Live and Dead Clostridium butyricumGKB7 Diminish Osteoarthritis Pain and Progression in Preclinical Animal Model

Author:

Chen Li‐Chai1,Lin Yen‐You2,Tsai You‐Shan3,Chen Chin‐Chu34,Chang Tzu‐Ching2,Chen Hsien‐Te56,Hsu Chin‐Jung67,Tang Chih‐Hsin28910ORCID

Affiliation:

1. Department of Pharmacy Tajen University Pingtung Taiwan

2. Department of Pharmacology School of Medicine, China Medical University Taichung Taiwan

3. Biotech Research Institute, Grape King Bio Ltd. Taoyuan Taiwan

4. Institute of Food Science and Technology, National Taiwan University Taipei Taiwan

5. Department of Sports Medicine College of Health Care, China Medical University Taichung Taiwan

6. Department of Orthopedic Surgery China Medical University Hospital Taichung Taiwan

7. School of Chinese Medicine, China Medical University Taichung Taiwan

8. Chinese Medicine Research Center, China Medical University Taichung Taiwan

9. Department of Medical Laboratory Science and Biotechnology College of Medical and Health Science, Asia University Taichung Taiwan

10. Department of Medical Research China Medical University Hsinchu Hospital Hsinchu Taiwan

Abstract

ABSTRACTOsteoarthritis (OA) is a degenerative joint disease primarily affecting the elderly. It is characterized by the progressive decline of joint cartilage and alterations in the underlying bone. Several probiotic strains have exhibited immunomodulatory and anti‐inflammatory properties. Here, we examined the functions of live and dead Clostridium butyricum GKB7 (GKB7‐L and GKB7‐D) in a preclinical anterior cruciate ligament transection (ACLT)‐enhanced OA procedure. Oral administration of GKB7‐L and GKB7‐D ameliorated ACLT‐induced bone pain as assessed by weight‐bearing behavioral testing but did not affect body weight. Micro‐computed tomography (CT) results showed that GKB7‐L and GKB7‐D diminished ACLT‐induced bone destruction and loss. GKB7‐L and GKB7‐D‐enriched therapies also reduced ACLT‐induced production of the pro‐inflammatory cytokines interleukin (IL)‐1β and tumor necrosis factor (TNF)‐α, as well as the chondrolytic factor matrix metalloproteinase (MMP)‐3, leading to inhibition of aggrecan and collagen type II degradation and thereby blocking cartilage breakdown. We therefore suggest that oral supplementation with GKB7‐L or GKB7‐D can be beneficial in the prevention and treatment of OA.

Funder

China Medical University Hospital

Publisher

Wiley

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