Disordered Expression of Tight Junction Proteins Is Involved in the Mo-induced Intestinal Microenvironment Dysbiosis in Sheep
Disordered Expression of Tight Junction Proteins Is Involved in the Mo-induced Intestinal Microenvironment Dysbiosis in Sheep
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DOI：
10.1007/s12011-022-03155-0
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发表时间：
2022-04
影响因子：
3.9
通讯作者：
Chen-Yu Zhang-;Jing-hong Zhao;M. Mao;Zhan-Qin Zhao;Feng-Jun Liu;Hong-wei Wang
中科院分区：
文献类型：
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作者：
Chen-Yu Zhang-;Jing-hong Zhao;M. Mao;Zhan-Qin Zhao;Feng-Jun Liu;Hong-wei Wang
为探讨钼(Mo)对绵羊肠道形态的影响及肠道紧密连接(TJ)蛋白表达与肠道屏障功能的关系，将20只健康绵羊随机分为5组：对照组、Mo5组、Mo10组、Mo20组和Mo50组，分别给予Na2MoO4·2H2O 0、5、10、20、50 mg/kgbw。钼处理28天后，取十二指肠、空肠和回肠组织。苏木精-伊红染色评价组织病理学和发育参数。TdT介导的dUTP缺口末端标记法检测肠上皮细胞DNA损伤。肠糖蛋白和杯状细胞分别用阿新蓝-高碘酸-席夫(AB-PAS)染色和PAS染色进行分析。用免疫荧光技术检测TJ蛋白。结果表明，过量钼可显著降低小肠绒毛高度(VH)、隐窝深度(CD)、VH/CD和粘膜厚度(P<； 0.0 5或 .0.0 1)，并引起小肠上皮细胞DNA损伤。此外，过量钼还可降低糖蛋白分布面积百分比(P<； )和肠杯状细胞相对密度(P<； )，从而损害肠屏障功能。钼处理导致闭锁小带-1、闭锁蛋白和克劳丁-1的表达降低(P<； )。综上所述，过量的钼干扰了TJ蛋白的表达，抑制了肠上皮细胞的发育，进一步加重了肠屏障功能的损害，导致了小肠微环境平衡的紊乱。
To evaluate the molybdenum (Mo)-induced changes of intestinal morphology and the relationship of intestinal tight junction (TJ) proteins expression and intestinal barrier function, a total of 20 healthy sheep were randomly divided into five groups of four: 0, 5, 10, 20, and 50 mg/kg BW/day Na2MoO4·2H2O were administrated in five groups named control group, Mo 5 group, Mo 10 group, Mo 20 group, and Mo 50 group, respectively. After 28 days of Mo treatment, the duodenum, the jejunum, and the ileum tissue were collected. The histopathology and the developmental parameters were evaluated by hematoxylin–eosin staining. The intestinal epithelial cell DNA damage was detected by TdT-mediated dUTP nick end labeling assay. The intestinal glycoprotein and the goblet cells were analyzed by Alcian Blue-Periodic Acid-Schiff (AB-PAS) staining and PAS staining, respectively. TJ proteins were determined by immunofluorescence technology. Results showed that excessive Mo significantly decreased the small intestinal villus height (VH), crypt depth (CD), VH/CD, and mucosal thickness (P< 0.05 orP< 0.01) while induced the damage of DNA in small intestinal epithelial cells. Moreover, excessive Mo injured intestinal barrier function by decreasing the percent of glycoprotein distribution area (P< 0.05) and the relative density of intestinal goblet cells (P< 0.05). Mo treatment induced decreased (P< 0.01) expression of Zonula Occludens-1, Occludin, and Claudin-1. In conclusion, excessive Mo interfered with the expression of TJ proteins, inhibited intestinal epithelial development, and further aggravated the intestinal barrier function damage, leading to disturbing the small intestinal microenvironment balance.