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[目的]观察商陆皂苷甲(esculentosideA,EsA)对BXSB小鼠肾组织细胞增殖核抗原(PCNA)、半胱氨酸天冬氨酸酶3(Caspase-3)、凋亡诱导因子(Fas)和凋亡诱导因子配体(FasL)蛋白表达影响。[方法]将24只18周龄雄性BXSB小鼠随机分为模型组、地塞米松组和商陆皂苷甲(EsA)组,8只/组。腹腔注射干预:模型组RPMI1640培养液0.2mL/d;地塞米松组,地塞米松溶液1mg/kg·d;商陆皂苷甲组,EsA溶液20mg/kg·d;每只小鼠1次/d,连续4周,处死小鼠取肾组织标本检测(终点为小鼠22周龄)。干预始点及结束前,留取尿标本检测尿蛋白和尿肌酐浓度。[结果]与模型组相比,商陆皂苷甲组和地塞米松组尿蛋白/肌酐比值下降,肾脏病理变化有不同程度改善,肾组织中PCNA表达减弱,肾组织Caspase-3、Fas和FasL表达增强(P<0.05)。[结论]实验剂量EsA和地塞米松能够降低BXSB小鼠尿蛋白,改善肾脏病理变化;EsA和地塞米松减轻BXSB小鼠肾损害可能机制是通过抑制BXSB小鼠肾组织细胞增殖和促进肾组织细胞凋亡实现。
[Objective] To observe the effects of Esculentoside A (EsA) on the expression of PCNA, Caspase-3, Fas in kidney of BXSB mice, And apoptosis inducing factor ligand (FasL) protein expression. [Methods] Twenty-four male BXSB mice of 18 weeks old were randomly divided into model group, dexamethasone group and EsA group (n = 8). Intraperitoneal injection intervention: model group RPMI1640 0.2mL / d; dexamethasone group, dexamethasone solution 1mg / kg · d; safronin A group, EsA solution 20mg / kg · d; 1 mouse / d, for 4 weeks, the mice were sacrificed to take kidney tissue samples (end point of mice 22 weeks of age). Before intervention and before the end, urine samples were collected for urinary protein and urinary creatinine concentrations. [Results] Compared with model group, urinary albumin / creatinine ratio in Esculentoside A group and dexamethasone group decreased, renal pathological changes improved to some extent, and PCNA expression in renal tissue decreased. Caspase-3, Fas and FasL The expression was enhanced (P <0.05). [Conclusion] The experimental doses of EsA and dexamethasone can reduce urinary protein in BXSB mice and improve renal pathological changes. The possible mechanism of EsA and dexamethasone in reducing renal damage in BXSB mice is that by inhibiting renal cell proliferation and promoting renal tissue Apoptosis is achieved.