Evidence map›Paper›PMID 40222728›Full record

ArticleAsian spine journal2025

Inhibitory effect of MLC901 on axonal demyelination in experimental animals undergoing circumferential lumbal stenosis by increasing transforming growth factor-β1 levels.

Kevin Jonathan Sjukur, Willy Adhimarta, Andi Asadul Islam, Bambang Priyanto, Andriany Qanitha

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Article in Asian spine journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Kevin Jonathan SjukurNeurosurgery Division, Department of Surgery, Faculty of Medicine, Universitas Hasanuddin, Makassar, Indonesia.
Willy AdhimartaNeurosurgery Division, Department of Surgery, Faculty of Medicine, Universitas Hasanuddin, Makassar, Indonesia.
Andi Asadul IslamNeurosurgery Division, Department of Surgery, Faculty of Medicine, Universitas Hasanuddin, Makassar, Indonesia.
Bambang PriyantoNeurosurgery Division, Department of Surgery, Faculty of Medicine, Universitas Mataram, Mataram, Indonesia.
Andriany QanithaDepartment of Physiology, Faculty of Medicine, Universitas Hasanuddin, Makassar, Indonesia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STUDY

designExperimental study using circumferential lumbar stenosis (CLS) rat model. PURPOSE: 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. OVERVIEW OF LITERATURE: 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.

methodsRats 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.

resultsLong 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).

conclusionsMLC901 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.

Indexed as

CytokinesLaminectomyMLC901Schwann cells

Identifiers

PMID40222728
PMCPMC12242253

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