分析异丙肾上腺素诱导的小鼠腓肠肌变化和血清乳酸脱氢酶表达。
Analysis of isoproterenol-induced changes in gastrocnemius muscle and serum lactate dehydrogenase expression in mice.
机构信息
Department of Biosciences, Himachal Pradesh University, Summer Hill, Shimla 171005, Himachal Pradesh, India.
出版信息
Singapore Med J. 2011 Apr;52(4):274-82.
INTRODUCTION
Beta-adrenergic agonists are highly abused by sportspeople for their muscle anabolic and lipolytic effects. Muscle growth effects are thought to result from beta-2 adrenoceptor activation. This study attempted to characterise muscle (gastrocnemius) tissue damage following the administration of isoproterenol.
METHODS
Adult male Balb-C mice were treated with a single oral dose of isoproterenol (100 mg/kg body weight) for 4, 8, 20, 48 and 72 hours. Control mice received equal doses of saline. The animals were killed at the respective stages, followed by the collection of gastrocnemius and blood. Serum was then separated from blood. Histopathology and lactate dehydrogenase (LDH) assays were performed.
RESULTS
Beta-adrenoceptor activation-induced histological changes began with structural aberrations, and ultimately resulted in myonecrosis and extensive degeneration within hours of the administration of isoproterenol. The effects of beta-agonist administration on muscle myofibre organisation were visible within four hours and became most prominent at 20 and 48 hours. Augmentation of more than 20 percent in muscle LDH activity was observed at 4, 8 and 72 hour stages, and was accompanied by a significant decline of 19 and 27 percent at 20 and 48 hour time points, respectively. Serum corroborated the above results.
CONCLUSION
Isoproterenol treatment produced considerable histopathological changes, including myonecrosis in mice gastrocnemius, resulting in a leaky sarcolemma and the release of marker enzyme, LDH into the serum (more evident after 20 and 48 hours). This suggests that isoproterenol promotes the process of necrosis in mice gastrocnemius at the concentration employed, which raises a significant question regarding the use and abuse of beta-agonists.
引言
β-肾上腺素能激动剂因其肌肉合成代谢和脂肪分解作用而被运动员高度滥用。肌肉生长作用被认为是由于β-2 肾上腺素能受体的激活。本研究试图描述异丙肾上腺素给药后肌肉(腓肠肌)组织损伤的特征。
方法
成年雄性 Balb-C 小鼠给予单次口服异丙肾上腺素(100mg/kg 体重),分别在 4、8、20、48 和 72 小时处死。对照组小鼠给予等量生理盐水。分别在相应阶段处死动物,收集腓肠肌和血液。然后从血液中分离血清。进行组织病理学和乳酸脱氢酶(LDH)检测。
结果
β-肾上腺素受体激活诱导的组织学变化始于结构异常,最终导致异丙肾上腺素给药后数小时内出现肌坏死和广泛变性。β-激动剂给药对肌肉肌纤维组织的影响在 4 小时内可见,并在 20 和 48 小时时最为明显。肌肉 LDH 活性增加超过 20%,在 4、8 和 72 小时时观察到,分别伴有 20 和 48 小时时的显著下降 19%和 27%。血清证实了上述结果。
结论
异丙肾上腺素治疗导致小鼠腓肠肌出现相当大的组织病理学变化,包括肌坏死,导致肌细胞膜渗漏和标记酶 LDH 释放到血清中(在 20 和 48 小时后更为明显)。这表明,在使用浓度下,异丙肾上腺素促进了小鼠腓肠肌的坏死过程,这对β-激动剂的使用和滥用提出了重大问题。