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1.宁波职业技术学院 乙烯工程副产物高质化利用浙江省应用技术协同创新中心,浙江 宁波 315800
2.浙江医药高等专科学校 中药学院,浙江 宁波 315100
3.中国药科大学 中药学院,南京 210009
刘兴艳,博士,讲师,从事中药药效物质基础研究,Tel:0574-86891952,E-mail:liuxingyan2002@163.com
收稿日期:2021-02-04,
网络出版日期:2021-05-09,
纸质出版日期:2021-07-05
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刘兴艳,马舒伟,李雄伟等.白芍总苷对干燥综合征小鼠肠道微环境的调节作用[J].中国实验方剂学杂志,2021,27(13):50-57.
LIU Xing-yan,MA Shu-wei,LI Xiong-wei,et al.Regulatory Mechanism of Total Glucosides of Paeony on Gut Microenvironment in Non-obese Diabetic Mice with Sjogren's Syndrome[J].Chinese Journal of Experimental Traditional Medical Formulae,2021,27(13):50-57.
刘兴艳,马舒伟,李雄伟等.白芍总苷对干燥综合征小鼠肠道微环境的调节作用[J].中国实验方剂学杂志,2021,27(13):50-57. DOI: 10.13422/j.cnki.syfjx.20211208.
LIU Xing-yan,MA Shu-wei,LI Xiong-wei,et al.Regulatory Mechanism of Total Glucosides of Paeony on Gut Microenvironment in Non-obese Diabetic Mice with Sjogren's Syndrome[J].Chinese Journal of Experimental Traditional Medical Formulae,2021,27(13):50-57. DOI: 10.13422/j.cnki.syfjx.20211208.
目的
2
通过研究白芍总苷(TGPs)对干燥综合征(SS)模型小鼠肠动力、肠屏障和肠道菌群的影响情况,探讨白芍总苷对SS小鼠肠道菌群微环境的影响。
方法
2
实验选BALB/c小鼠为正常组,雌性非肥胖型糖尿病(NOD)小鼠30只随机分为模型组、果寡糖组(700 mg∙kg
-1
),TGPs低、中、高(160,320,640 mg∙kg
-1
)剂量组,每组各6只。观察小鼠摄食量、饮水量、粪便排出颗粒数和粪便含水率,评价TGPs对于SS小鼠肠动力的影响;采用酶联免疫吸附法测定
D
-乳酸(
D
-Lac)含量、二胺氧化酶(DAO)活性和连接复合物蛋白闭锁小带蛋白-1(ZO-1)表达量;收集不同时间的粪便样品,采用平板涂布和气相色谱法检测肠道菌群结构和短链脂肪酸含量。
结果
2
与正常组比较,模型组小鼠饮水量、摄食量均减少(
P
<
0.01),肠推进率显著下降(
P
<
0.01),
D
-Lac含量和DAO活性明显升高(
P
<
0.05,
P
<
0.01),ZO-1表达量降低(
P
<
0.01),肠道菌总菌数量下降(
P
<
0.01),短链脂肪酸浓度降低(
P
<
0.05,
P
<
0.01)。与模型组相比,TGPs显著增加SS小鼠粪便数量和含水率(
P
<
0.05,
P
<
0.01),提高肠推进率(
P
<
0.05,
P
<
0.01)。TGPs降低小鼠血清中
D
-Lac含量和DAO活性(
P
<
0.05,
P
<
0.01),增加ZO-1表达水平(
P
<
0.01);TGPs提高肠道菌群中双歧杆菌和乳酸杆菌比例、降低肠杆菌比例;TGPs促进乙酸和丁酸的产生(
P
<
0.05,
P
<
0.01)。
结论
2
TGPs通过增加粪便含水量,提高肠动力改善SS小鼠便秘症状;TGPs调节肠道菌群结构,增加乙酸和丁酸含量,增加紧密连接蛋白的表达,降低SS小鼠肠道屏障通透性,促进受损肠道屏障功能的恢复。
Objective
2
To investigate the effects of total glucosides of paeony (TGPs) on intestinal motility, barrier function, and gut microbiota in non-obese diabetic (NOD) mice with Sjogren's syndrome (SS).
Method
2
Thirty NOD mice were randomly assigned into the model group (deionized water), prebiotic fructo-oligosaccharide (FOS) group (700 mg∙kg
-1
), and the low- (160 mg∙kg
-1
), medium- (320 mg∙kg
-1
), and high-dose (640 mg∙kg
-1
) TGP groups, with six mice in each group. Moreover, the BALB/c mice were employed as the normal control and administered with deionized water. The food and water intakes, number of discharged fecal particles, and fecal moisture content were observed to evaluate the effect of TGPs on intestinal motility in SS mice. The levels of
D
-lactate (
D
-Lac) content, diamine oxidase (DAO), and junction-associated protein zonula occludens-1 (ZO-1) in mouse serum were detected by enzyme linked immunosorbent assay (ELISA). The fecal samples collected at different time points were determined by spread plate method and gas chromatography for uncovering the intestinal microbial communities and the content of short-chain fatty acids.
Result
2
Compared with the normal group, the model group exhibited decreased food and water intakes (
P
<
0.01), weakened intestinal propulsion (
P
<
0.01), elevated
D
-Lac and DAO (
P
<
0.05,
P
<
0.01), lowered ZO-1 and SCFAs (
P
<
0.05,
P
<
0.01), and reduced number of intestinal bacteria (
P
<
0.01). The comparison with the model group revealed that TGPs significantly increased the number of discharged fecal particles and fecal moisture content (
P
<
0.05,
P
<
0.01), enhanced intestinal propulsion (
P
<
0.05,
P
<
0.01), decreased serum
D
-Lac and DAO levels (
P
<
0.05,
P
<
0.01), and up-regulated ZO-1 expression (
P
<
0.01). Apart from increasing the proportions of
Bifidobacterium
and
Lactobacillus
and decreasing the proportion of
Enterobacter
in intestinal flora (
P
<
0.05,
P
<
0.01), TGPs also accelerated the production of acetic acid and butyric acid (
P
<
0.05,
P
<
0.01).
Conclusion
2
TGPs attenuate SS-mediated constipation and restore the impaired intestinal barrier function in mice by increasing fecal moisture content, boosting intestinal motility, regulating intestinal microbial communities, elevating acetic acid and butyric acid levels, and up-regulating tight junction protein expression.
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