Examination of exercise-induced accommodation in the transcription control of the heat shock protein (HSP7O) and biophylaxis function
| Project/Area Number |
14580062
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
体育学
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| Research Institution | Nippon Medical School |
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Principal Investigator |
MIKAMI Toshio Nippon Medical School, Department of Health and Sports Science, Assistant Professor, 医学部, 助教授 (60199966)
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| Co-Investigator(Kenkyū-buntansha) |
OHTA Shijeo Nippon Medical School, Institute of Gerontology, Department of Biochemistry and Cell Biology, Professor, 大学院・医学研究科, 教授 (00125832)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2002: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | heat shock protein 70 / stress resistance / skeletal muscle damage / β-glucuronidase / creatine kinase / primary culture / exercise training / lactate dehydrogenase / ストレス抵抗性 / β-グルクロニダーゼ活性 / クレアチンキナーゼ活性 / LDH / 伸長性筋収縮 |
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| Research Abstract |
At 2003 years, we investigated the inhibitory effects of heat shock protein 70 (HSP7O) on in vivo skeletal muscle damage induced by exercise. For this purpose, ICR male mice were exposed to heat environment (42℃) for 30 min one day before treadmill running. This heat exposure induced to the increase of HSP70 in skeletal muscle (soleus and extensor digitrium longus (EDL). Twenty-four hours after heat exposure, both heat-exposed and non-heat-exposed mice were performed 60 min of down-hill running on treadmill. Plasma creatine kinase actitity at 12 h after down-hill running was significantly lower in heat-exposed mice than in non-heat-exposed mice. The increase of β-glucuronidase activities in soleus and EDL muscle were significantly lower in heat-exposed than non-heat-exposed, too. In addition, the level of muscle damage, which was histochemically determined by HE stain, was obviously severe in non-heat-exposed mice. These findings suggested that heat exposure prior to exercise inhibit t
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he level of muscle damage induced by exercise and that this inhibitory effects my be related to the increase of skeletal muscle HSP70 induced by heat exposure. At 2004 years, to investigate whether the exercise training may enhance stress-resistance, we performed the cellular experiment using the primary culture of hepatocytes. Male wistar rats, aged 10 wk, were randomly divided two groups, sedentary and exercise-trained rats. Exercise-trained rats were performed 60 min of running exercise on treadmill for 8 wk. Eight weeks later, hepatocytes were isolated from both groups of rats by collagenase perfursion method. To separate intact cells from injured cells, isoltaed hepatocytes were applied on percoll density gradient. Collected intact hepatocytes were primary cultured in medium containing 10% fatal bovine serum for 48 h. After fourty-eight hour of culture, this cultured hepatocytes were incubated in medium contained hydrogen peroxide for 6 h. Hydrogen peroxide resulted in the decrease of cell viability and the increase of LDH released into the medium from hepatcytes. In these parameters, there was less changed in hepatocytes derived from exercise-trained rats than that of sedentary rats. In addition, induction of HSP7O was significantly higher in hepatocytes derived from exercise-trained rats than in that of sedentary rats. These findings suggested that exercise training led to the enhancement of stress resistance by improvement of HSP7O induction. Less
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Report
(3 results)
Research Products
(4 results)
