Platelet-rich plasma ameliorates dexamethasone-induced myopathy by suppressing autophagy and enhancing myogenic potential through modulation of Myo-D, Pax-7, and myogenin expression

IF 2.7 4区 生物学 Q1 ANATOMY & MORPHOLOGY Tissue & cell Pub Date : 2024-11-05 DOI:10.1016/j.tice.2024.102602
Sally M. Safwat , Dalia M. Abdel Ghaffar , Mamdouh Eldesoqui , Sally Abdallah Mostafa , Eman A.E. Farrag , Fardous El-Senduny , Basma Osman , Eman Mohamad El Nashar , Shaker Hassan Alshehri , A. Alhefzi , Mohammed Saeed Alasmry , Omar Aboubakr Elnashar , Zienab Helmy Eldken
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引用次数: 0

Abstract

Background

Muscle tissue is essential for overall well-being that declines with age and different illnesses. Glucocorticoids, despite being efficient in treating inflammation, can induce muscle weakness (known as glucocorticoid-induced myopathy) by affecting protein breakdown and synthesis. Glucocorticoids have a negative impact on satellite cells, which play a role in muscle regeneration. Platelet rich plasma (PRP), containing concentrated growth factors, has a potential role in enhancing tissue repair and could be used to ameliorates combat muscle wasting caused by glucocorticoids.

Aim

The purpose of this study was to identify how PRP can affect dexamethasone-induced myopathy in a rat model.

Methods

Twenty-four male rats were divided into four equal groups: control, PRP, steroid (dexamethasone) treated for induction of myopathy, and steroid then treated with PRP for three weeks. Skeletal muscle contractile properties, protein content of the muscle, oxidative stress markers, histological structure, myogenin gene expression and immunohistochemical expression of Myo-D, Pax-7 and LC3 were assessed.

Results

dexamethasone caused significant muscle weakness, decreased protein content, increased oxidative stress, decreased expression of myogenic genes and upregulated LC3 expression. PRP administration significantly improved muscle function, increased protein content, reduced oxidative stress, and upregulated myogenic genes. Histological results confirmed these findings. Additionally, PRP decreased autophagy marker LC3 expression and increased muscle stem cell markers MyoD and Pax7.

Conclusion

These results suggested that PRP could effectively prevent and reverse dexamethasone-induced muscle atrophy by promoting muscle protein synthesis, reducing oxidative stress, decreasing autophagy, and enhancing muscle stem cell activity. This study supports the potential role of PRP as a therapeutic strategy for muscle wasting disorders.
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富血小板血浆可抑制自噬,并通过调节Myo-D、Pax-7和肌原蛋白的表达增强肌生成潜能,从而改善地塞米松诱发的肌病。
背景:肌肉组织对整体健康至关重要,但随着年龄的增长和不同疾病的发生,肌肉组织的功能会下降。糖皮质激素虽然能有效治疗炎症,但会影响蛋白质的分解和合成,从而诱发肌无力(称为糖皮质激素诱发的肌病)。糖皮质激素对卫星细胞有负面影响,而卫星细胞在肌肉再生中发挥作用。富血小板血浆(PRP)含有浓缩的生长因子,具有促进组织修复的潜在作用,可用于改善糖皮质激素引起的肌肉萎缩:24只雄性大鼠被分为四个等量组:对照组、PRP组、类固醇(地塞米松)治疗诱导肌病组、类固醇治疗后再用PRP治疗三周组。结果:地塞米松会导致明显的肌肉无力、蛋白质含量下降、氧化应激增加、致肌基因表达下降和 LC3 表达上调。给予 PRP 可明显改善肌肉功能、增加蛋白质含量、减少氧化应激和上调肌生成基因。组织学结果证实了这些发现。此外,PRP 还减少了自噬标记 LC3 的表达,增加了肌肉干细胞标记 MyoD 和 Pax7:这些结果表明,PRP 可通过促进肌肉蛋白质合成、降低氧化应激、减少自噬和增强肌肉干细胞活性,有效预防和逆转地塞米松诱导的肌肉萎缩。这项研究支持了 PRP 作为肌肉萎缩疾病治疗策略的潜在作用。
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来源期刊
Tissue & cell
Tissue & cell 医学-解剖学与形态学
CiteScore
3.90
自引率
0.00%
发文量
234
期刊介绍: Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed. Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.
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