Chronic Exposure to Subtherapeutic Antibiotics Aggravates Ischemic Stroke Outcome in Mice.
Chronic Exposure to Subtherapeutic Antibiotics Aggravates Ischemic Stroke Outcome in Mice.
复制标题
长期接触亚治疗抗生素会加重小鼠的缺血性中风结果。
DOI：
10.1016/j.ebiom.2017.09.002
复制
发表时间：
2017-10
期刊：
影响因子：
11.1
通讯作者：
Xie HH
中科院分区：
文献类型：
--
作者：
Dong XH;Peng C;Zhang YY;Tao YL;Tao X;Zhang C;Chen AF;Xie HH
亚治疗性抗生素自20世纪50年代以来广泛应用于农业，可通过各种途径在人体内积累，并可能产生长期后果。然而，关于慢性亚治疗性抗生素暴露与缺血性脑损伤结果之间的联系的信息有限。本研究表明，经美国食品和药物管理局（FDA）批准在农业中广泛使用的亚治疗性氯四环素、青霉素或万古霉素长期治疗可损害小鼠EPC功能，减少缺血性脑血管生成，加重脑缺血损伤和长期卒中结局。此外，与对照组相比，慢性抗生素处理小鼠的EPCs移植对脑缺血损伤的减轻和局部血管生成的促进作用较低，并且来自供体动物的EPCs可以融入受体小鼠的缺血脑。此外，移植的EPCs可能对小鼠脑缺血损伤的减轻具有旁分泌作用，这种作用可能被慢性抗生素暴露损害。综上所述，慢性亚治疗性抗生素暴露加重了小鼠的脑缺血损伤，这可能部分归因于EPCs介导的血管生成和EPCs的旁分泌作用的损害。这些发现揭示了以前未被认识到的慢性亚治疗性抗生素暴露对缺血性损伤的影响。慢性暴露于亚治疗性抗生素会加重小鼠的长期中风结果。慢性暴露于亚治疗性抗生素损害小鼠内皮祖细胞功能。慢性暴露于亚治疗性抗生素可减少小鼠缺血性脑血管生成。亚治疗性抗生素自20世纪50年代以来广泛应用于农业，可通过各种途径在人体内积累，并可能产生长期后果。然而，关于慢性亚治疗性抗生素暴露与缺血性脑损伤结果之间的联系的信息有限。本研究表明，经美国食品和药物管理局（FDA）批准在农业中广泛使用的亚治疗性氯四环素、青霉素或万古霉素慢性治疗可损害内皮祖细胞介导的血管生成，并加重小鼠的长期卒中结局。这些发现揭示了以前未被认识到的慢性亚治疗性抗生素暴露对缺血性损伤的影响。
Subtherapeutic antibiotics have been widely used in agriculture since the 1950s, which can be accumulated in human body through various approaches and may have long-term consequences. However, there is limited information about the link between chronic subtherapeutic antibiotic exposure and the outcome of ischemic brain injury. Here we showed that long-term treatment with subtherapeutic chlortetracycline, penicillin or vancomycin, which were widely used in agriculture approved by US Food and Drug Administration (FDA), could impair EPC functions, reduce ischemic brain angiogenesis and aggravate cerebral ischemic injury and long-term stroke outcomes in mice. In addition, transplantated EPCs from chronic antibiotic-treated mice showed a lower therapeutic effect on cerebral ischemic injury reduction and local angiogenesis promotion compared to those from control mice, and EPCs from the donor animals could integrate into the recipient ischemic brain in mice. Furthermore, transplanted EPCs might exert paracrine effects on cerebral ischemic injury reduction in mice, which could be impaired by chronic antibiotic exposure. In conclusion, chronic subtherapeutic antibiotic exposure aggravated cerebral ischemic injury in mice, which might be partly attributed to the impairment of both EPC-mediated angiogenesis and EPCs' paracrine effects. These findings reveal a previously unrecognized impact of chronic subtherapeutic antibiotic exposure on ischemic injury. Chronic exposure to subtherapeutic antibiotics aggravates long-term stroke outcome in mice. Chronic exposure to subtherapeutic antibiotics impairs endothelial progenitor cell functions in mice. Chronic exposure to subtherapeutic antibiotics reduces ischemic brain angiogenesis in mice. Subtherapeutic antibiotics have been widely used in agriculture since the 1950s, which can be accumulated in human body through various approaches and may have long-term consequences. However, there is limited information about the link between chronic subtherapeutic antibiotic exposure and the outcome of ischemic brain injury. Here we showed that chronic treatment with subtherapeutic chlortetracycline, penicillin or vancomycin, which were widely used in agriculture approved by US Food and Drug Administration (FDA), could impair endothelial progenitor cells-mediated angiogenesis and aggravate long-term stroke outcome in mice. These findings reveal a previously unrecognized impact of chronic subtherapeutic antibiotic exposure on ischemic injury.
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影响因子：
82.9
作者：
Benakis C;Brea D;Caballero S;Faraco G;Moore J;Murphy M;Sita G;Racchumi G;Ling L;Pamer EG;Iadecola C;Anrather J
通讯作者：
Anrather J
GTP 环水解酶 I/BH4 通路通过抑制盐敏感性高血压中的氧化应激和血小板反应蛋白-1 来保护 EPC
DOI：
10.1161/hypertensionaha.110.160622
发表时间：
2010-12
期刊：
Hypertension (Dallas, Tex. : 1979)
影响因子：
--
作者：
Xie HH;Zhou S;Chen DD;Channon KM;Su DF;Chen AF
通讯作者：
Chen AF
影响因子：
20.1
作者：
Zhang, ZG;Zhang, L;Chopp, M
通讯作者：
Chopp, M
影响因子：
6.3
作者：
Chen, JL;Zhang, CL;Chopp, M
通讯作者：
Chopp, M
影响因子：
15.9
作者：
Marrotte, Eric J.;Chen, Dan-Dan;Chen, Alex F.
通讯作者：
Chen, Alex F.