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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。
To study the protective effect of sea buckthorn polysaccharides on acute hepatic injury induced by lipopolysaccharide (LPS) in mice. Methods: Kunming mice were randomly divided into blank group (A), model group (B), low dose of sea buckthorn polysaccharide group (C 100mg / kg) and high dose group (D 200mg / kg). Seabuckthorn polysaccharide 30 days after continuous gavage, except for the blank group, the other groups were intraperitoneal injection of LPS (10mg / kg) model of acute liver injury. After 4h and 9h after LPS treatment, blood and liver tissues were collected. Serum levels of various indicators of the kit, Elisa kit determination of indicators, and QPCR determination of tumor necrosis factor (TNF-α) and interleukin -6 (IL-6) expression levels. Results: Seabuckthorn polysaccharide could inhibit LPS-induced elevation of ALT, AST and MDA in liver tissue in a dose-dependent manner. Seabuckthorn polysaccharides also reduced the expression of tumor necrosis factor (TNF-α) and interleukin-6 (IL-6). Compared with the model group, the superoxide dismutase (SOD) Glutathione peroxidase (GSH-Px) activity was also significantly increased. Conclusion: The polysaccharides from Hippophae rhamnoides have a good protective effect on LPS-induced acute liver injury in mice, and its mechanism may be related to its antioxidant and anti-inflammatory activity.