摘要
目的考察金丝桃苷对内毒素(LPS)诱导的小鼠急性肾损伤的保护作用。方法通过采用腹腔注射7 mg·kg-1LPS建立小鼠急性肾损伤模型,通过检测血清尿素氮(BUN)和肌酐(Cr)水平,HE染色法观察肾脏病理组织学改变,Western blot法检测p50、p65、IκB-α和TLR4的蛋白表达,考察金丝桃苷对小鼠急性肾损伤保护作用。结果与模型组相比,金丝桃苷降低小鼠血清中BUN、Cr水平及肾组织p50、p65、和TLR4的蛋白表达量,升高IκB-α的蛋白表达量,组织切片观察发现其可缓解肾组织损伤,且具有一定的剂量依赖关系。结论金丝桃苷对内毒素所致的小鼠急性肾损伤具有一定的保护作用,其机制可能与抑制NF-κB炎症通路有关。
Objective To characterize the protective effects of hyperoside on endotoxin（LPS）-induced acute kidney injury in mice. Methods The acute kidney injury model of mice, which established by intraperitoneal injection（ i. p. ）of LPS, was used to evaluate the protective effects of hyperoside. Biochemical indicator ser- um urea nitrogen （BUN）and creatinine （Cr）were investigated. Renal tissues histological were observed using HE staining. Expression of p50, p65, IκB-α and TLR4 protein were measured using Western Blotting Assay. Results Hyperoside protected endotoxin（LPS）-induced acute kidney injury in mice by reduced serum BUN and Cr. The mechanism involved decrease p50, p65, TLR4 and increase IκB-α expression in renal tissue. Re- nal tissues histological showed hyperoside protected kidney injury in a dose-depend manner. Conclusions Hyperoside could protect endotoxin（LPS）-induced acute kidney injury in mice through inhibition of NF-κB inflammatory pathway.
出处
《沈阳药科大学学报》
CAS
CSCD
北大核心
2014年第10期799-803,共5页
Journal of Shenyang Pharmaceutical University
