| ObjectiveBy observing the effect of Knee Arthritis Therapeutic Apparatus (KATA) on cartilage morphology and cytokines IL-1β, IL-6, TNF-a, MMP-3, HA in synovial fluid in osteoarthritis in vivo, respectively, so as to discuss the effect of KATA on osteoarthritis cartilage degeneration, further to illustrate its possible mechanism in the treatment of osteoarthritis, and provide experimental data for its clinical application.MethodsNew Zealand White rabbits of average gender (n=64) were randomly divided into blank group (n=16) and osteoarthritis model group (n=48). Osteoarthritis model was operated in left knee of rabbits according to the modified Hulth’s modeling method. After operation, the rabbits were randomly divided into three groups:the model group (without any treatment), the control group [received the treatment of Infrared Therapy Apparatus (2 times/day,30 min/time)] and the experimental group [received the treatment of KATA (2 times/day,30 min/time)]. The blank group also does not receive any treatment. After every 8 weeks of continuous treatment, the animals were sacrificed, synovial fluid and tibial plateau cartilage tissues were obtained. The cartilage morphological changes were observed under an optical microscope following staining with hematoxylin and eosin (H&E) and the chondrocyte ultrastructural changes were investigated by transmission electron microscopy (TEM). The levels of IL-β, IL-6, TNF-a, MMP-3 and HA from synovial tissue were measured by Enzyme-linked immunosorbnent assay (ELISA).Results1. The macroscopic observation showed the appearance of the normal articular cartilage, smooth articular surface in blank group, while in model group, the articular surface was grayish yellow and ulceration and joint marginal appeared desmoplastic hyperplasia serious. After 16 weeks, the subchondral bone plate exposure and osteophyte formation with the exacerbation of the disease. The periarticular connective tissue hyperplasias of the experimental group and the control group were lighter than in the model group, the articular surface was still shiny and without ulceration.2. HE staining results showed that the articular cartilage surfaces of the blank group were smooth, the four layers’ structures of the articular cartilage were legible, the chondrocytes line up in neat rows and the caryotin uniformity and the caryon is clear. In the model group, the articular cartilage surfaces were rough, the cartilage layer become thinner and the chondrocytes line up in disorder and four layers’ structures were uneasy to distinguish, part of districts the bone marrow vascular Granulation tissue invades cartilage layer. The articular cartilage surface of the experimental group and the control group were not smooth, and four layers’ structure could be still distin-guished and slightly thin cartilage layer. Mankin cartilage rating of the model group, the control group and the experimental group were significantly higher than that of blank group (P<0.05), it was significantly lower in the experimental group and contr-ol group than the model group (P<0.05).3. TEM results showed that the normal chondrocytes were nearly oval, cells and cell membrane were integrity, in intracytoplasic, there were abundant rough endoplasmic reticulums (RER), dictyosomes, mitochondria and glycogen scattered. In the model group, the chondrocytes were obviously atrophy, degeneration and necrosis, and their shape showed irregularity and the areolae around cells disappear, in intracytoplasmic, organelles were dissolving and uneasy to distinguish. Compared with the model group, the chondrocytes’ degradation of the experimental group and the control group were not very serious.4. ELISA measured showed that the expression of IL-1(3, IL-6, TNF-α and MMP-3 of the model group were dramaticlly higher than the blank group (P<0.01), meanwhile, the level of HA was obviously lower than the blank group (P<0.01). The expression of IL-1β, IL-6, TNF-a and MMP-3 of the experimental group and the control group were distinctly lower than the model group respectively (P<0.01),the level of HA was overtly higher than the model group (P<0.01).And they were significantly different between 8 weeks and 16 weeks (P<0.01). In addition, the contents of IL-1β, IL-6, TNF-α, MMP-3 and HA in the experimental group and in the control group were significant difference (P<0.01).Conclusions1. KATA could delay the articular cartilage degeneration by improving the function of chondrocytes and the morphology of cartilage matrix.2. KATA could protect the chondrocytes via up-regulating the expression of HA and down-regulating the expressions of cytokines IL-1β, IL-6, TNF-α and inflammatory mediator MMP-3 in synovial fluid in osteoarthritis. |
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