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BACKGROUND:Breviscapine has been shown to impact the reproductive capacity in rats with type 2 diabetes mel itus, but few reports concerned its mechanism of action. OBJECTIVE:To study the effects of breviscapine on proliferating cel nuclear antigen and proto-oncogene c-fos expression in testis of type 2 diabetes mel itus rats. METHODS:Total y 36 healthy male rats were randomly divided into control group, model group and breviscapine group with 12 rats in each group. In the model group and breviscapine group, rat models of type 2 diabetes mel itus were established by continuous intraperitoneal injection of streptozotocin. Blood glucose reaching 16.7 mmol/L in rats was considered as the standard of model induction. In the control group, rats were given an equal volume of citrate buffer solution by single intraperitoneal injection. In the breviscapine group, rats were administered breviscapine 10 mg/(kg?d) for 4 consecutive weeks by intraperitoneal injection. Rats in the other two groups were injected with an equal volume of physiological saline at the same time point. RESULTS AND CONCLUSION:After 4 weeks of intervention, serum testosterone testing, immunohistochemistry and PCR results showed that serum testosterone levels, proliferating cel nuclear antigen, c-Fos protein and mRNA expression:control group>breviscapine group>model group (P<0.05);blood glucose concentration:the control group
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Objective To explore the effects of keratinocyte growth factor receptor (KGFR) transgene on sodium channel in alveolar type Ⅱ cells with LPS-induced acute lung injury, to provide the evidence for gene treatment in acute lung injury. Method Totally 40 male Sprague-Dawtey rats were randomly divided into four groups, including normal control (n=8), injured control (n=10), normal transgene (n=10) and injured transgene (n=12). The models of acute lung injury were produced using LPS, and the successful criteria was the obvious enlargement in the lung tissue. The rats in normal transgene group and injured transgene group were injected with 1 mL of KGFR adenovirus vector through rats' tail vein. At 72 hours later, the rats in injured control group and injured transgene group were injected with LPS in dose of 5 mg/kg (BW). While rats in normal control group and normal transgene group were injected with equivalent saline simultaneously. Another 48 hours later, rats in the four groups were killed. The lung tissue were collected for analysis. The expression of sodium channel in rats' alveolar type Ⅱ cells were detected by immunohistochemistry and immunoeectron microscope. Difference among the experimental groups were estimated by ANOVA analysis (LSD-t-test). There was statistical signifi-cance when P<0.05. Results The levels of sodium channel expression in rats' alveolar type Ⅱ cells were differ-era, with normal control group (47.7±3.33), normal transgene group (46.9±5.21), injured tramgene group (29.19±4.11) and injured control group (5.1±2.3). The level of sodium channel expression in injured trans-gene group was lower than that in normal transgene group (t=9.134, P<0.001) and normal control group (t=10.601,P<0.001), but signifieantly higher than that in injured control group (t=16.466, P<0.001). Conclusions The transgene vector can effectively promote the expression of sodium channel in alveolar type Ⅱ cells in rats with LPS-indueed acute lung injury, and can alleviate sodium and water reteraion in alveolar.