栀子苷对糖尿病肾病小鼠的改善作用

目的：探讨栀子苷改善糖尿病肾病的作用效果。方法：利用链脲佐菌素（STZ）建立1型糖尿病小鼠模型，随机分为模型组、栀子苷低剂量组（100 mg/kg）、栀子苷高剂量组（200 mg/kg）和正常组。模型组和正常组给予0.9%氯化钠溶液，栀子苷剂量组给予相应剂量栀子苷，连续灌胃8周，观察记录小鼠生活状态，检测体质量和血糖，HE染色观察肾组织病理变化，RT-qPCR法检测TNF-α、IL-6和IL-1β mRNA表达情况。结果：与正常组比较，模型组小鼠生活质量降低，体质量增长缓慢（P＜0.01），血糖增高（P＜0.01），病理染色显示肾小球结构明显受损，肾间质炎性细胞大量浸润，RT-qPCR法检测结果显示肾组织中TNF-α、IL-6和IL-1β mRNA表达量上升（P＜0.01）。相较于模型组，栀子苷低、高剂量组小鼠生活状态尚可，体质量增长较快（P＜0.05），血糖明显下降（P＜0.01），肾组织病理形态明显改善，肾组织中TNF-α、IL-6和IL-1β mRNA表达量下降（P＜0.01）。结论：栀子苷能有效改善小鼠的糖尿病肾病状态，降低血糖，保护肾组织，其调控机制可能与其能改善糖尿病小鼠炎症状态有关。

The effect of geniposide on mice with diabetic nephropathy

Objective: To investigate the effect of geniposide on diabetic nephropathy. Methods: Diabetic mice were established by streptozotocin and randomly divided as model group, geniposide low dose group (100 mg/kg), high dose group (200 mg/kg) and normal control group. The model group and the normal group were given normal saline, and the geniposide dose groups were given the corresponding dose intragastrically for 8 weeks. The living conditions of the mice were observed and recorded. The body weight and blood glucose were measured. The pathological changes of renal tissue were observed by HE staining, and the expression of TNF-α, IL-6 and IL-1β mRNA were detected by RT-qPCR. Results: Compared with the normal control group, the model group had poorer life quality, slower weight gain (P<0.01), increased blood glucose (P<0.01), and obviously damaged glomerular structure shown by pathological staining. A large number of interstitial inflammatory cells were infiltrated, and the expression of TNF-α, IL-6 and IL-1β in renal tissue was increased, as detected by RT-qPCR assay (P<0.01). Compared with the model group, the mice in the low and high dose groups had a better living conditions, more rapid increase of the body weight (P<0.05), significantly decreased blood glucose (P<0.01) but improved pathological morphology of renal tissue and decreased expression of TNF-α, IL-6 and IL-1β in renal tissue (P<0.01). Conclusion: Geniposide can improve the symptoms of diabetes in mice and protect the kidney tissues. Its regulatory mechanism may be related to the improvement of inflammation in diabetic mice.