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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: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: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.