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OBJECTIVE:To study the effects of ulinastatin on pathological state of lung tissue and aquaporin 1(AQP-1)and matrix metalloproteinases (MMP-2),MMP-9 expressions in silicosis rats. METHODS:Wistar rats were divided into normal con-trol group,model group,ulinastatin high-dose,medium-dose,low-dose groups(50×104,10×104,2×104 u/kg),20 in each group. Except for normal control group,rats in other groups were given 40 mg/mL SiO2 suspension 1 mL by non-exposed endotracheal per-fusion to induce silicosis model;1 h before modeling administration,corresponding doses of ulinastatin were intraperitoneally in-jected,for 3 d. Hematoxylin-eosin staining was used to observe silicon nodules in lung tissue of rats in each group;immunofluores-cence method was used to detect AQP-1 expression in lung tissue;real-time fluorescence quantitative polymerase chain reaction method was used to detect MMP-2,MMP-9 mRNA expressions in lung tissue;Western blot method was used to detect MMP-2, MMP-9 protein expressions in lung tissue. RESULTS:There were obvious silicon nodules and serious structural damage in lung tis-sue in model group,ulinastatin groups showed macrophage foci visible dust,but pulmonary fibrosis was obviously reduced. Com-pared with normal control group,AQP-1 expression in lung tissue in other groups were reduced,MMP-2,MMP-9 mRNA and pro-tein expressions were enhanced (P<0.05). Compared with model group,AQP-1 expression in lung tissue in ulinastatin groups were increased,MMP-2,MMP-9 mRNA and protein expressions were decreased (P<0.05),in which improvement effects in high-dose,medium-dose groups were superior to low-dose group(P<0.05). CONCLUSIONS:Ulinastatin can reduce the patholog-ical state of silicosis rats,increase AQP-1 expression and decrease MMP-2,MMP-9 expressions.
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BACKGROUND:Studies have shown that tanshinone II can improve microcirculation, dilate cerebral blood vessels, increase cerebral blood flow, reduce infarct size, and improve brain function after cerebral metabolic disorder. OBJECTIVE:To investigate the effect of tanshinone II combined with bone marrow mesenchymal stem cel transplantation on nerve regeneration folowing cerebral infarction in rats. METHODS:Rat models of acute cerebral infarction were prepared using the thread occlusion method and then given tanshinone II combined with bone marrow mesenchymal stem cel transplantation (combined group), bone marrow mesenchymal stem cel transplantation (cel transplantation group), and no treatment (model group), respectively. Neuromotor function was assessed using Longa scores. Expression of brain-derived neurotrophic factor gene around the infarction region was detected using RT-PCR. Cel apoptosis was detected using TUNEL. Immunohistochemistry staining was used to determine peri-cortex Nogo-A and NgR protein expression at the infarction region. RESULTS AND CONCLUSION:Longa scores, apoptotic index, and expression of Nogo-A and NgR proteins exhibited significant differences among three groups (P< 0.05) as folows: combined group < cel transplantation group < model group. Conversely, the expression of brain-derived neurotrophic factor gene was highest in the combined group successively folowed by the cel transplantation group and model group (P< 0.05). These data show that tanshinone II combined with bone marrow mesenchymal stem cel transplantation accelerate the recovery of neurologic function and promote nerve regeneration after cerebral infarction by incresing mRNA expression of brain-derived neurotrophic factor.
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BACKGROUND:Cel transplantation becomes a new approach for treatment of cerebral infarction. In recent years, bone marrow mesenchymal stem cels (BMSCs) have become an important kind of seed cels in cel transplantation. OBJECTIVE: To investigate the effect of fleabane injection combined with BMSC transplantation on S100B protein and superoxide dismutase expression in acute cerebral infarction rats. METHODS:Animal models of acute cerebral infarction were made in Sprague-Dawley rats using suture method. After successful modeling, 80 model rats were randomly divided into control group, fleabane group, BMSC group and combined group (fleabane combined with BMSC transplantation). Changes of serum S100B protein and serum superoxide dismutase levels were detected using enzyme-linked immunosorbent assay and xanthine oxidase method, respectively, before and after treatment. NIHSS neurological function scores were measured to observe neurological behavior changes in model rats. The infarct volume was measured by TTC staining. RESULTS AND CONCLUSION:At 36, 7, 14 days after treatment, S100B protein levels in the fleabane group and BMSC group were significantly lower than that in the control group, but higher than that in the combined group (P <0.05); serum superoxide dismutase levels in the fleabane group and BMSC group were significantly higher than that in the control group, but lower than that in the combined group (P < 0.05). At 1, 2, 3 weeks after treatment, NIHSS neurological function scores were ranked as folows: combined group < fleabane group and BMSC group < control group, and there was a significant difference between groups (P < 0.05). At 2 weeks after treatment, the infarct volume in the fleabane group and BMSC group was higher than that in the combined group but lower than that in the control group (P < 0.05). These findings indicate that fleabane combined with BMSC transplantation can inhibit the expression of S100B protein in rats with acute cerebral infarction, and promote the activity of superoxide dismutase, thereby playing a neuroprotective role.
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Objective To investigate the relationship of polymorphisms at codons 333 and 637 of TAP-1 allele gene to recurrent condyloma acuminatum (CA) in a Chinese population. Methods Amplificatory refraction mutation system-PCR (ARMS-PCR) was performed to detect TAP1 polymorphic residues at codon 333 in 88 patients with recurrent CA and 81 age- and sampling date-matched controls and at codon 637 in 60 patients with recurrent CA and 60 age- and sampling date-matched controls. Results The frequencies of AA,GG and AG genotypes at codon 333 of TAP-1 gene were 86.36%, 0, 13.64%, respectively, in patients with recurrent CA, 79.01%, 0 and 20.99%, respectively, in the controls, and no significant difference was observed between the two groups (χ2 = 1.604, P ＞ 0.05). However, a significant difference was observed in the frequencies of AA, GG and AG genotypes at codon 637 of TAP-1 gene between the patients and controls (3.33% vs 10.0%, 95.00% vs 60.00%, 1.67% vs 30.00%, χ2 = 21.551, P ＜ 0.01 ). Conclusions The recurrence of CA may be associated with the polymorphism at codon 637, but not with that at codon 333, of TAP-1 gene.