Protective effect of β-(1,3 → 1,6)-d-glucan against irritant-induced gastric lesions

Protective effect of β-(1,3 → 1,6)-d-glucan against irritant-induced gastric lesions
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β-(1,3 → 1,6)-d-葡聚糖对刺激性胃损伤的保护作用

DOI:
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发表时间:
2011
影响因子:
3.6
通讯作者:
T. Mizushima
T. Mizushima
中科院分区:
医学3区
文献类型:
--
作者:
Ken;Yuta Tanaka;Toshio Suzuki;T. Mizushima

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具有β-(1,6)支链的β-(1,3)-d-葡聚糖具有多种药理活性,如抗肿瘤和抗感染活性,这是由于其免疫调节作用。胃病变是攻击性和防御性因素失衡的结果。在本研究中,我们研究了从出芽短梗霉中分离的具有β-(1,6)分支的β-(1,3)-d-葡聚糖对小鼠胃溃疡反应的影响。口服β-葡聚糖可改善乙醇(EtOH)或盐酸诱导的胃损伤。β-葡聚糖的这种给药还抑制EtOH诱导的炎症反应,例如中性粒细胞的浸润以及促炎细胞因子、趋化因子和细胞粘附分子(CAM)在胃粘膜的表达。在各种防御因子中,热休克蛋白(HSP)70和粘蛋白的水平通过给予β-葡聚糖而增加,但不增加PGE 2。在体外培养的细胞中还观察到β-葡聚糖依赖性诱导HSP 70和粘蛋白的表达以及抑制促炎细胞因子、趋化因子和CAM的表达。本研究的结果表明,β-葡聚糖通过增加防御因子(如HSP 70和粘蛋白)的水平来保护胃粘膜免受刺激诱导的损伤的形成。
β-(1,3)-d-Glucan with β-(1,6) branches has been reported to have various pharmacological activities, such as anti-tumour and anti-infection activities, which result from its immunomodulating effects. Gastric lesions result from an imbalance between aggressive and defensive factors. In the present study, we examined the effect of β-(1,3)-d-glucan with β-(1,6) branches isolated from Aureobasidium pullulans on the gastric ulcerogenic response in mice. Oral administration of β-glucan ameliorated gastric lesions induced by ethanol (EtOH) or HCl. This administration of β-glucan also suppressed EtOH-induced inflammatory responses, such as infiltration of neutrophils and expression of pro-inflammatory cytokines, chemokines and cell adhesion molecules (CAM) at the gastric mucosa. Of the various defensive factors, the levels of heat shock protein (HSP) 70 and mucin but not PGE2 were increased by the administration of β-glucan. β-Glucan-dependent induction of the expression of HSP70 and mucin proteins and suppression of the expression of pro-inflammatory cytokines, chemokines and CAM were also observed in cultured cells in vitro. The results of the present study suggest that β-glucan protects the gastric mucosa from the formation of irritant-induced lesions by increasing the levels of defensive factors, such as HSP70 and mucin.
DOI: 10.5555/uri:pii:0016508584902026
发表时间: 1984
期刊: Gastroenterology
影响因子: 29.4
作者:
J. E. Krawisz;P. Sharon;W. Stenson
通讯作者: J. E. Krawisz;P. Sharon;W. Stenson