潜在益生菌抗高脂血症机制的研究

Fatma E. Salem, Mohamed M. Aboulwafa, Shahenda Mahgoub, Riham M. Shawky, Shima Ali Ibrahim
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引用次数: 0

摘要

高胆固醇血症导致心血管疾病,这几乎是世界范围内导致死亡的主要原因。益生菌的降胆固醇作用越来越受到人们的关注,尤其是化学药物产生的一些不良副作用。了解益生菌的潜在作用并选择正确的使用方法,需要研究它们控制血清胆固醇的机制。方法:本研究采用乳酸菌(Lactococcus lactis ssp.)和乳酸菌(Lactococcus lactis .)乳酸菌和Pediococcus sp.)在我们之前的工作中从乳制品中分离出来,具有高的体外胆固醇去除活性以及有希望的体内抗高脂血症作用。在研究益生菌抗高脂血症作用的仓鼠实验中,切除不同组的肝脏,测定肝脏总胆固醇和细胞色素P450家族7亚家族A成员1 (CYP7A1)的水平。统计分析采用单因素方差分析(ANOVA)和事后检验。p值< 0.05的概率认为有统计学意义。结果:乳酸乳球菌;与饮食性高脂血症对照组相比,乳酸链球菌和Pediococcus sp.显著降低了肝脏总胆固醇水平24.96%和35.80% (p < 0.05),使肝脏CYP7A1水平分别提高了49.60%和37.84% (p < 0.05)。两种分离药物与对照药物阿托伐他汀在两项检测参数水平上的影响均无显著差异。结论:我们引入了两种与阿托伐他汀对肝脏总胆固醇和肝脏CYP7A1水平影响相似的潜在益生菌。因此,这些分离物可以作为辅助治疗,以减少阿托伐他汀的剂量,从而减少其副作用。抗高血脂作用的可能机制可能是通过上调肝脏CYP7A1基因,导致胆固醇合成更多胆汁酸,从而降低肝脏胆固醇水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Investigation of the Antihyperlipidemic Mechanism of Potential Probiotics
Hypercholesterolemia leads to cardiovascular diseases that are almost the leading cause of death worldwide. The cholesterol-lowering effect of probiotics is getting increased attention especially that the chemical drugs produce several undesirable side effects. Understanding probiotics' potential effects and choosing the right way to use them requires research into the mechanisms through which they control serum cholesterol. Methods: In this study, we used two lactic acid bacteria (LAB) ( Lactococcus lactis ssp. lactis and Pediococcus sp.) that were isolated in a previous work of ours from dairy products and had a high in vitro cholesterol removal activity together with promising antihyperlipidemic effect in vivo . In the laboratory animal experiment conducted on hamsters for studying the antihyperlipidemic effect of probiotics, the livers of the different groups were excised, and the levels of hepatic total cholesterol and Cytochrome P450 Family 7 Subfamily A Member 1 ( CYP7A1) were determined. Statistical analyses were conducted by one-way analysis of variance (ANOVA) then post-hoc test. A probability of p -value < 0.05 was considered statistically significant. Results: Lactococcus lactis ssp. lactis and Pediococcus sp. significantly ( p < 0.05) decreased the hepatic total cholesterol levels by 24.96 % and 35.80 %, respectively and increased hepatic CYP7A1 levels by about 49.60% and 37.84 %, respectively in comparison to the diet-induced hyperlipidemic control group. There was no significant difference between the effect of the two isolates and the reference drug, atorvastatin in the levels of both test parameters. Conclusion: We introduce two potential probiotics with similar effect as atorvastatin on both hepatic total cholesterol and hepatic CYP7A1 levels. Thus, these isolates can act as adjuvant therapy to decrease the atorvastatin dose and consequently its side effects. The possible mechanism for the antihyperlipidemic effect could be through upregulation of hepatic CYP7A1 genes that leads to more bile acid synthesis from cholesterol and consequently decreasing liver cholesterol level.
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