【摘要】 目的 通过原发性高血压大鼠（spontaneouslyhypertensiverat,SHR）验证益生菌BPL1(Bifidobacterium animalis subsp. lactis BPL1)降血压的功效并探讨可能机制。方法 将50只SHR随机分为模型对照组、卡托普利阳性对照组、益生菌BPL1高[BPL1(H)]、中[BPL1(M)]、低[BPL1(L)]剂量组，每组10只，并取10只正常血压大鼠(Wistar-Kyoto,WKY)作为空白对照组。连续灌胃30d干预，期间监测大鼠体质量、收缩压（systolic blood pressure,SBP）、舒张压（diastolic blood pressure,DBP）、平均压(mean arterial pressure,MAP)、心率（Heart rate,HR）；实验结束后观察大鼠肾脏病理切片，检测肾脏血管紧张素I转换酶（angiotensinIconvertingenzyme,ACE）蛋白表达、生化及免疫学相关指标，分析动物肠道菌群构成与变化。结果 BPL1各剂量组SBP均显著低于模型组（P<0.05）;BPL1(M)、BPL1(H)组DBP显著低于模型组，且BPL1各剂量组DBP均接近阳性对照组，差异无统计学意义；BPL1各剂量组MAP显著低于模型组（P<0.05）;BPL1 (L)、BPL1 (H)组干预后血管紧张素Ⅱ（angiotensin II,AngⅡ）显著低于模型组（P<0.05）;BPL1各剂量组醛固酮（aldosterone,ALD）水平显著低于模型组（P<0.05）;BPL1 (L)干预后免疫球蛋白A(immunoglobulin A,Ig A)的水平显著高于模型组（P<0.05）;BPL1各剂量组干预后主动脉肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的水平较模型组有显著的降低，BPL1 (M)干预后主动脉白细胞介素-1(interleukin-6,IL-1β)显著低于模型组（P<0.05）;BPL1各剂量组的ACE蛋白表达量的均值均低于模型组；BPL1各剂量组的厚壁菌门和拟杆菌门的比值F/B值的均数均低于模型组，并且随着BPL1剂量的升高存在下降的趋势。结论 益生菌BPL1的降压效果可能是通过影响机体的肾素-血管紧张素-醛固酮系统，抑制ACE活性，限制Ang II转化途径，同时恢复肠道菌群的平衡来实现。[营养学报，2024,46(6):574-582]更多还原

【Abstract】 Objective To verify the effect of Bifidobacterium animalis subsp. lactis(BPL1) on blood pressure in spontaneously hypertensive rats(SHR) and to explore the possible mechanisms. Methods Fifty SHR rats were randomly divided into model control group(MC), captopril positive control group(PC), probiotic BPL1 high-dose [BPL1(H)], medium-dose [BPL1(M)] and low-dose groups [BPL1(L)] with 10 rats in each group. Ten Wistar-Kyoto(WKY) rats were selected as blank control group. Body mass, systolic blood pressure(SBP), diastolic blood pressure(DBP), mean arterial pressure(MAP) and heart rate were monitored during 30 days. After the experiment, the pathological sections of rat kidney were observed and the expression of renal angiotensin I converting enzyme(ACE) protein, biochemical and immunological related indexes, and the composition and changes of intestinal flora were analyzed. Results The SBP of the BPL1 dose groups was significantly lower than that of the model group(P<0.05). The DBP of the BPL1(M) and BPL1(H) groups was significantly lower than that in the model group, and the DBP of the BPL1 dose groups was close to the positive control group. However, the difference was not statistically significant. The MAP of the BPL1 dose groups was significantly lower than that of model group(P<0.05). Serum angiotensin II(AngⅡ)in the BPL1(L) and BPL1(H) groups was significantly lower than that in the model group(P<0.05). The level of aldosterone(ALD) in the BPL1 dose groups was significantly lower than that in the model group(P<0.05). The level of immunoglobulin A(Ig A) in the BPL1(L) group was significantly higher than that in the model group(P< 0.05). The level of tumor necrosis factor-α(TNF-α) in aorta after BPL1(M) treatment was significantly lower than that in the model group, and the level of interleukin-1β(IL-1β) in aorta after BPL1(M) treatment was significantly lower than that in the model group(P<0.05). The kidney expression of ACE protein in BPL1 dose groups was lower than that in the model group. The average F/B ratio in BPL1 dose groups was lower than that in the model group, and there was a downward trend with the increase of BPL1 dose. Conclusion Probiotic BPL1 has a remarkable antihypertensive effect by affecting renin-angiotensin-aldosterone system, inhibiting angiotensin I converting enzyme(ACE) activity, restricting Ang II conversion pathway, and restoring the balance of intestinal flora. [ACTA NUTRIMENTA SINICA,2024,46(6):574-582]更多还原