Melatonin as a shield against skeletal muscle damage: A study on ischemia-reperfusion injury.

Ertan Demirdaş, Gökhan Arslan, Hakan Kartal, Gökhan Erol, Tayfun Özdem, Başak Büyük Yavuz, Celalettin Günay, Bilgehan Savaş Öz
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Abstract

We evaluated the protective effects of melatonin against skeletal muscle ischemia-reperfusion injury, a significant cause of skeletal muscle damage. Ischemia-reperfusion (I/R) injury occurs due to a temporary restriction of blood flow (ischemia) followed by its restoration (reperfusion), triggering oxidative stress, inflammation, and cell death. Although current treatments are limited, melatonin's antioxidant and anti-inflammatory properties suggest potential benefits.

Methods: We studied 30 male mice divided into five groups: control, melatonin control, I/R, melatonin + I/R, and dimethyl sulfoxide control. After the designated treatments, we assessed muscle tissue for antioxidant capacity (total antioxidant status [TAS]), oxidative stress markers (total oxidative status [TOS] and malondialdehyde [MDA]), inflammation (myeloperoxidase [MPO]), and cell death (terminal deoxynucleotidyl transferase dUTP nick-end labeling [TUNEL] assay and histological analysis).

Results: Melatonin significantly increased antioxidant capacity (TAS) compared to all other groups. Conversely, oxidative stress (TOS) was significantly lower in the melatonin + I/R group compared to the I/R group alone. Histological analysis revealed greater necrosis, edema, inflammation, and cell death in the I/R group compared to others. Interestingly, the melatonin + I/R group exhibited significantly less damage than the I/R group, highlighting melatonin's protective effect.

Conclusion: This study demonstrates that exogenous melatonin effectively reduces oxidative stress, inflammation, and cell death in skeletal muscle tissue subjected to I/R injury. These findings suggest that melatonin may be a promising therapeutic agent for mitigating I/R-induced complications in skeletal muscle injury.

褪黑素是骨骼肌损伤的防护盾:缺血再灌注损伤研究
我们评估了褪黑素对骨骼肌缺血再灌注损伤的保护作用,这是骨骼肌损伤的一个重要原因。缺血-再灌注(I/R)损伤的发生是由于血流暂时受限(缺血),随后血流恢复(再灌注),引发氧化应激、炎症和细胞死亡。虽然目前的治疗方法有限,但褪黑素的抗氧化和抗炎特性表明了潜在的益处。方法:将30只雄性小鼠分为5组:对照组、褪黑素对照组、I/R组、褪黑素+ I/R组和二甲亚砜对照组。在指定的处理后,我们评估了肌肉组织的抗氧化能力(总抗氧化状态[TAS])、氧化应激标志物(总氧化状态[TOS]和丙二醛[MDA])、炎症(髓过氧化物酶[MPO])和细胞死亡(末端脱氧核苷酸转移酶dUTP nick末端标记[TUNEL]测定和组织学分析)。结果:与其他各组相比,褪黑素显著提高抗氧化能力(TAS)。相反,与单独使用I/R组相比,褪黑素+ I/R组的氧化应激(TOS)显著降低。组织学分析显示,与其他组相比,I/R组的坏死、水肿、炎症和细胞死亡更严重。有趣的是,褪黑激素+ I/R组的损伤明显小于I/R组,这突出了褪黑激素的保护作用。结论:本研究表明外源性褪黑素可有效降低I/R损伤骨骼肌组织的氧化应激、炎症和细胞死亡。这些发现表明,褪黑素可能是一种有前景的治疗药物,可以减轻I/ r诱导的骨骼肌损伤并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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