Abstract：
In this study, we evaluated the effects of Lactobacillus reuteri NCIMB (LRC™) supplementation on hypercholesterolemia by researching its effects on cellular cholesterol metabolism in hypercholesterolemic rats (KHGASP-22-170) and HepG2 cell line. Rats were separated into six groups after adaptation and were then fed a normal control (NC), a high-cholesterol diet (HC), or a HC supplemented with simvastatin 15 mg/kg body weight (positive control [PC]), LRC 1 × 109 colony-forming units (CFU)/rat/day, LRC 4 × 109 CFU/rat/day, or LRC 1 × 1010 CFU/rat/day (1 × 109, 4 × 109, or 1 × 1010). The rats were dissected to study the effects of LRC on cholesterol metabolism and intestinal excretion at the end of experimental period. We discovered that LRC mainly participated in the restraint of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the uptake of low-density lipoprotein (LDL) cholesterol into tissues, partially in the transport of cholesteryl esters into high density lipoprotein for maturation, and intestinal excretion of cholesterol. These results are supported by the expression of transcription factors and enzymes such as HMG-CoA reductase, SREBP2, CYP7A1, CETP, and LCAT in both messenger RNA (mRNA) and protein levels in serum and hepatic tissue. Furthermore, the LRC treatment in HepG2 significantly reduced the mRNA expression of HMG-CoA reductase, SREBP2, and CEPT and significantly increased the mRNA expression of LDL-receptor, LCAT, and CYP7A1 at all doses. Hence, we suggest that LRC supplementation could alleviate the serum cholesterol level by inhibiting the intracellular cholesterol synthesis, and augmenting excretion of intestinal cholesterol.
摘要：
在这项研究中,我们通过研究补充罗伊氏乳杆菌NCIMB(LRC™)对高胆固醇血症大鼠(KHGASP-22-170)和HepG2细胞系细胞胆固醇代谢的影响,评估了其对高胆固醇血症的影响.适应后将大鼠分为六组，然后喂食正常对照组（NC），高胆固醇饮食（HC），或补充辛伐他汀15mg/kg体重的HC（阳性对照[PC]），LRC1×109菌落形成单位（CFU）/大鼠/天，LRC4×109CFU/鼠/天，或LRC1×1010CFU/大鼠/天（1×109、4×109或1×1010）。在实验期结束时解剖大鼠以研究LRC对胆固醇代谢和肠排泄的影响。我们发现LRC主要参与抑制3-羟基-3-甲基戊二酰辅酶A（HMG-CoA）还原酶，低密度脂蛋白（LDL）胆固醇进入组织的摄取，部分在胆固醇酯运输到高密度脂蛋白成熟，和胆固醇的肠道排泄。这些结果得到了转录因子和酶如HMG-CoA还原酶的表达的支持。SREBP2,CYP7A1,CETP,和LCAT在血清和肝组织中的信使RNA（mRNA）和蛋白质水平。此外，LRC治疗HepG2显著降低HMG-CoA还原酶的mRNA表达,SREBP2和CEPT，并显着增加LDL受体的mRNA表达，LCAT,和CYP7A1在所有剂量。因此，我们建议补充LRC可以通过抑制细胞内胆固醇合成来减轻血清胆固醇水平，增加肠道胆固醇的排泄。
