芍药苷对PFOS致小鼠肝脏氧化损伤的保护研究

目的 研究不同浓度的芍药苷对全氟辛烷磺酸基化合物（PFOS）损伤小鼠肝脏的抑制作用。方法 通过给小鼠灌服全氟辛烷酸钾（10 mg/kg,连续 灌胃18 d）建立小鼠肝脏氧化损伤模型。建模后,40只小鼠采用随机数表的方法分为模型对照组,高、中、低剂量组芍药苷100、50、10 mg/（kg·d）]及阳性对照组益肝灵片100 mg/（kg·d）],连续灌胃给药3周。分别检测小鼠血清和肝脏各种酶的水平,包括ALT、AST和血清碱性磷酸酶（ALP）以及肝脏丙二醛和超氧化物歧化酶（SOD）,另外采用HE染色法检测肝脏中组织学是否发生改变。结果 芍药苷不仅使肝脏中的SOD水平升高,而且使丙二醛水平降低（P均< 0.05）,进而有效缓解了PFOS导致的肝脏氧化损伤;芍药苷能有效降低小鼠血清ALT、AST及ALP的水平（P均< 0.05）,有效缓解PFOS导致的肝脏氧化损伤;在病理学上,芍药苷能有效改善PFOS导致的肝组织淤血、肝脏局部组织紊乱、细胞及组织水肿、炎症细胞浸润、局部组织坏死;PFOS对于小鼠体质量增长起到了抑制作用;在给予芍药苷治疗后,小鼠的体质量抑制得到缓解（P均< 0.05）。结论 PFOS可以引起肝脏的氧化应激反应,在一定程度上对肝脏组织造成氧化性损伤,芍药苷对于PFOS导致的肝脏氧化损伤具有一定的保护作用。

Protective effect of paeoniflorin on PFOS-induced oxidative liver damage in mouse models

Objective To investigate the effect of perfluorooctane sulfonate （PFOS） in mice. Methods The mouse models of oxidative liver injury were established by gavage of potassium perfluorooctane at a dose of 10 mg/kg for consecutive 18 d. After model establishment, 40 mice were divided into the model control group, high-dose, medium-dose and low-dose paeoniflorin groups （100 mg/（kg·d）, 50mg/（kg·d）, 10mg/（kg·d）） and positive control group （100 mg/（kg·d）, Yiganling tablet） by random number table method, and were given with intragastric administration for consecutive 3 weeks. The serum levels of alkaline phosphatase （ALP）, aspartate aminotransferase （AST） and alanine aminotransferase （ALT）, and the levels of superoxide dismutase （SOD） and malondialdehyde （MDA） in the liver tissues of mice were determined. The histological changes of liver were observed by hematoxylin-eosin staining. Results Paeoniflorin significantly increased the SOD level, whereas decreased the MDA level in the liver tissues （both P < 0.05）, thereby effectively alleviating the oxidative liver damage caused by PFOS. Paeoniflorin could significantly reduce the serum levels of ALT, AST and ALP （all P < 0.05）, and effectively mitigated the oxidative liver damage caused by PFOS. Pathologically, paeoniflorin could effectively alleviate liver tissue congestion, local liver tissue disorder, cell and tissue edema, inflammatory cell infiltration, and local tissue necrosis induced by PFOS. PFOS could also inhibit the weight gain of mice. After paeoniflorin treatment, the inhibitory effect upon mouse weight was significantly alleviated （all P < 0.05）. Conclusions PFOS can provoke oxidative stress responses to the liver, and lead to oxidative liver injury to certain extent. Paeoniflorin exerts certain protective effect on the development of oxidative liver injury caused by PFOS.