Amelioration of colitis in mouse model by exploring antioxidative potentials of an indigenous probiotic strain of Lactobacillus fermentum Lf1.

Amelioration of colitis in mouse model by exploring antioxidative potentials of an indigenous probiotic strain of Lactobacillus fermentum Lf1.
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通过探索乳酸乳杆菌发酵液LF1的本地益生菌菌株的抗氧化潜力,改善结肠炎。

DOI:
10.1155/2014/206732
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发表时间:
2014
影响因子:
--
通讯作者:
Grover S
Grover S
中科院分区:
生物学3区
文献类型:
--
作者:
Chauhan R;Vasanthakumari AS;Panwar H;Mallapa RH;Duary RK;Batish VK;Grover S

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在对8株本土益生菌进行初步筛选的基础上,筛选出发酵乳杆菌Lf 1,并对其在DSS结肠炎小鼠模型中的抗氧化作用进行了评价。结果表明,发酵乳杆菌Lf 1在H2 O2应激下可使HT-29细胞中“Nrf 2”的表达增加6.43倍,MDA抑制率为78.1 ± 0.24%。Lf 1处理组小鼠的疾病活动指数和组织学评分低于对照组。然而,在Lf 1处理的小鼠中未观察到“Nrf 2”的表达。在两组中记录到抗氧化酶如SOD 2和TrxR-1的表达显著增加。与对照组相比,结肠炎诱导小鼠中SOD 2的表达显著下调了−100.00倍,结肠炎Lf 1治疗组中下调幅度大幅降低至−37.04倍。几乎,在“硫氧还蛋白”表达的情况下记录了类似的趋势,尽管“CAT”对表达是无活性的。与结肠炎对照组相比,Lf 1给药组的丙二醛水平降低(37.92 ± 6.31 vs 91.13 ± 5.76 μM/g)。这些结果指向Lf 1诱导的小鼠模型中抗氧化酶系统的激活及其作为IBD管理的新策略的前景。
Based on the preliminary screening of eight indigenous putative probiotic Lactobacilli, Lactobacillus fermentum Lf1 was selected for assessing its antioxidative efficacy in DSS colitis mouse model based on its ability to enhance the expression of “Nrf2” by 6.43-fold and malondialdehyde (MDA) inhibition by 78.1  ±  0.24% in HT-29 cells under H2O2 stress. The Disease Activity Index and histological scores of Lf1-treated mice were lower than the control group. However, expression of “Nrf2” was not observed in Lf1-treated mice. A significant increase in the expression of antioxidative enzymes such as SOD2 and TrxR-1 was recorded in both of the groups. The expression of SOD2 was significantly downregulated in colitis-induced mice by −100.00-fold relative to control group, and the downregulation was considerably reduced to −37.04-fold in colitis Lf1 treatment group. Almost, a similar trend was recorded in case of “thioredoxin” expression, though “CAT” was refractile to expression. The Lf1-treated group had decreased malondialdehyde level as compared to colitis control (37.92  ±  6.31 versus 91.13  ±  5.76 μM/g). These results point towards Lf1-induced activation of the antioxidant enzyme system in the mouse model and its prospects to be explored as a new strategy for IBD management.
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