Huang Ying, Wang Jinfeng, Quan Guihua, Wang Xiaojun, Yang Longfei, Zhong Lili
Central Research Laboratory, Second Hospital of Jilin University, Changchun, People's Republic of China
Central Research Laboratory, Second Hospital of Jilin University, Changchun, People's Republic of China.
Appl Environ Microbiol. 2014 Dec;80(24):7496-504. doi: 10.1128/AEM.02926-14. Epub 2014 Sep 26.
The objective of this study was to investigate the effect of Lactobacillus acidophilus ATCC 4356 on the development of atherosclerosis in apolipoprotein E-knockout (ApoE(-/-)) mice. Eight-week-old ApoE(-/-) mice were fed a Western diet with or without L. acidophilus ATCC 4356 daily for 16 weeks. L. acidophilus ATCC 4356 protected ApoE(-/-) mice from atherosclerosis by reducing their plasma cholesterol levels from 923 ± 44 to 581 ± 18 mg/dl, likely via a marked decrease in cholesterol absorption caused by modulation of Niemann-Pick C1-like 1 (NPC1L1). In addition, suppression of cholesterol absorption induced reverse cholesterol transport (RCT) in macrophages through the peroxisome proliferator-activated receptor/liver X receptor (PPAR/LXR) pathway. Fecal lactobacillus and bifidobacterium counts were significantly (P < 0.05) higher in the L. acidophilus ATCC 4356 treatment groups than in the control groups. Furthermore, L. acidophilus ATCC 4356 was detected in the rat small intestine, colon, and feces during the feeding trial. The bacterial levels remained high even after the administration of lactic acid bacteria had been stopped for 2 weeks. These results suggest that administration of L. acidophilus ATCC 4356 can protect against atherosclerosis through the inhibition of intestinal cholesterol absorption. Therefore, L. acidophilus ATCC 4356 may be a potential therapeutic material for preventing the progression of atherosclerosis.
本研究的目的是调查嗜酸乳杆菌ATCC 4356对载脂蛋白E基因敲除(ApoE(-/-))小鼠动脉粥样硬化发展的影响。给8周龄的ApoE(-/-)小鼠每日喂食含或不含嗜酸乳杆菌ATCC 4356的西式饮食,持续16周。嗜酸乳杆菌ATCC 4356通过将ApoE(-/-)小鼠的血浆胆固醇水平从923±44降至581±18mg/dl,保护其免受动脉粥样硬化影响,这可能是通过调节尼曼-匹克C1样1蛋白(NPC1L1)导致胆固醇吸收显著减少实现的。此外,胆固醇吸收的抑制通过过氧化物酶体增殖物激活受体/肝脏X受体(PPAR/LXR)途径诱导巨噬细胞中的胆固醇逆向转运(RCT)。嗜酸乳杆菌ATCC 4356治疗组的粪便中乳酸杆菌和双歧杆菌计数显著高于对照组(P<0.05)。此外,在喂养试验期间,在大鼠小肠、结肠和粪便中检测到嗜酸乳杆菌ATCC 4356。即使在停止给予乳酸菌2周后,细菌水平仍保持较高。这些结果表明,给予嗜酸乳杆菌ATCC 4356可通过抑制肠道胆固醇吸收预防动脉粥样硬化。因此,嗜酸乳杆菌ATCC 4356可能是预防动脉粥样硬化进展的潜在治疗物质。