和DM + HS组小鼠下半身浸泡在42℃热水中30 min,诱导热应激;注射链脲佐菌素后第7天开始,每天1次,每周5次,连续3周。测定糖尿病大鼠和非糖尿病大鼠EDL肌的肌纤维横截面积;western blotting分析热应激蛋白(HSP) 72和HSP25的表达水平。热应激可减轻糖尿病大鼠的肌肉纤维萎缩。与DM组比较,DM + HS组HSP72、HSP25表达上调。我们的研究结果表明,热应激通过上调HSP72和HSP25的表达来减轻EDL肌肉的萎缩。
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Heat stress attenuates skeletal muscle atrophy of extensor digitorum longus in streptozotocin-induced diabetic rats.
To investigate whether heat stress attenuates skeletal muscle atrophy of the extensor digitorum longus (EDL) muscle in streptozotocin-induced diabetic rats, 12-week-old male Wistar rats were randomly assigned to four groups (n = 6 per group): control (Con), heat stress (HS), diabetes mellitus (DM), and diabetes mellitus/heat stress (DM + HS). Diabetes was induced by intraperitoneal injection of streptozotocin (50 mg/kg). Heat stress was induced in the HS and DM + HS groups by immersion of the lower half of the body in hot water at 42 °C for 30 min; it was initiated 7 days after injection of streptozotocin, and was performed once a day, five times a week for 3 weeks. The muscle fiber cross-sectional area of EDL muscles from diabetic and non-diabetic rats was determined; heat stress protein (HSP) 72 and HSP25 expression levels were also analyzed by western blotting. Diabetes-induced muscle fiber atrophy was attenuated upon heat stress treatment in diabetic rats. HSP72 and HSP25 expression was upregulated in the DM + HS group compared with the DM group. Our findings suggest that heat stress attenuates atrophy of the EDL muscle by upregulating HSP72 and HSP25 expression.
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来源期刊
Acta physiologica Hungarica
Acta physiologica Hungarica 医学-生理学
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