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探讨特发性脊柱侧凸中椎旁肌胶原的病理作用。

Exploring the Pathological Role of Collagen in Paravertebral Muscle in the Progression of Idiopathic Scoliosis.

机构信息

Department of Rehabilitation, Changzheng Hospital, Second Military Medical University, Shanghai, China.

Shanghai University of Medicine & Health Sciences, Shanghai, China.

出版信息

Biomed Res Int. 2020 Aug 3;2020:1527403. doi: 10.1155/2020/1527403. eCollection 2020.

DOI:10.1155/2020/1527403
PMID:32802834
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7421238/
Abstract

BACKGROUND

Paravertebral muscle (PVM) is considered as a contributing factor of idiopathic scoliosis (IS); collagen is crucial for maintaining the mechanical properties of PVM, but only a few researches have described this field. In this study, we observed the muscle stiffness of PVM and the curvature of the spine by adjusting the content of collagen in PVM of rats and explored the role of collagen in the progression of IS.

METHODS

32 female Sprague Dawley rats were randomly divided into four groups: neutralizing antibody (NA) group (group 1), normal control group (group 2), IS group (group 3), and IS with NA group (group 4). TGF-1 NA was injected into PVM in group 1 and group 4, while Normal saline in group 2 and group 3. The Cobb angle and muscle stiffness were measured before and after injection; the rats were sacrificed at one week after injection, and performed histological, Western Blot, and qRT-PCR examinations.

RESULTS

X-rays showed that scoliosis occurred in group 1 and relieved in group 4. The stiffness of PVM was decreased significantly on the convex side in group 1, while on the concave side in group 4. The expression of TGF-1 and COL1 on the concave side in IS rats (group 3) was significantly increased than that in normal rats (group 2), the concentration of COL1 and COL3 in group 3 was significantly higher than that in group 2, and the addition of TGF-1 NA significantly downregulated COL1 and COL3 in group 1 and group 4. The concentration of COL1 in convex PVM was negatively related to Cobb angle in group 1 and group 2, and in concave PVM was positively related to Cobb angle in group 3 and group 4. However, no significant correlation was found between COL3 and Cobb angle in group 3 and group 4.

CONCLUSIONS

Asymmetric biomechanical characteristics of PVM was an important etiological factor of IS, which was directly correlated with collagen, it could be adjusted by local intramuscular injecting of TGF-1 NA, and finally had an effect on the shape of the spine.

摘要

背景

椎旁肌(PVM)被认为是特发性脊柱侧凸(IS)的一个致病因素;胶原蛋白对于维持 PVM 的机械性能至关重要,但只有少数研究描述了这一领域。在这项研究中,我们通过调整大鼠 PVM 中的胶原蛋白含量来观察 PVM 的肌肉僵硬和脊柱的弯曲程度,并探讨胶原蛋白在 IS 进展中的作用。

方法

32 只雌性 Sprague Dawley 大鼠随机分为四组:中和抗体(NA)组(第 1 组)、正常对照组(第 2 组)、IS 组(第 3 组)和 IS 加 NA 组(第 4 组)。第 1 组和第 4 组向 PVM 中注射 TGF-1 NA,第 2 组和第 3 组注射生理盐水。在注射前后测量 Cobb 角和肌肉僵硬度;注射后一周处死大鼠,进行组织学、Western Blot 和 qRT-PCR 检查。

结果

X 光片显示第 1 组发生脊柱侧凸,第 4 组缓解。第 1 组 PVM 凸侧的僵硬度显著降低,而第 4 组 PVM 凹侧的僵硬度显著降低。IS 大鼠(第 3 组)PVM 凹侧 TGF-1 和 COL1 的表达明显高于正常大鼠(第 2 组),第 3 组 COL1 和 COL3 的浓度明显高于第 2 组,TGF-1 NA 的加入显著下调了第 1 组和第 4 组的 COL1 和 COL3。第 1 组和第 2 组凸侧 PVM 中 COL1 的浓度与 Cobb 角呈负相关,第 3 组和第 4 组凹侧 PVM 中 COL1 的浓度与 Cobb 角呈正相关。然而,第 3 组和第 4 组中 COL3 与 Cobb 角之间没有显著相关性。

结论

PVM 的不对称生物力学特征是 IS 的一个重要病因因素,与胶原蛋白直接相关,可通过局部肌内注射 TGF-1 NA 进行调节,最终对脊柱形态产生影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/06124714c79c/BMRI2020-1527403.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/ae09bd491f0d/BMRI2020-1527403.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/fc781aff4f47/BMRI2020-1527403.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/a8c6976a24ef/BMRI2020-1527403.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/f9247d9c569d/BMRI2020-1527403.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/aaf8a3bca135/BMRI2020-1527403.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/c05ab8b28f32/BMRI2020-1527403.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/2024756e5024/BMRI2020-1527403.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/036f1f3fdba7/BMRI2020-1527403.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/06124714c79c/BMRI2020-1527403.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/ae09bd491f0d/BMRI2020-1527403.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/fc781aff4f47/BMRI2020-1527403.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/a8c6976a24ef/BMRI2020-1527403.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/f9247d9c569d/BMRI2020-1527403.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/aaf8a3bca135/BMRI2020-1527403.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/c05ab8b28f32/BMRI2020-1527403.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/2024756e5024/BMRI2020-1527403.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/036f1f3fdba7/BMRI2020-1527403.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aa6/7421238/06124714c79c/BMRI2020-1527403.009.jpg

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