基于UPLCQTOF/MS的黑灵芝多糖对大鼠急性肠道炎症作用机制研究

李露; 付王威; 吴睿婷; 吴文英; 尹术华; 宋也好; 万敏; 李文娟

doi:10.13386/j.issn1002-0306.2020050103

基于UPLCQTOF/MS的黑灵芝多糖对大鼠急性肠道炎症作用机制研究

1. 南昌大学食品学院, 江西南昌 330047;
2. 江西省食品检验检测研究院, 江西南昌 330001

基金项目:

国家自然科学基金地区项目（81860713）；南昌大学研究生创新项目（CX2018116）。

详细信息

作者简介:
李露(1995-),女,硕士研究生,研究方向:食品科学与工程,E-mai:1752003235@qq.com。

通讯作者:
李文娟(1982-),女,博士,教授,研究方向:天然产物与功能性食品,E-mail:Liwenjuan8211@126.com。

中图分类号: TS207.3
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出版历程
- 收稿日期: 2020-05-08
- 网络出版日期: 2021-03-15
- 刊出日期: 2021-03-14

Effect of Ganoderma lucidum Polysaccharides on Intestinal Inflammation in Rats Based on UPLC-Q-TOF/MS

1. College of Food Science, Nanchang University, Nanchang 330047, China;
2. Food Inspection and Testing Institute of Jiangxi Province, Nanchang 330001, China

摘要

摘要: 探究黑灵芝多糖（PSG）对脂多糖（LPS）诱导的大鼠急性肠道炎症的作用机制。本实验将大鼠随机分为正常组（Con）、模型组（LPS）、阳性对照组（DEX）和黑灵芝多糖低、中、高剂量组（PSG），每组10只。PSG低、中、高剂量组分别灌胃黑灵芝多糖20、40、80 mg/kg。Con组、LPS组与PSG组则每天灌胃等量的生理盐水，连续灌胃7 d。第7 d灌胃结束后，腹腔注射0.8 mg/kg的LPS溶液建立急性肠道炎症模型。通过观察大鼠空肠组织形态、检测细胞因子IL-1β及IL-10含量等指标，结果发现，PSG对LPS诱导的大鼠具有抗炎作用。与LPS组相比，PSG组空肠组织形态明显得到改善，肠道组织中IL-1β和IL-10含量被调节至正常水平。进一步，利用超高效液相色谱-四级杆串联飞行时间质谱（UPLC-Q-TOF/MS）方法获得了四组大鼠盲肠内容物样品的代谢轮廓图。结果发现，与Con组相比，LPS组大鼠盲肠内容物中存在22种代谢物。同时，PSG干预可回调PC （24：0/20：4（5Z，8Z，11Z，14Z））、DG （16：0/20：3（5Z，8Z，11Z）/0：0）等12种差异代谢物，进而影响甘油磷脂代谢、亚油酸代谢和α-亚麻酸代谢等三条代谢通路，发挥其对LPS诱导大鼠的抗炎作用。综上，PSG可改善LPS所致急性肠道炎症，作用机理与其抑制促炎因子的释放和代谢紊乱有关。
- 黑灵芝多糖 /
- 急性肠道炎症 /
- 超高效液相色谱-四级杆串联飞行时间质谱 /
- 代谢组学 /
- 抗炎
Abstract: The protective effects of Ganoderma atrum polysaccharide(PSG) on acute intestinal inflammation caused by lipopolysaccharide(LPS) were investigated. Rats were randomly divided into a control group(Con), a model group(LPS), positive control group(DEX) and three groups treated with PSG: Low-dose group(PSG-20), middle-dose group(PSG-40) and high-dose group(PSG-80), with 10 rats in each group. Rats were orally administered either vehicle(0.9% saline) alone or vehicle composition containing PSG(20, 40, and 80 mg/kg/d) for 7 days. After intragastric administration on the 7th day, 0.8 mg/kg LPS was injected intraperitoneally to establish an acute intestinal inflammation model. The results indicated that PSG has an anti-inflammatory effect on LPS-induced rats by observing jejunum histology, detecting the content of IL-1β and IL-10 in intestinal tissue. Compared with LPS group, the morphology of the jejunum tissue and the content of IL-1β and IL-10 were adjusted to normal levels. Furthermore, the metabolic effects of PSG were evaluated by screening and identifying differential metabolites and exploring metabolic pathways in rats based on UPLC-Q-TOF/MS metabolomics analysis. Accordingly, results indicated that 22 metabolites were significantly(P<0.05) changed in acute intestinal inflammation rats when compared to control rats. Meanwhile, PSG pretreatment could restore 12 different metabolites such as PC(24: 0/20: 4(5Z, 8Z, 11Z, 14Z)), DG(16: 0/20: 3(5Z, 8Z, 11Z)/0:0), and then participated in three metabolic pathways of glycerophospholipid metabolism, linoleic acid metabolism and α-linolenic acid metabolism, exerting its anti-inflammatory effects on LPS-induced rats. Altogether, PSG could improve LPS-induced acute intestinal inflammation and its mechanism were linked to inhibit release of proinflammatory mediators and reverse metabolic pathway disturbances

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