Sjukur Kevin Jonathan, Adhimarta Willy, Islam Andi Asadul, Priyanto Bambang, Qanitha Andriany
Neurosurgery Division, Department of Surgery, Faculty of Medicine, Universitas Hasanuddin, Makassar, Indonesia.
Neurosurgery Division, Department of Surgery, Faculty of Medicine, Universitas Mataram, Mataram, Indonesia.
Asian Spine J. 2025 Jun;19(3):333-345. doi: 10.31616/asj.2024.0364. Epub 2025 Apr 11.
Experimental study using circumferential lumbar stenosis (CLS) rat model.
To investigate the effect of MLC901 administration on transforming growth factor (TGF)-β1 level and the degree of axonal demyelination in the CLS rat model.
CLS is common in older adults, causing neuropathic pain that impairs daily functioning. TGF-β1 plays an essential role in nerve regeneration and reducing axonal demyelination in CLS. MLC901, a traditional therapeutic formula, has shown promise in preclinical studies, including modulating proinflammatory cytokines. While MLC901's effect on serum TGF-β1 levels in the CLS rat model has been explored, its impact on tissue TGF-β1 expression remains understudied.
Rats were randomly allocated into one of six groups: no CLS (baseline), CLS only (pretreatment), short treatment (1 day) with MLC901, short treatment with placebo, longer treatment (7 days) with MLC901, and longer treatment with placebo. The CLS model was induced by laminectomy at the lumbar 5th vertebra, followed by teflon insertion around the dura mater. Serum TGF-β1 levels were measured using enzyme-linked immunosorbent assay. Tissue TGF-β1 expression and the degree of axonal demyelination were assessed by immunohistochemistry and histopathology, respectively.
Long treatment MLC901 group had significantly higher serum TGF-β1 levels than the pretreatment group (p<0.001). Long treatment MLC901 group also exhibited the highest TGF-β1 tissue expression among all treatment groups, including the baseline group (p=0.013). Axonal demyelination was lowest in the long treatment MLC901 group, indicated by the highest number of Schwann cells (p<0.001), the fewest inflammatory cells (except versus baseline) (p=0.001), and the fewest vacuoles (except versus baseline) (p=0.015).
MLC901 can inhibit axonal demyelination in experimental animals undergoing CLS surgery by upregulating TGF-β1 levels. MLC901 has the potential to be used as an adjuvant therapy in CLS surgery.
使用腰椎管狭窄（CLS）大鼠模型的实验研究。
研究给予MLC901对CLS大鼠模型中转化生长因子（TGF）-β1水平及轴突脱髓鞘程度的影响。
CLS在老年人中常见，可导致神经性疼痛，影响日常功能。TGF-β1在神经再生及减少CLS中的轴突脱髓鞘方面起重要作用。MLC901是一种传统治疗方剂，在临床前研究中已显示出前景，包括调节促炎细胞因子。虽然已探讨了MLC901对CLS大鼠模型血清TGF-β1水平的影响，但其对组织TGF-β1表达的影响仍研究不足。
将大鼠随机分为六组之一：无CLS（基线）、仅CLS（预处理）、用MLC901短期治疗（1天）、用安慰剂短期治疗、用MLC901长期治疗（7天）、用安慰剂长期治疗。通过第5腰椎椎板切除术诱导CLS模型，随后在硬脑膜周围插入聚四氟乙烯。使用酶联免疫吸附测定法测量血清TGF-β1水平。分别通过免疫组织化学和组织病理学评估组织TGF-β1表达及轴突脱髓鞘程度。
长期治疗的MLC901组血清TGF-β1水平显著高于预处理组（p<0.001）。长期治疗的MLC901组在所有治疗组（包括基线组）中也表现出最高的TGF-β1组织表达（p=0.013）。长期治疗的MLC901组轴突脱髓鞘程度最低，表现为施万细胞数量最多（p<0.001）、炎性细胞最少（与基线组相比除外）（p=0.001）、空泡最少（与基线组相比除外）（p=0.015）。
MLC901可通过上调TGF-β1水平抑制接受CLS手术的实验动物的轴突脱髓鞘。MLC901有潜力用作CLS手术的辅助治疗。
