Investigation of the Antihyperlipidemic Mechanism of Potential Probiotics

Abstract

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.