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肌纤维凋亡发生在大鼠离心收缩后的炎症和再生阶段。

Myofiber apoptosis occurs in the inflammation and regeneration phase following eccentric contractions in rats.

机构信息

Department of Applied Physics and Chemistry, University of Electro-Communications, Chofu, Tokyo, 1828585, Japan.

出版信息

J Physiol Sci. 2009 Nov;59(6):405-12. doi: 10.1007/s12576-009-0049-3. Epub 2009 Jul 28.

Abstract

Eccentric contractions (ECC) induce myofibrillar collapse, edema, and inflammation in muscle cells. Although apoptosis of myonuclei following ECC is activated during the inflammatory phase, the apoptosis response of the regenerative phase remains to be elucidated. The aim of the present study was to determine the inflammatory and regenerative phase of the apoptosis responses induced by ECC. In anesthetized rats, the tibialis anterior muscles were subjected to ECC repeated 40 times, evoked by surface electric stimulation (100 Hz, 10 V) with mechanical muscle stretch. Apoptosis was examined in the control group and in groups 1, 3, 7, and 14 days after ECC (each group, n = 4-6). Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive myonuclei were assessed by further labeling with dystrophin staining and DAPI. The expression of proteins related to apoptosis (Bcl-2 and Bax) was examined by Western blot assay. At 1 and 3 days, focal edema and necrotic myofibers invaded by mononuclear phagocytes were present, whereas regenerated myofibers with central nuclei were detected at 7 and 14 days. The occurrence of TUNEL-positive myonuclei increased significantly at 7 (7.0 +/- 1.5%) and 14 days (5.6 +/- 0.6%) compared with control (0.9 +/- 0.5%). Further we found that myonuclear apoptosis was restricted to the subsarcolemmal space at 7 and 14 days and markedly absent from the central nucleus. The Bax/Bcl-2 ratio was significantly higher at 3 (4.5 +/- 0.9) and 7 days (3.4 +/- 0.5) after ECC. In conclusion, myofiber apoptotic responses following ECC are present not only in the inflammatory phase but also persist during the regenerative phase.

摘要

离心收缩(ECC)会导致肌纤维细胞中的肌原纤维崩溃、水肿和炎症。虽然 ECC 后炎症期会激活肌核凋亡,但再生期的凋亡反应仍有待阐明。本研究旨在确定 ECC 诱导的细胞凋亡的炎症和再生期。在麻醉大鼠中,通过表面电刺激(100 Hz,10 V)和机械肌肉拉伸,使胫骨前肌反复进行 40 次 ECC。在对照组和 ECC 后 1、3、7 和 14 天的各组(每组 n = 4-6)中检查凋亡。通过进一步用抗肌营养不良蛋白染色和 DAPI 标记,评估末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记(TUNEL)阳性肌核。通过 Western blot 检测法检查与凋亡相关的蛋白质(Bcl-2 和 Bax)的表达。在 1 天和 3 天,可见局灶性水肿和单核吞噬细胞浸润的坏死肌纤维,而在 7 天和 14 天则检测到具有中央核的再生肌纤维。与对照组(0.9 ± 0.5%)相比,TUNEL 阳性肌核在 7 天(7.0 ± 1.5%)和 14 天(5.6 ± 0.6%)时显著增加。此外,我们发现肌核凋亡仅局限于 7 天和 14 天的肌小节下空间,并且从中核明显缺失。ECC 后 3 天(4.5 ± 0.9)和 7 天(3.4 ± 0.5)的 Bax/Bcl-2 比值显著升高。总之,ECC 后肌纤维的凋亡反应不仅存在于炎症期,而且在再生期也持续存在。

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