Zhou Yuyan, Lu Xiaoya, Xia Li, Yao Weiqiang, Qin Guozheng, Wang Guodong
Drug Research and Development Center//School of Pharmacy, Wannan Medical College, Wuhu 241002, China.
Anhui Provincial Engineering Research Center for Polysaccharide Drugs//Anhui Provincial Key Laboratory of Active Biological Macro-molecules, Wuhu 241002, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2020 Oct 30;40(10):1399-1405. doi: 10.12122/j.issn.1673-4254.2020.10.04.
To investigate the protective effect of arctiin with anti-inflammatory bioactivity against triptolide-induced nephrotoxicity in rats and explore the underlying mechanism.
Forty SD rats were divided into 4 groups for gastric lavage of normal saline, arctiin (500 mg/kg), triptolide (500 μg/kg), or both arctiin (500 mg/kg) and triptolide (500 μg/kg). Blood samples were collected for analysis of biochemical renal parameters, and the renal tissues were harvested for determining the kidney index and for pathological evaluation with HE staining. In the experiment, HK-2 cells were treated with arctiin and triptolide either alone or in combination, and the cell viability was determined with MTT assay; the cell morphological changes was observed using laser confocal microscopy, cell apoptosis was detected using flow cytometry, and the expressions of inflammation-related protein expression were detected by Western blotting.
In SD rats, arctiin significantly antagonized triptolide-induced elevation of BUN, Scr and kidney index ( < 0.05) and obviously improved renal tissue damages induced by triptolide including cell swelling, vacuolization and spotty necrosis. Arctiin significantly inhibited triptolide-induced cytotoxicity in HK-2 cells and increased the cell viability at 24 h ( < 0.05). Arctiin also attenuated triptolide-induced cell morphological changes, decreased cell apoptosis rate ( < 0.05) and reversed the expressions of IκBα and nuclear p65 ( < 0.05).
Arctiin can protect the kidney from triptolide-induced damages in rats possibly through the anti-inflammatory pathway.
研究具有抗炎生物活性的牛蒡子苷对雷公藤甲素诱导的大鼠肾毒性的保护作用，并探讨其潜在机制。
将40只SD大鼠分为4组，分别灌胃生理盐水、牛蒡子苷（500mg/kg）、雷公藤甲素（500μg/kg）或牛蒡子苷（500mg/kg）与雷公藤甲素（500μg/kg）。采集血样分析肾脏生化指标，摘取肾组织测定肾脏指数并进行HE染色病理评估。实验中，HK-2细胞单独或联合用牛蒡子苷和雷公藤甲素处理，用MTT法测定细胞活力；用激光共聚焦显微镜观察细胞形态变化，用流式细胞术检测细胞凋亡，用蛋白质免疫印迹法检测炎症相关蛋白表达。
在SD大鼠中，牛蒡子苷显著拮抗雷公藤甲素诱导的血尿素氮、血肌酐升高及肾脏指数增加（P<0.05），并明显改善雷公藤甲素诱导的肾组织损伤，包括细胞肿胀、空泡化和点状坏死。牛蒡子苷显著抑制雷公藤甲素诱导的HK-2细胞毒性，并在24小时时提高细胞活力（P<0.05）。牛蒡子苷还减轻了雷公藤甲素诱导的细胞形态变化，降低细胞凋亡率（P<0.05），并逆转IκBα和核p65的表达（P<0.05）。
牛蒡子苷可能通过抗炎途径保护大鼠肾脏免受雷公藤甲素诱导的损伤。
