摘要
目的:研究没食子对IgA肾病大鼠血清与肾组织核转录因子-κB(NF-κB)的影响。方法:采用CCl4+脂多糖+牛血清白蛋白联合法复制大鼠IgA肾病模型。80只SD大鼠随机均分为正常对照(等容生理盐水)组、模型(等容生理盐水)组与没食子高、中、低剂量(300、150、75 mg/kg)组,灌胃给药,每天1次,连续4周。测定大鼠24 h尿蛋白量;酶标仪法测定大鼠血清NF-κB含量;免疫组化法测定大鼠肾组织NF-κB的表达;观察大鼠肾脏病理损害程度。结果:与正常对照组比较,模型组大鼠24 h尿蛋白量增加,血清NF-κB含量增加,肾组织NF-κB表达增强,差异有统计学意义(P<0.05);大鼠肾小球系膜增宽(节段)伴/不伴细胞增生,肾间质轻度纤维化,部分小管扩张。与模型组比较,没食子高、中、低剂量组大鼠24 h尿蛋白量减少;没食子高剂量组大鼠血清NF-κB含量减少,肾组织NF-κB表达减弱,差异有统计学意义(P<0.05);大鼠肾脏病理情况有一定改善。结论:没食子能够减轻IgA肾病模型大鼠肾损害,其机制可能与下调NF-κB水平有关。
ABSTRACT OBJECTIVE: To study the effects of Quercus infectoria on NF-kB in serum and renal tissue of IgA nephropathy rats. METHODS: lgA nephropathy model was induced by carbon tetrachloride+ lipopolysaccharide+BSA. 80 SD rats were randomly divided into normal control group (constant volume of normal saline), model group (constant volume of normal saline) and Q. infectoria gallnut high-dose, medium-dose and low-dose groups (300,150,75 mg/kg). They were given relevant medicines intragas- trically once a day for consecutive 4 weeks. 24 h albuminuria of rats was determined. ELISA method was used to detect the content of NF-κB; Immunohistochemical method was adopted to determine the expression of NF-κB. Semi-quantitative score method was used to calculate the pathological score to observe kidney pathological damage. RESULTS: Compared with normal control group, 24 h albuminuria, serum content of NF-~B and the expression of NF-kB were all increased in model group; there was statistical significance (P〈0.05). Glomerular mesangium (segment) rats were broadened with or without cell proliferation, and slight renal interstitial fibrosis and some tubular ectasia were found. Compared with model group, 24 h albuminuria, in Q. infectoria high-dose, medium-dose and low-dose groups; serum content of NF-κB and the expression of NF-κB were all decreased in Q. infectoria high-dose groups; there was statistical significance(P〈0.05), renal pathological symptom was improved. CONCLUSIONS:Q. infectoria can relieve renal damage in IgA nephropathy model rats, and the mechanism may be related to down-regulation of NF-κB
出处
《中国药房》
CAS
CSCD
2014年第43期4036-4039,共4页
China Pharmacy
基金
新疆维吾尔自治区心血管病研究重点实验室开放课题(No.XJDX-0903-2011-06)