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Objective To observe the effect of platelet rich plasma(PRP)combined with core decompression on the steroid-induced avascular necrosis of the femoral head(SANFH)and on MMP/TIM in rabbits.Methods A total of 42 New Zealand white rabbits were used in this study,and were randomly divided into 3 groups(decompression,combination and control groups,each n=14). The rabbit model of SANFH was established by i.m. injecting prednisolone acetate in the decompression group and combination group. The improved Landesberg method was used to make the platelet rich plasma. The decompression group received core decompression treatment while the combination group received PRP combined with core decompression for bone repair. X-ray photography of the hip joint of the two groups were taken at 2,6 and 10 weeks after the surgery,and the Lane-Sandhu X-ray scores and new bone area ratio were compared. Venous blood samples of the 3 groups were collected and the bilateral femoral heads were taken for further examination. The left femoral heads were used for histopathological observation and the right ones were used to determine the expression of the mRNA of MMP-2,MMP-9, TIMP-1, and TIMP-2. Results The levels of MMP-2 and MMP-9 in the decompression group were higher than that in the combination group and control group after surgery. The levels of TIMP-1 and TIMP-2 in the decompression group were significantly lower than the combination group and control group(P < 0.05). The IL-6 level and the rate of empty bone lacunae in the decompression group were significantly higher than the combination group and control group(P < 0.05), and that of the combination group was higher than the control group(P < 0.05). The combination group had a better joint imaging and histopathological evaluation than the decompression group after surgery. Conclusions Our findings demonstrate that PRP combined with core decompression can exert a positive effect on the MMP/TIMP and bone tissue repair in the treatment of steroid-induced avascular necrosis of the femoral head in rabbits.
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BACKGROUND:Cirrhosis is a long-term consequence of chronic hepatic injury, which has no effective therapy. Mesenchymal stem cels have been shown to play a potential role in the treatment of liver fibrosis/cirrhosis. OBJECTIVE:To investigate the therapeutic effect and mechanism of human umbilical cord-derived mesenchymal stem cels on CCl4 induced liver fibrosis/cirrhosis in rats. METHODS:A CCl4-induced liver fibrotic/cirrhotic rat model was used, and human umbilical cord-derived mesenchymal stem cels were injectedvia the tail vein after modeling. Liver biochemical profile was measured by Beckman Coulter analyzer. Histopathological changes were assessed by Sirius red staining. The expressions of colagen type I, colagen type III, matrix metaloproteinases-2 and tissue inhibitor of matrix metaloproteinases-2 protein and mRNA in liver tissues were observed by immunohistochemistry, western blot and real-time PCR, respectively. RESULTS AND CONCLUSION:Liver biochemical profile indicated the transplantation of human umbilical cord-derived mesenchymal stem cels could improve the liver function of rats with liver fibrosis and cirrhosis. After cel transplantation, except 1-week cel transplantation group, the expressions of the matrix metaloproteinases-2 mRNA and protein were significantly increased, while the expressions of colagen type I, colagen type III and tissue inhibitor of matrix metaloproteinases-2 mRNA and protein significantly decreased, compared with the corresponding model groups. Human umbilical cord-derived mesenchymal stem cels play a role in the treatment of liver fibrosis and cirrhosis through upregulating the expression of matrix metaloproteinases-2 and lowering the expression of inhibitor of matrix metaloproteinases-2. With the continued presence of pathogenic factors, human umbilical cord-derived mesenchymal stem cel transplantation cannot reverse liver fibrosis or cirrhosis, and only delay the process of liver fibrosis or cirrhosis.
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BACKGROUND:Tissue inhibitor of matrix metaloproteinase 1 (TIMP-1) is the corresponding antagonist of matrix metaloproteinase 13 (MMP-13), and their balance between expression and functional activity exerts an important role in the metabolic state of the extracelular matrix. During the development of osteoarthritis, however, TIMP-1 and MMP-13 expressions and their expression ratio show unclear changes in DH guinea pigs. OBJECTIVE:To explore the expression levels of MMP-13 and TIMP-1 in DH guinea pigs with different ages, and to analyze the relationship between the ratio of MMP-13 to TIMP-1 and the age-dependent degenerative changes in the articular cartilage. METHODS:Twenty-four female Dunkin Hartley guinea pigs were sacrificed at age of 2, 4, 8, 12 months separately, with six animals at each time point. The knee joints were colected and gross visual appearance of the articular cartilage was observed, then were decalcified and prepared for paraffin sections. VG staining and Mankin score were used to analyze the histological changes. Immunohistochemistry was conducted to assess the expression levels of MMP-13 and TIMP-1 in the cartilage. Integrated absorbance values were used as the quantitive analysis calculated by Image pro-Plus 6.0. Linear regression analysis was done to analysis the relationship between Mankin score and the ratio of MMP-13/TIMP-1. RESULTS AND CONCLUSION:Normal appearance in the articular cartilage was observed in 2-month-old DH guinea pigs, while degenerative changes in the articular cartilage were shown in 4-month-old animals, which became severer with age. Significant difference was found in Mankin score between any two groups (P < 0.05). The ratio of MMP-13 to TIMP-1 increased with age, and the ratio was positively correlated to the Mankin score (P < 0.05). Age-related articular cartilage degeneration occurred in Dunkin Hartley guinea pigs at 4 months of age, and devoloped with age, which is related with the imbanlance of the expression ratio of MMP-13 to TIMP-1.
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A Periodontite Crônica é uma doença imunoinflamatória caracterizada pela perda óssea alveolar em indivíduos susceptíveis, tendo como fator etiológico principal o biofilme dental. O tratamento convencional desta doença é a terapia periodontal mecânica. Na tentativa de melhorar os parâmetros clínicos no controle da periodontite, a terapia de modulação do hospedeiro pode ser usada como auxiliar ao tratamento convencional, uma vez que diminui a resposta inflamatória do paciente, tendo em vista que as metaloproteinases da matriz têm um papel importante na regulação da destruição do tecido periodontal. Tal terapia pode ser realizada com doxiciclina em dose subantimicrobiana (DDS) de 20 mg administrada 2 vezes ao dia, para regular a atividade excessiva de colagenase no tecido gengival e fluido gengival crevicular. Dessa maneira, o presente estudo teve como objetivo avaliar o mecanismo de ação dessa droga, a eficácia do tratamento e a segurança no seu uso em longo prazo. Os dados obtidos a partir da revisão de literatura demonstram que a DDS como coadjuvante a raspagem e alisamento radicular (RAR) foi capaz de promover benefícios clínicos significativos, reduzir os níveis de colagenase, marcadores inflamatórios, reabsorção óssea e citocinas pró-inflamatórias, além de não alterar a microflora subgengival e não causar resistência a antibióticos. Os resultados sugerem ser eficaz e seguro o uso da DDS em longo prazo como coadjuvante na terapia periodontal quando usada por no mínimo 3 meses, com melhores resultados em 9 meses de uso. Futuros estudos longitudinais necessitam ser conduzidos a fim de definir a eficácia desse tratamento na história da doença periodontal.
The Chronic Periodontitis is an immuno-inflammatory disease characterized by alveolar bone loss in susceptible individuals, with the dental biofilm as main etiological factor. Conventional treatment of this disease is mechanical periodontal therapy. In an attempt to improve the clinical parameters in controlling periodontitis, host modulation therapy can be used as an adjunct to conventional treatment, since it reduces the inflammatory response of the patient, considering that matrix metalloproteinases have a role in regulation of periodontal tissue destruction. Such therapy can be accomplished with subantimicrobial dose doxycycline (SDD) 20 mg taken twice daily to regulate the excessive collagenase activity in gingival tissue and gingival crevicular fluid. Thus, the present study aimed to evaluate the mechanism of action of this drug, treatment efficacy and safety as long-term use treatment. The data obtained from the literature review shows that the SDD as an adjunct to scaling and root planing (SRP) was able to promote significant clinical benefits, reducing levels of collagenase, inflammatory markers, bone resorption and proinflammatory cytokines, and does not lead to change the subgingival microflora and antibiotic resistance. The results suggest that it is effective and safe the long-term use of SDD as an adjunct in periodontal therapy when used for at least 3 months, with better results at 9 months of use. Future longitudinal studies need to be conducted to establish the efficacy of this treatment in the history of periodontal disease.
Subject(s)
Humans , Doxycycline , Matrix MetalloproteinasesABSTRACT
The left ventricular (LV) myocardial remodeling process that occurs in various settings of congestive heart failure (CHF) had historically been attributed to intrinsic changes in the cardiac myocyte. However, it is now recognized that important changes also occur within the extracellular matrix (ECM) of the myocardium, contributing to the remodeling process. Matrix metalloproteinases are a family of proteolytic enzymes responsible for myocardial extracellular protein degradation.Several MMP species identified within the human myocardium may be dysregulated in congestive heart failure (CHF). The purpose of the present review is to present a brief overview of the matrix metalloproteinases (MMPs) within the myocardium that likely contributes to myocardial remodeling,to examine the results from basic studies to explore relationship with respect to MMPs activation and congestive heart failure.-