金花葵花多糖对LPS诱导致炎小鼠的抗炎作用

Anti-inflammatory effect of Abelmoschus manihot L.flower polysaccharides on LPS-induced inflammatory mice

研究旨在探究金花葵花多糖对炎症模型小鼠抗炎效果。将54只昆明小鼠分为空白对照(CK)组(0.9%NaCl)、脂多糖(LPS)模型组(0.01 mg/g LPS)、地塞米松(Dex)组(0.01 mg/g地塞米松)、L组(0.2 mg/g金花葵花多糖)、M组(0.4 mg/g金花葵花多糖)和H组(0.6 mg/g金花葵花多糖),每组9个重复,每个重复1只小鼠。连续灌胃3 d,除CK组外,其余各组均给予0.01 mg/g LPS腹腔注射,12 h后处死小鼠。结果表明,与Dex组相比,3个金花葵花多糖组小鼠肝脏系数和脾脏系数均具有显著差异(P<0.05)。与LPS组相比,M组NO释放量增加(P<0.05)。H组淋巴细胞活力和巨噬细胞吞噬率均高于LPS组(P<0.05)。M组和H组小鼠肝脏白细胞介素-6(IL-6)与肿瘤坏死因子-α(TNF-α)的表达量均低于LPS组(P<0.05)。研究表明,适宜剂量的金花葵花多糖对LPS致炎小鼠具有一定的抗炎效果,具有提高机体免疫的功效。

The study aimed to investigate the anti-inflammatory effects of Abelmoschus manihot L.flower polysaccharides on a mouse inflammation model.Fifty-four Kunming mice were divided into a blank control(CK)group(0.9%NaCl),a lipopolysaccharide(LPS)model group(0.01 mg/g LPS),a dexamethasone(Dex)group(0.01 mg/g DXMS),a L group(0.2 mg/g Abelmoschus manihot L.flower polysaccharides),a M group(0.4 mg/g Abelmoschus manihot L.flower polysaccharides),and a H group(0.6 mg/g Abelmoschus manihot L.flower polysaccharides).Each group had nine replicates and one mice per repliate.Continuous gavage was performed for three days,and except for the CK group,all other groups were intraperitoneally injected with 0.01 mg/g LPS.The mice were euthanized 12 h later.The results showed that compared to the Dex group,the liver index and spleen index of mice in the three groups ofAbelmoschus manihot L.flower polysaccharides had significant differences(P<0.05).Compared to the LPS group,the M group exhibited an increase in NO release(P<0.05).The H group showed a higher lymphocyte vitality and macrophage phagocytosis rate than the LPS group(P<0.05).The expression levels of IL-6 and TNF-αin the liver of mice in the M group and H group were lower than those in the LPS group(P<0.05).The study indicates that an appropriate dose ofAbelmoschus manihot L.flower polysaccharides has a certain anti-inflammatory effect on LPS-induced inflammatory mice and has the potential to enhance the body's immune response.