A Comparison of the Effects of Neuronal Nitric Oxide Synthase and Inducible Nitric Oxide Synthase Inhibition on Cartilage Damage
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Tarih
2016
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Hindawi Ltd
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
The objective of this study was to investigate the effects of selective inducible nitric oxide synthase and neuronal nitric oxide synthase inhibitors on cartilage regeneration. The study involved 27 Wistar rats that were divided into five groups. On Day 1, both knees of 3 rats were resected and placed in a formalin solution as a control group. The remaining 24 rats were separated into 4 groups, and their right knees were surgically damaged. Depending on the groups, the rats were injected with intra-articular normal saline solution, neuronal nitric oxide synthase inhibitor 7-nitroindazole (50mg/kg), inducible nitric oxide synthase inhibitor aminoguanidine (30mg/kg), or nitric oxide precursor L-arginine (200mg/kg). After 21 days, the right and left knees of the rats were resected and placed in formalin solution. The samples were histopathologically examined by a blinded evaluator and scored on 8 parameters. Although selective neuronal nitric oxide synthase inhibition exhibited significant(p = 0.044) positive effects on cartilage regeneration following cartilage damage, it was determined that inducible nitric oxide synthase inhibition had no statistically significant effect on cartilage regeneration. It was observed that the nitric oxide synthase activation triggered advanced arthrosis symptoms, such as osteophyte formation. The fact that selective neuronal nitric oxide synthase inhibitors were observed to have mitigating effects on the severity of the damage may, in the future, influence the development of new agents to be used in the treatment of cartilage disorders.
Açıklama
Anahtar Kelimeler
Reduced Chondrocyte Proliferation; Human Articular Chondrocytes; Experimental Osteoarthritis; Proteoglycan Turnover; Joint Pain; Expression; Apoptosis; Cytokines; Model; Degradation
Kaynak
Biomed Research International
WoS Q Değeri
Q3
Scopus Q Değeri
Q1
Cilt
2016
