摘要
目的探讨当归补血汤(当归、黄芪以5∶1的比例配制)对糖尿病大鼠肾组织损伤的保护作用及可能机制。方法采用腹腔注射链脲佐菌素(STZ,60 mg/kg)的方法建立糖尿病大鼠模型,分为正常组,模型组,当归补血汤高、低剂量组[3.6、1.8 g/(kg·d)]及氯沙坦钾组[0.03 g/(kg·d)],灌胃给药,每日1次;12周后,检测当归补血汤对模型大鼠体质量、肾质量体质量比、24 h尿蛋白定量、尿素氮(BUN)、血肌酐(SCr)、超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、超敏C反应蛋白(hs-CRP)、磷酸化酪氨酸激酶2(p-JAK2)及磷酸化信号转导及转录激活蛋白3(p-STAT3)的影响。结果当归补血汤组大鼠体质量显著增加,肾质量体质量比显著减小,24 h尿蛋白定量、BUN及SCr水平显著降低;当归补血汤可以提高模型组大鼠肾组织SOD活性、降低MDA含有量及降低TNF-α、IL-6和hs-CRP表达;同时有效抑制p-JAK2及p-STAT3蛋白的表达。结论当归补血汤具有保护糖尿病大鼠肾组织损伤的作用与其降低氧化应激水平,抑制JAK2/STAT3信号通路的激活,进而产生抗炎活性有关。
AIM To explore the protective effects of Danggui Buxue Decoction（ 5 ∶ 1 ratio of Angelicae sinensis Radix and Astragali Radix） on the renal injury in diabetic rats and its mechanism of action. METHODS The diabetic rats models were established by intraperitoneal injection of STZ（ 60 mg / kg） and the diabetic rats were divided into normal group,model group,high-,low-dose Danggui Buxue Decoction groups [3. 6,1. 8 g /（ kg · d） ],and losartan potassium group [0. 03 g /（ kg·d） ]. The corresponding agents were intragastrically administrated to the rats once daily. Twelve weeks later,the rats＇ body weights,ratio of kidney mass to body mass,24-hour urine protein,blood urea nitrogen（ BUN）,serum creatinine（ SCr）,superoxide dismutase（ SOD）,melondialdehyde（ MDA）,TNF-α,IL-6,hs-CRP,p-JAK2,and p-STAT3 were tested to observe the effects of Danggui Buxue Decoction on them. RESULTS The body weight was significantly increased; the ratio of kidney mass to body mass was significantly decreased; 24-hour urine protein,BUN,and SCr were significantly reduced in Danggui Buxue Decoction groups. The SOD activity was elevated; the MDA level was reduced significantly,and the expressions of TNF-α,IL-6,and hs-CRP were significantly down-regulated in Danggui Buxue Decoction groups,at the same time,the expression of p-JAK2 and p-STAT3 was significantly inhibited. CONCLUSION Danggui Buxue De-coction has protective effects on the renal injury in diabetic rats,which may be related to its anti-inflammatory effects by reducing the oxidative stress level and inhibiting the activation of JAK2 / STAT3 signaling pathway.
出处
《中成药》
CAS
CSCD
北大核心
2016年第12期2541-2545,共5页
Chinese Traditional Patent Medicine
基金
河南省医学科技攻关计划项目(2011010016)
