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Probiotic properties of Pediococcus acidilactici Z123 and its intervention effects and mechanisms on hypercholesterolemia in mice

ABSTRACT:

The intervention effects and underlying mechanisms of Lactobacillus strains against hypercholesterolemia in mice have been extensively documented. However, fewer studies have focused on the cholesterol-lowering potential and the corresponding metabolic regulatory mechanisms of Pediococcus acidilactici. In the present study, we first characterized the in vitro probiotic properties of a novel lactic acid bacterial strain, Pediococcus acidilactici Z123 (P. acidilactici Z123), which exhibited prominent cholesterol-lowering activity. Subsequently, intragastric administration of P. acidilactici Z123 was carried out in a mouse model of high-fat diet-induced hypercholesterolemia to assess its intervention effect and elucidate the underlying molecular mechanisms. The results revealed that P. acidilactici Z123 possessed desirable probiotic characteristics such as auto-aggregation, adhesion ability, and gastrointestinal fluid tolerance, and showed good biosafety, including antibiotic susceptibility and no hemolytic activity. In vivo results demonstrated that supplementation with P. acidilactici Z123 effectively alleviated excessive body weight gain and reduced visceral fat accumulation, improved serum lipid profiles, and ameliorated the histological morphology of the liver and epididymal adipose tissue. Untargeted metabolomics indicated that P. acidilactici Z123 exerted a significant regulatory effect on lipolysis in adipocytes, PPAR and AMPK signaling pathways, primary bile acid metabolism, bile secretion, tryptophan metabolism, etc. Notably, such metabolic regulation was further verified at the transcriptional level. Quantitative reverse transcription PCR (qRT-PCR) analysis revealed that P. acidilactici Z123 intervention could inhibit cholesterol synthesis by downregulating the expression of Hmgcr and Srebf1, and upregulating the expression of Prkaa1. Meanwhile, it also elevated the expression of genes related to fatty acid oxidation (Cpt1a, Pparalpha) and bile acid synthesis (Cyp7a1). All these molecular changes jointly modulated systemic lipid metabolism. The present findings will provide valuable theoretical evidence for the development and application of novel functional probiotic products with lipid-regulating properties.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS14733 | MetaboLights | 2026-06-13

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS14733_LC-MS_negative_reverse-phase.txt	Txt
	a_MTBLS14733_LC-MS_positive_reverse-phase.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS14733_LC-MS_negative_reverse-phase_v2_maf.tsv	Tabular
	m_MTBLS14733_LC-MS_positive_reverse-phase_v2_maf.tsv	Tabular

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Project description:In previous in vitro study, we reported potential mechanism of cholesterol-lowering effect of Lactobacillus brevis119-2 (119-2) isolated from turnip M-bM-^@M-^\Tsuda kabuM-bM-^@M-^] is due to incorporation of cholesterol into 119-2 cell. In this study, we analyzed serum cholesterol and hepatic gene expression of Sprague-Dawley (SD) rat fed diet containing cholesterol with or without 119-2 for 2 weeks, to evaluate the cholesterol-lowering effect of 119-2 in vivo. Serum cholesterol of SD rat fed diet with 119-2 significantly decreased compared to SD rat fed diet without 119-2, and both viable and dead 119-2 indicated the effect. The result of hepatic gene analysis using DNA microarray suggested that potential mechanism of the cholesterol-lowering effect of 119-2 in vivo is inhibiting the activity of 3-hydroxy-3-methylglutaryl-CoA reductase by Insig (insulin induced gene) that is endoplasmic reticulum membrane protein, and catabolizing cholesterol to bile acid by Cyp7a1 (cytochrome P450 a1) that is the rate-limiting enzyme in the synthesis of bile acid from cholesterol. In addition, we concluded feeding 119-2 decreased serum low density lipoprotein (LDL) cholesterol by overexpression of Ldlr (LDL receptor gene). On the other hand, feeding Lactobacillus acidophilus ATCC43121 (ATCC) increased high density lipoprotein (HDL) cholesterol by over expression of Abca1 (ATP binding cassette sub-family A member 1 gene) and Angplt3 (Angiopoietin-like 3). These results suggested that 119-2 decrease the risk of atherosclerosis by serum cholesterol-lowering effect and improving effect of fatty liver and the LH (LDL cholesterol / HDL cholesterol) ratio. Lactobacillus brevis119-2 (119-2) was isolated from turnip M-bM-^@M-^\Tsuda kabuM-bM-^@M-^] harvested in Matsue city, Shimane Prefecture, Japan, and was stored at Shimane Institute for industrial Technology. Male Jcl: SD rat (4 weeks of age) were obtained from CLEA Japan, Inc. (Tokyo, Japan). Rats were maintained under controlled environmental conditions (temperature 23 M-BM-1 3 M-KM-^ZC, relative humidity 55% M-BM-1 25%, 12/12hr light - dark cycle) and given food and water ad libitum. All rats were acclimated 1 week prior to the experiment. Two groups of 11 rats each were treated respective group diets for 2weeks. Control group was fed high-cholesterol diet containing 10 g cholesterol/kg, 5 g cholic acid/kg, 985 g mouse & rat & rabbit diet (CRF-1) /kg obtained from Oriental yeast Co., Ltd (Tokyo, Japan). The other group was fed same highcholesterol diet with 10 g freeze-dried viable 119-2 /kg. This study and all procedures were approved by regulations and code of ethics in experimental animals Chitose Japan Food Research Laboratories.

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Probiotic properties of Pediococcus acidilactici Z123 and its intervention effects and mechanisms on hypercholesterolemia in mice

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