Background Epidural fibrosis (EF) and peridural adhesions remain important causes of adverse outcomes after laminectomy, and no standard preventive strategy has yet been established. This study investigated the antifibrotic effect of oral ginsenoside Rg1 administration in a rat model of laminectomy-induced EF using histopathological assessment, TUNEL staining, and RT-qPCR-based analysis of Tgfb1, Smad2, and Smad3 gene expression. Methods Thirty-two adult male rats were randomized into four groups (n = 8/group): Control, Rg1, LAM (laminectomy), and LAM+Rg1 (Rg1 administered after laminectomy; 72 mg/kg/day by oral gavage for 28 days). Lumbar specimens were harvested on postoperative day 28. EF and adhesion severity were evaluated histologically on hematoxylin and eosin-stained sections. Collagen deposition was assessed with Masson’s trichrome staining, dural thickness was measured morphometrically, fibroblast density was scored semiquantitatively, and DNA fragmentation/apoptotic activity was assessed by TUNEL staining. Relative mRNA expression levels of Tgfb1, Smad2, and Smad3 were determined by RT-qPCR. Results The LAM group showed marked epidural scar formation, extensive collagen deposition, increased fibroblast density, severe adhesions, and considerable dural thickening relative to the Control and Rg1 groups. Administration of Rg1 following laminectomy significantly reduced dural thickening, fibroblast accumulation, adhesion severity, and EF scores compared with the LAM group (p < 0.05 for all), with less collagen deposition observed on Masson’s trichrome staining. The LAM group exhibited a significant elevation in TUNEL-positive nuclei compared to both the Control and Rg1 groups (p = 0.0002 and p = 0.0003, respectively). The LAM+Rg1 group demonstrated the highest TUNEL positivity, with a further significant increase compared with the LAM group (p < 0.0001). RT-qPCR analysis showed significant intergroup differences in Tgfb1, Smad2, and Smad3 expression (p = 0.002, p = 0.023, and p = 0.003, respectively), with the lowest expression levels observed in the LAM+Rg1 group. Conclusions Post-laminectomy Rg1 administration attenuated EF and reduced peridural adhesions in rats. These effects were accompanied by increased TUNEL positivity within scar-associated regions and lower Tgfb1, Smad2, and Smad3 transcript levels on postoperative day 28. Together, these findings support the antifibrotic potential of Rg1 in experimental post-laminectomy EF, while further protein-level, pathway-specific, and functional studies are required to clarify the mechanisms underlying this effect and its translational relevance.

Ginsenoside Rg1 mitigates epidural fibrosis after laminectomy in rats: histopathological, TUNEL, and transcriptional evidence

期刊论文
发表日期：

2026年7月25日

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Ziya Yurtal,
Kadri Kulualp,
Hasan Hüseyin Keçeli,
Hüseyin Özkan,
Ufuk Kaya,
Meltem Kumaş

摘要

Background

Epidural fibrosis (EF) and peridural adhesions remain important causes of adverse outcomes after laminectomy, and no standard preventive strategy has yet been established. This study investigated the antifibrotic effect of oral ginsenoside Rg1 administration in a rat model of laminectomy-induced EF using histopathological assessment, TUNEL staining, and RT-qPCR-based analysis of Tgfb1, Smad2, and Smad3 gene expression.

Methods

Thirty-two adult male rats were randomized into four groups (n = 8/group): Control, Rg1, LAM (laminectomy), and LAM+Rg1 (Rg1 administered after laminectomy; 72 mg/kg/day by oral gavage for 28 days). Lumbar specimens were harvested on postoperative day 28. EF and adhesion severity were evaluated histologically on hematoxylin and eosin-stained sections. Collagen deposition was assessed with Masson’s trichrome staining, dural thickness was measured morphometrically, fibroblast density was scored semiquantitatively, and DNA fragmentation/apoptotic activity was assessed by TUNEL staining. Relative mRNA expression levels of Tgfb1, Smad2, and Smad3 were determined by RT-qPCR.

Results

The LAM group showed marked epidural scar formation, extensive collagen deposition, increased fibroblast density, severe adhesions, and considerable dural thickening relative to the Control and Rg1 groups. Administration of Rg1 following laminectomy significantly reduced dural thickening, fibroblast accumulation, adhesion severity, and EF scores compared with the LAM group (p < 0.05 for all), with less collagen deposition observed on Masson’s trichrome staining. The LAM group exhibited a significant elevation in TUNEL-positive nuclei compared to both the Control and Rg1 groups (p = 0.0002 and p = 0.0003, respectively). The LAM+Rg1 group demonstrated the highest TUNEL positivity, with a further significant increase compared with the LAM group (p < 0.0001). RT-qPCR analysis showed significant intergroup differences in Tgfb1, Smad2, and Smad3 expression (p = 0.002, p = 0.023, and p = 0.003, respectively), with the lowest expression levels observed in the LAM+Rg1 group.

Conclusions

Post-laminectomy Rg1 administration attenuated EF and reduced peridural adhesions in rats. These effects were accompanied by increased TUNEL positivity within scar-associated regions and lower Tgfb1, Smad2, and Smad3 transcript levels on postoperative day 28. Together, these findings support the antifibrotic potential of Rg1 in experimental post-laminectomy EF, while further protein-level, pathway-specific, and functional studies are required to clarify the mechanisms underlying this effect and its translational relevance.