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Glyburide Accelerates the Process of Tendon Healing by Inhibiting NLRP3 Inflammasome in Calcific Tendinopathy
WeiYi Chen1,2,3, WanQing Qi1,2,3, MengYang Jia1,2,3
1Department of Sports Medicine, Xinhua Hospital affiliated to Dalian University, Dalian, Liaoning, China.
Background:
The NOD-like receptor protein 3 (NLRP3) inflammasome activated by calcific crystals is particularly relevant to the initiation and progression of calcific tendinopathy. Moreover, NLRP3 inflammasome-driven inflammation controlled at low-grade levels could promote collagen regeneration of the tendon. Recently, it has been reported that glyburide, a hypoglycemic drug, inhibits the NLRP3 inflammasome, a possible diagnostic biomarker and therapeutic target for calcific tendinopathy.
Study Design:
Controlled laboratory study.
Purpose:
To investigate whether glyburide has therapeutic effects on calcific tendinopathy and to determine the role of the NLRP3 inflammasome in such an effect.
Methods:
A total of 60 Sprague-Dawley rats underwent collagenase injection into the Achilles tendon to induce calcific tendinopathy. Sixteen weeks later, the rats were randomly assigned to 3 groups: (1) 10% dimethyl sulfoxide (DMSO) group, (2) celecoxib group, and (3) glyburide group. Gross morphological and histological analyses were conducted to evaluate tendon healing. Additionally, real-time quantitative polymerase chain reaction and Western blotting were performed to assess whether glyburide degeneration influences the expression of components of the NLRP3 inflammasome, including NLRP3, apoptosis-associated speckle-like protein (ASC), caspase-1, IL-1β, and IL-18, within Achilles tendon enthesis at 2 weeks after treatment.
Results:
The Achilles tendon tissues in the glyburide group exhibited significantly less degeneration and fewer calcium deposits compared with the celecoxib and DMSO groups. The mRNA and protein expression levels of NLRP3, ASC, caspase-1, IL-1β, and IL-18 were reduced in the glyburide group compared with both the celecoxib and DMSO groups.
Conclusion:
Glyburide targets the upstream NLRP3 signaling pathway, potentially accelerating tendon healing, which may contribute to advancements in the treatment of calcific tendinopathy.
Clinical Relevance:
Glyburide acts as an NLRP3 inflammasome inhibitor and may be a new option for tendon healing in calcific tendinopathy.
Insights
Glyburide effectively reduced degeneration and calcium deposits in calcific tendinopathy by inhibiting the NLRP3 inflammasome pathway. This suggests glyburide may accelerate tendon healing and offer a new treatment option.
Area of Science:
- Biomedical Science
- Molecular Biology
- Orthopedics
Background:
- Calcific tendinopathy involves NLRP3 inflammasome activation by calcific crystals, driving inflammation and progression.
- Low-grade NLRP3 inflammasome activity may promote tendon collagen regeneration.
- Glyburide, a hypoglycemic drug, is a known inhibitor of the NLRP3 inflammasome.
Purpose of the Study:
- To evaluate the therapeutic potential of glyburide in calcific tendinopathy.
- To elucidate the role of the NLRP3 inflammasome in glyburide's effects on tendon healing.
Main Methods:
- A rat model of collagenase-induced calcific tendinopathy was established.
- Rats were treated with DMSO, celecoxib, or glyburide.
- Tendon healing was assessed via morphological and histological analyses; NLRP3 inflammasome component expression (NLRP3, ASC, caspase-1, IL-1β, IL-18) was quantified using RT-qPCR and Western blotting.
Main Results:
- Glyburide treatment significantly reduced Achilles tendon degeneration and calcium deposition compared to control and celecoxib groups.
- Expression of NLRP3 inflammasome components (NLRP3, ASC, caspase-1, IL-1β, IL-18) at both mRNA and protein levels was significantly decreased in the glyburide group.
Conclusions:
- Glyburide effectively inhibits the NLRP3 inflammasome pathway in calcific tendinopathy.
- Glyburide demonstrates therapeutic potential for accelerating tendon healing in this condition.
- Glyburide represents a promising new therapeutic strategy for calcific tendinopathy treatment.
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