Abstract
The ongoing chronic inflammation and subsequent fibrosis play an important role in ligamentum flavum (LF) fibrosis and hypertrophy in patients with lumbar spinal canal stenosis (LSCS). Leptin is a chronic inflammatory mediator and involved in the fibrotic process in multiple organ systems. The present study aimed to investigate the role of leptin in LF fibrosis and its related regulatory mechanisms. The LF specimens were obtained during the surgery from 12 patients with LSCS (LSCS group) and 12 control patients with lumbar disc herniation (LDH) group. The morphologic changes and fibrosis score of LF were assessed by Hematoxylin and eosin (H&E) and Masson’s trichrome staining respectively. The location and expression of leptin in LF tissues were determined. Then, the LF cells were cultured and exposed to recombinant human leptin (rhleptin). Collagen I and III were used as fibrosis markers and IL-6 was used as the inflammatory factor. As a result, the LF thickness and fibrosis score in the LSCS group were significantly higher than those in the LDH group (P<0.05). Leptin was detected in the hypertrophied LF and its expression was substantially increased in the LSCS group and positively correlated with LF thickness and fibrosis score (P<0.05). Moreover, our in vitro experiments revealed that rhleptin treated LF cells elevated the expression of collagen I and III. Finally, leptin administration induced IL-6 expression via nuclear factor-κB (NF-κB) pathway in LF cell (P<0.05). Our study demonstrated novel molecular events for leptin-induced inflammation in LF tissue by promoting IL-6 expression and thus might have potential implications for clarifying the mechanism underlying LF fibrosis and hypertrophy.
Highlights
Lumbar spinal canal stenosis (LSCS) is one of the most common diseases in the elderly population often with symptoms of low back and leg pain, numbness, and intermittent claudication arising from nerve compression [1]
Despite the fact that the etiology of LSCS is poorly understood, it is clear that ligamentum flavum (LF) hypertrophy is known to be one of the main causes contributing to LSCS [1,2]
The experiment explored in this investigation demonstrated that LF thickness in LSCS group was significantly greater than that in the lumbar disc herniation (LDH) group
Summary
Lumbar spinal canal stenosis (LSCS) is one of the most common diseases in the elderly population often with symptoms of low back and leg pain, numbness, and intermittent claudication arising from nerve compression [1]. Numerous causative factors such as disc protrusion, the bony proliferation of the facet joints, and hypertrophy of the ligamentum flavum (LF) contribute to the development of LSCS. Several studies have explored the mechanism of LF fibrosis at the histological and cellular levels, and c 2018 The Author(s)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
