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BACKGROUND:At present, there is no effective treatment strategy for cavernous transformation of portal vein and basic research about its etiology is rarely reported. OBJECTIVE:To establish the models of cavernous transformation of portal vein, detect the expression of matrix metal oproteinase-2,-9 (MMP-2, MMP-9) and tissue inhibitors 1, 2 of metal oproteinase (TIMP-1, TIMP-2) in rat portal vein and peripheral tissue, and discuss the roles in the process of peripheral angiogenesis. METHODS:Eighty Sprague-Dawley rats were randomly divided into three groups. The rat models of cavernous transformation of portal vein were established with partial coarctation in portal vein by using 21 G blunt pinhead. Control group was normal rats without operation (samples were harvested after portal vein radiography). Model group and sham operation group were divided into three groups respectively according to different time points, namely 2, 4 and 6 weeks after operation. Rats of each group were randomly chosen at week 2, 4 and 6 after operation to observe the formation of col ateral circulation of portal vein and its peripheral tissues by performing portal vein radiography. CD31 was detected by immunohistochemistry. The expression of MMP-2, MMP-9, TIMP-1, TIMP-2 mRNA and protein in portal vein and peripheral tissue were determined by RT-PCR and immunohistochemistry respectively. RESULTS AND CONCLUSION:Peripheral angiogenesis of model group was increased obviously by portal vein radiography and immunohistochemistry. RT-PCR and immunohistochemistry results demonstrated that, compared with the control group and sham operation group, the expression of MMP-2 mRNA and protein in model group were significantly increased at weeks 2, 4, and 6 (P0.05). Ratio of MMP-2/TIMP-2 of model group was significantly higher than that of control group and sham operation group (P<0.05) at week 2. the rat models of cavernous transformation of portal vein have low mortality, high success rate and are stable. Upregulation of the expression of MMP-2, MMP-9 and the disbanlance of the ratio of MMP-2/TIMP-2 might contribute to the peripheral angiogenesis in rats with cavernous transformation of portal vein.
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BACKGROUND:Conventional treatments for hypertrophic scars include excision, steroid hormones, anti-metabolite drugs, immunosuppressive agents and radiation therapy. Easy to relapse or serious reaction limits their clinical use. In recent years, application of calcium channel blockers in treatment of hypertrophic scars has made more good progresses, but little adverse reactions are obtained. OBJECTIVE:To explore the effects of calcium channel blocker trifluoperazine on hypertrophic scar of rabbit ears. METHODS:A total of 24 rabbits were enrol ed in this study. After 1 week of accommodation, models of rabbit ear scar were established in accordance with the method of Morris and Li et al. Rabbit models were randomly assigned to three group (n=8). At 30 days after model induction, when scar formed, trifluoperazine and triamcinolone acetonide groups received trifluoperazine and triamcinolone acetonide injection. Blank control group was left intact. Changes in hyperplastic scar, hypertrophic index, levels of matrix metal oproteinase-2, tissue inhibitor of metal oproteinase-2, transforming growth factorβ1,α-smooth muscle actin and proliferating cellnuclear antigen were compared and observed in each group. RESULTS AND CONCLUSION:At 10 and 20 days after treatment, in the three groups, skin bulge was visible in rabbit ears and no rabbit hair grew. Rabbit ears had obvious softening in the trifluoperazine group compared with the triamcinolone acetonide group, showing dark red. In the blank control group, rabbit ear scar was evident and showed red color. At 20 days after treatment, scar thickness and scar index were lower in the trifluoperazine and triamcinolone acetonide groups than in the blank control group. Matrix metal oproteinase 2 expression was significantly higher, but tissue inhibitor of metal oproteinase-2 and transforming growth factorβ1 levels were lower in the trifluoperazine and triamcinolone acetonide groups than in the blank control group. Results indicated that trifluoperazine obtained good proliferative effects on rabbit ear scar, and could decrease scar thickness.
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BACKGROUND:It is presumed that urinary trypsin inhibitor could have protective effects on local and systemic tissues and could inhibit osteoclast proliferation and activation under long-term chronic inflammation conditions and in ischemic and anoxic environment which was induced by prosthetic wear. OBJECTIVE:To investigate the inhibitory effect of ulinastatin on receptor activator for nuclear factor-κb ligand-induced differentiation, proliferation and osteoclastogenesis of RAW264.7 cells and its effects on matrix metal oproteinase-2, matrix metal oproteinase-9 expression level and activity. METHODS:Mouse monocyte/macrophage cellline RAW264.7 was treated with different concentrations of urinary trypsin inhibitor (0, 500, 5 000 U/mL) for 24, 48 and 72 hours. Experiments were divided into four groups:the blank group (RAW264.7 cells), receptor activator for nuclear factor-κb ligand-induced group (0 U/mL ulinastatin), 500 U/mL ulinastatin group and 5 000 U/mL ulinastatin group. RESULTS AND CONCLUSION:(1) MTT results indicated that there was no significant difference on the proliferation of RAW264.7 cells treated with urinary trypsin inhibitor at 0-5 000 U/mL (P>0.05) (2) Tartrate-resistant acid phosphatase staining results revealed that compared with receptor activator for nuclear factor-κb ligand-induced group, the number of tartrate-resistant acid phosphatase-positive cells was significantly less in the ulinastatin group (P<0.05), showing a time-dose dependent manner. (3) Immunohistochemisical results found that compared with receptor activator for nuclear factor-κb ligand-induced group, the percentage of matrix metal oproteinase-9-positive cells was apparently lower in the ulinastatin group. (4) Western blot assay results demonstrated that matrix metal oproteinase-9 expression was low in the RAW264.7 cells alone. At 48 hours after addition of receptor activator for nuclear factor-κb ligand, matrix metal oproteinase-9 protein expression was large. At 72 hours after culture in the 5 000 U/mL ulinastatin group, matrix metal oproteinase-9 protein expression was evidently reduced. (5) Gelatin zymography results showed that compared with the receptor activator for nuclear factor-κb ligand-induced group, matrix metal oproteinase-9 expression was significantly lower in the 5 000 U/mL ulinastatin group (P<0.05). Results suggested that urinary trypsin inhibitor inhibited receptor activator for nuclear factor-κb ligand-induced osteoclastogenesis and diminished matrix metal oproteinase-9 expression and activity.
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BACKGROUND:Interleukin-1βand matrix metal oproteinase-13 can promote the metabolism of chondrocytes, inhibit the capacity of synthesizing and repairing, induce the degradation of extracellular matrix, and play a crucial role in the occurrence of osteoarthritis. OBJECTIVE:To observe the effects of extracorporeal shock wave therapy on the interleukin-1βand matrix metal oproteinase-13 expression in rabbits with experimental knee osteoarthritis. METHODS:Thirty New Zealand rabbits were randomly and equal y divided into treatment group, model group and control group, with 10 rabbits in each group. Model of knee osteoarthritis was established in both the treatment group and model group, using modified plaster cast in extension position for 6 weeks. Then the rabbits of treatment group were treated with extracorporeal shock wave therapy, each 1 000 impulse, at the energy flux density of 0.1 mJ/mm2. There were no treatments in the control group. The rabbits in each group were sacrificed at 4 weeks after treatment, the knee synovial fluid and articular cartilage were col ected from the rabbits. The pathological changes of knee joint were detected using hematoxylin-eosin staining and toluidine blue staining. The interleukin-1βand matrix metal oproteinase-13 expression in the synovia was detected using ELISA and immunohistochemical staining respectively. RESULTS AND CONCLUSION:The interleukin-1βconcentration in the synovial fluid was significantly higher in the treatment group and model group than the control group (P<0.01), and the treatment group after treatment showed a lower concentration than the model group (P<0.05). Mankin scores in treatment group and model group were significantly increased compared with the control group (P<0.01), and the treatment group after treatment showed a lower score than the model group (P<0.05). The interleukin-1βand matrix metal oproteinase-13 positive expression rates in the treatment group and model group were significantly increased compared with the control group (P<0.01), and the treatment group after treatment showed a lower rate than the model group (P<0.05). The extracorporeal shock wave therapy can downregulate the expression of interleukin-1βand matrix metal oproteinase-13, promote the synthesis of new col agen.
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BACKGROUND:There are few reports concerning effects of warming the yang and benefiting the marrow for the knee osteoarthritis on the expression of matrix metal oproteinase. OBJECTIVE:To observe the effect of warming the yang and benefiting the marrow on the expression of matrix metal oproteinase in rabbit models of knee osteoarthritis. METHODS:Of 96 healthy adult New Zealand rabbits, 72 rabbits were randomly selected for making rabbit models of knee osteoarthritis using plaster external fixation. After success model establishment, the rabbits were randomly assigned to three groups. Model group was left intact. Chinese medicine group received daily intragastric administration of drug extract 24 mL/kg. Drug control group was daily intragastrical y administered Puli Capsule (glucosamine hydrochloride) 24 mg/kg, once a day, until the eighth week of success model induction. An additional 24 New Zealand rabbits served as blank controls. RESULTS AND CONCLUSION:Using quantitative PCR, matrix metal oproteinase-1, matrix metal oproteinase-3 and matrix metal oproteinase-13 expression was significantly higher in the model group than that in the other three groups. Matrix metal oproteinase-1, matrix metal oproteinase-3 and matrix metal oproteinase-13 expression was significantly lower in the Chinese medicine group and drug control group than that in the model group. These results indicated that warming the yang and benefiting the marrow for knee osteoarthritis in rabbits could effectively inhibit the expression of matrix metal oproteinase in rabbits.
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[Objective]To explore the mechanism of bioactive tanshinones in Salviae Miltiorrhiae regulating angiogenesis and lay the foundation for the prevention and treatment of cancer, atherosclerosis, ischemic heart disease and other angiogenesis-related diseases. [Method]Based on angiogenesis mechanisms, infer to recent 10 years of articles from home and abroad, analyze and summarize the angiogenesis regulatory mechanisms of various bioactive ingredients in Danshen on endothelial cells, in vitro tumour cells and in vivo xenograft tumor. [Result] Among various bioactive ingredients of Salvia, Salvianolic acid B, Tanshinone IIA, Cryptotanshinone, Dihydrotanshinone I can promote or inhibit angiogenesis. Furthermore, Salvianolic acid B and Tanshinone IIA are considered to be the most important bioactive ingredients in Danshen and exhibit a dual angiogenic regulating activity through regulating various approaches, such as pro-angiogenic factors, MMPs, HIF-1α, the PI3K/AKT/eNOS signal pathway and so on. [Conclusion]Various bioactive ingredients of Salvia can serve as a regulator of angiogenesis, and it may provide new ideas for the prevention of angiogenesis-related diseases.
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BACKGROUND:Many studies have shown that matrix metal oproteinases 1, 3, 9 and 13 play an important role in articular cartilage degeneration and destruction, but there is less special research on the articular synovium. OBJECTIVE:To observe the effect of long-distance running on the expressions of matrix metal oproteinases 1, 3, 9 and 13 in the synovium. METHODS:Fifteen male Wistar rats were divided into three groups:control group, tablet group and uphil group. Rats in the control group received ordinary captivity;rats in the tablet group ran on the horizontal treadmil (0°) at the speed of 1 km/h for 1 hour daily, and lasted for 45 days;rats in the uphil group daily ran on the horizontal treadmil (0°) at the speed of 1 km/h for 1 hour, and lasted for 15 days, and then the rats ran on the uphil treadmil (+20°) at the speed of 1 km/h for 1 hour daily and lasted for 30 days. The knee joint synovium injury models with varying degrees were established. The dual hind knee joints were obtained after modeling for paraffin-embedded. Then the overal sagittal slices were obtained for hematoxylin-eosin staining and immunohistochemical staining, and the experimental results were observed and analyzed. RESULTS AND CONCLUSION:After long-distance running, the expression of matrix metal oproteinases 1 in synovium of the tablet group and uphil group was increased when compared with that of the control group (P0.05). There was no significant difference in matrix metal oproteinases 3 expression (P>0.05). The expressions of matrix metal oproteinase 9 and matrix metal oproteinase 13 in synovium were in gradient increasing state (Pexercise can influence the normal physiological structure of rat knee joint synovium by changing the expression of matrix metal oproteinases.
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BACKGROUND:Cel transplantation offers a new promise of rebuilding the damaged myocardium. But the results of them are not consistent. It is not clear if the transplanted cel s can permanently improve heart function and the mechanism underlying this therapeutic effect. OBJECTIVE:To study the effect of intracoronary autologous bone marrow mononuclear cel transplantation on cardiac function, and angiogenesis and cytokine production in canines with acute myocardial infarction. METHODS:Left anterior descending coronary artery ligation was used to produce acute myocardial infarction models in hybrid canines. Bone marrow mononuclear cel s were harvested by using puncture of anterior crest and posterior superior iliac spine to prepare cel suspension. Sixteen hybrid canines were randomly divided into transplantation group (n=10) and control group (n=6). Bone marrow mononuclear cel s (transplantation group, n=10) or normal saline (control group, n=6) were intracoronarily infused into infarction-related arteries 2 hours after acute myocardial infarction. To evaluate the heart function, we used echocardiography at 2 hours and 6 weeks after acute myocardial infarction. Capil ary density was assessed 6 weeks after transplantation by using von Wil ebrand factor test. The mRNA levels of vascular endothelial growth factor 188, vascular endothelial growth factor 164, basic fibroblast growth factor and matrix metal oproteinase-9 in the infarct area were determined by reverse transcription-PCR at 6 weeks after transplantation. RESULTS AND CONCLUSION:In contrast to the control group, ejection fraction and stroke volume at 6 weeks after transplantation increased significantly in the transplantation group. The transplantation group had a greater amount of new vessels in the peri-infarct area than the control group. Compared with the control group, the mRNA levels of vascular endothelial growth factor 188, vascular endothelial growth factor 164, and basic fibroblast growth factor significantly increased in the transplantation group, but the mRNA level of matrix metal oproteinase-9 significantly decreased in the transplantation group. These findings suggest that intracoronary transplantation of autologous bone marrow mononuclear cel s may improve the cardiac function, and increase capil ary density, especial y in the border zone of infarcted myocardium. Otherwise, bone marrow mononuclear cel transplantation can increase the mRNA levels of vascular endothelial growth factor 188, vascular endothelial growth factor 164, and basic fibroblast growth factor, but decrease the mRNA level of matrix metal oproteinase-9.
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BACKGROUND: p38 mitogen-activated protein kinase signal transduction pathway is a member of the mitogen-activated protein kinase family. It plays an important role in the development of osteoarthritis. OBJECTIVE: To review the progress of p38 mitogen-activated protein kinase signal transduction pathway in the pathological process of osteoarthritis. METHODS: An online search of CNKI and PubMed databases was performed for articles using keywords of “p38 mitogen-activated protein kinase signal transduction pathway, osteoarthritis, articular cartilage, chondrocyte” in Chinese and English, respectively. Relevant articles were summarized from three aspects of introduction of p38 signal transduction pathway, the role of p38 mitogen-activated protein kinase signal transduction pathway in osteoarthritis and the inhibitor of p38 in osteoarthritis. A total of 90 articles were included. According to inclusion criteria, a number of 46 articles were retained at last. RESULES AND CONCLUSION: p38 mitogen-activated protein kinase signal transduction pathway has a close relation with chondrocyte hypertrophy and calcification, chondrocyte apoptosis, synthesis of cartilage matrix metal oproteinase, production of proinflammatory cytokines, and exerts a significant effect on the development of osteoarthritis. p38 mitogen-activated protein kinase is involved in the formation and development of osteoarthritis through a variety of complex mechanisms and plays a very important role. Therefore, blocking p38 mitogen-activated protein kinase signaling pathway may be a new target in the treatment of osteoarthritis.