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中国精品科技期刊2020
吕芳芳,高阳阳,陈锦丽,等. 小蓬草乙醇提取物对葡聚糖硫酸钠诱导的溃疡性结肠炎小鼠的抗炎作用[J]. 食品工业科技,2021,42(15):314−320. doi: 10.13386/j.issn1002-0306.2020070360.
引用本文: 吕芳芳,高阳阳,陈锦丽,等. 小蓬草乙醇提取物对葡聚糖硫酸钠诱导的溃疡性结肠炎小鼠的抗炎作用[J]. 食品工业科技,2021,42(15):314−320. doi: 10.13386/j.issn1002-0306.2020070360.
LV Fangfang, GAO Yangyang, CHEN Jinli, et al. Anti-inflammatory Effects of Ethanol Extract from Conyza canadensis on DSS-induced Ulcerative Colitis in Mice Model[J]. Science and Technology of Food Industry, 2021, 42(15): 314−320. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2020070360.
Citation: LV Fangfang, GAO Yangyang, CHEN Jinli, et al. Anti-inflammatory Effects of Ethanol Extract from Conyza canadensis on DSS-induced Ulcerative Colitis in Mice Model[J]. Science and Technology of Food Industry, 2021, 42(15): 314−320. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2020070360.

小蓬草乙醇提取物对葡聚糖硫酸钠诱导的溃疡性结肠炎小鼠的抗炎作用

Anti-inflammatory Effects of Ethanol Extract from Conyza canadensis on DSS-induced Ulcerative Colitis in Mice Model

  • 摘要: 探讨小蓬草乙醇提取物(CME)对葡聚糖硫酸钠(dextran sodium sulfate,DSS)诱导的溃疡性结肠炎小鼠的抗炎能力的影响。将小鼠随机分成正常组、模型组、低剂量和高剂量CME组。除正常组外,其余各组小鼠采用DSS诱导结肠炎小鼠模型,并对低剂量和高剂量CME组分别灌胃50和200 mg·kg−1 CME,持续7 d。观察各组小鼠的体重、结肠长度、结肠重量长度比、疾病活动指数(disease activity index,DAI)及结肠组织病理学变化。检测结肠组织中髓过氧化物酶(myeloperoxidase,MPO)、谷胱甘肽(glutathione,GSH),超氧歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)的水平和结肠肿瘤坏死因子(tumor necrosis factor, TNF)-α、白介素(Interlukin, IL)-1β、IL-6的分泌水平,以及TNF-α、IL-1β、IL-6、诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)和环氧合酶-2(cyclooxygenase-2,COX-2)的mRNA表达水平。结果表明,相较于模型组,CME组能显著抑制DSS诱导的体重减轻、结肠缩短和肠壁增厚(P<0.05),结肠长度恢复至7.5 cm(低剂量CME组)和8.6 cm(高剂量CME组);改善结肠病理组织的粘膜损伤,隐窝丧失和炎症程度;显著提高结肠组织中GSH和SOD的水平(P<0.05),降低MPO和MDA水平。此外,高剂量CME组还能显著抑制结肠组织中的炎性细胞因子(TNF-α、IL-1β、IL-6)的分泌和iNOS、COX-2以及TNF-α、IL-1β、IL-6的mRNA转录(P<0.05)。综合而言,CME通过抑制炎性细胞因子的分泌及炎性介质在结肠组织中的表达而对DSS诱导的结肠炎小鼠的具有抗炎作用。

     

    Abstract: To observe the anti-inflammatory effects of ethanol extract from Conyza canadensis (CME) on dextran sodium sulfate (DSS)-induced ulcerative colitis in mice, the mice were divided into normal control group, model group, low dose and high dose CME groups. Except the normal control group, all the other groups were treated with DSS to induce the ulcerative colitis model, and the low-dose and high-dose CME groups were respectively given 50 mg·kg−1 and 200 mg·kg−1 CME by gavage for 7 days continuously. Body weight, colon length, ratio of colon length/weight, disease activity index (DAI) and histological changes of each group of mice were observed. The levels of colonic myeloperoxidase (MPO), glutathione (GSH), superoxide dismutase (SOD) and malondialdehyde (MDA) and the secretion levels of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β) and interleukin-6(IL-6), and expression levels of TNF-α, IL-1β, IL-6, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (cox-2) were also measured. The results showed CME groups significantly inhibited DSS-induced weight loss, colon shortening and intestinal wall thickening compared with the model group (P<0.05), the length of colon recovered to 7.5 cm (low dose CME group) and 8.6 cm (high dose CME group); CME groups significantly improved the mucosal damage, crypt loss and the degree of inflammation. It also resulted in significant increase of GSH and SOD levels(P<0.05), reduced MPO and MDA levels in the colon tissue. In addition, CME could also significantly inhibit the secretion of inflammatory cytokines (TNF-α, IL-1β, IL-6) and the transcription of mRNA of iNOS, COX-2, TNF-α, IL-1β, and IL-6 in colon tissues. Overall, CME had anti-inflammation effects on DSS-induced colitis mice by inhibiting the secretion of inflammatory cytokines and the expression of inflammatory mediators in colon tissues.

     

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