Effect of aging on the production and the action of nitric oxide in articular cartilage.
- Author:
Gun Il IM
1
;
Sung Ryong SHIN
;
Do Young KIM
;
Joo Ho SHIN
;
Won Ho CHO
Author Information
1. Department of Orthopedic Surgery, College of Medicine, Hallym University, Chunchon, Korea.
- Publication Type:Original Article
- Keywords:
Articular cartilage;
Chondrocyte;
Aging;
Nitric Oxide;
Cell proliferation;
Immunohistiochemical staining
- MeSH:
Aging*;
Cartilage, Articular*;
Cell Proliferation;
Chondrocytes;
Femur;
Humans;
Immunohistochemistry;
Nitric Oxide Synthase Type III;
Nitric Oxide*;
Rabbits
- From:The Journal of the Korean Orthopaedic Association
2001;36(3):215-220
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: We investigate the age-related changes in the production of nitiric oxide (NO) in the articular cartilage and its effects on cell proliferation. MATERIALS AND METHODS: Forty New Zealand white rabbits of four different age groups were used. There were 10 rabbits in each group and the age groups were 1 month, 6 months, 1 year and 3 years of age. We measured the basal and induced production of NO in cultured articular chondrocytes that were obtained from distal femur by using a nitrite assay. We observed the changes in the proliferative activity of the chondrocytes after exogenous NO administration using a nonradioisotopic proliferation assay. In addition, we also detected endothelial nitric oxide synthase (eNOS) in articular cartilage using immunohistochemical staining. RESULTS: The basal and induced levels of NO were lower in the cultured chondrocytes from older rabbits. Exogenous NO administration suppressed the proliferative activity of chondrocytes to a greater degree in the younger rabbits than in the older ones. Immunohistochemistry showed a predominance of eNOS positive chondrocytes in the superficial layer. The number of eNOS positive chondrocytes decreased in older rabbits. CONCLUSION: The production of NO decreased with aging in normal articular cartilage. The suppression of proliferative activity in chondrocytes by exogenous NO declined with aging.