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作 者:张晓慧[1] 宋亮[1] 赵世敏[1] 王雪[1] 邹凯[1] 王玉珍[1]
机构地区:[1]内蒙古农业大学生命科学学院,呼和浩特010018
出 处:《内蒙古农业大学学报(自然科学版)》2017年第3期1-7,共7页Journal of Inner Mongolia Agricultural University(Natural Science Edition)
基 金:国家自然科学基金(81260662;81560677);内蒙古杰出青年培育基金(2016JQ08);内蒙古自然科学基金(2015MS0884);内蒙古农业大学本科生科研创新基金(DC201557)
摘 要:研究沙棘多糖对脂多糖(LPS)所致小鼠急性肝损伤的保护作用。方法:昆明小鼠被随机分为空白组(A)、模型组(B)、沙棘多糖低剂量组(C 100mg/kg)和高剂量组(D 200mg/kg)。沙棘多糖连续灌胃30天后,除空白组外,其他每组均腹腔注射LPS(10mg/kg)构建急性肝损伤模型。分别在LPS作用后4h和9h后,采血和收集肝组织。利用血清各项指标的试剂盒、Elisa试剂盒测定各项指标含量,以及QPCR测定肿瘤坏死因子(TNF-α)和白细胞介素-6(IL-6)的表达水平。结果:沙棘多糖能剂量依赖性抑制LPS诱导的血清中谷丙转氨酶(ALT)和谷草转氨酶(AST)以及肝组织丙二醛(MDA)含量的升高。沙棘多糖也降低了肿瘤坏死因子(TNF-α)和白细胞介素-6(IL-6)的表达水平,与模型组相比,沙棘多糖组肝组织的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物(GSH-Px)的活性也显著升高。结论:沙棘多糖对LPS诱导的小鼠急性肝损伤有较好的保护作用,其作用机制可能与其抗氧化和抗炎活性有关。The paper aims to investigate the protective effects of seabuckthorn polysaccharides (SP) on mice with Lipopolysaccha- ride (LPS) -induced acute liver injury. Mice were randomly divided into four groups: Blank control (A), Model (B), Lowdose of seabuckthorn polysaccharides(C 100 mg/kg), High dose group (D 200 mg/kg). After continuous intragastric administration with 30 days SP, mice were intraperitoneally injected with 10mg/kg LPS to induce acute liver injury. Blood and liver samples were collected following 4h and 9h post LPS challenge. The result indicated that SP can significantly inhibit the enhance of ALT , AST and MDA content, the expression of TNF - α and 1L - 6 wasmarkedly decrease as well, the activity of SOD and GSH - Pxin damaged liver tis- sues was significantly improved by SP. SP can obviously protect against the LPS induced acute liver injury in mice. The mechanism of this role of SP may be related to its anti - oxidative and anti - inflammatory effects.
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