Chen Yu-Zhong, Li Chao, Gu Jia, Lv Si-Chen, Song Jia-Ying, Tang Zhi-Bing, Duan Guang-Xin, Qin Li-Qiang, Zhao Lin, Xu Jia-Ying
State Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, China.
Suzhou Kowloon Hospital, Shanghai Jiaotong University School of Medicine, Suzhou, China.
Dose Response. 2021 Mar 30;19(1):15593258211003798. doi: 10.1177/15593258211003798. eCollection 2021 Jan-Mar.
The main objective is to investigate the protective effect of camel milk (CM) on radiation-induced intestinal injury.
The C57BL/6 J mice in 2 experiments were assigned into control group (Con), irradiation group (IR), and CM+irradiation group (CM+IR). After receiving the CM via gavage for 14 days, the mice in the first experiment were exposed to 6 Gy X-ray whole body irradiation, and survival rate was compared among the groups. Mice in the second experiment were exposed to 4 Gy irradiation and sacrificed at day 7. The small intestines were collected to examine the histopathological changes and to determine the anti-oxidative index and HMGB1/TLR4 inflammatory pathway. Fasting blood was used to measure serum pro-inflammatory factors.
Compared with the IR group, the survival time was prolonged, and survival rate was increased in the CM+IR group. CM increased levels of SOD and GSH and decreased MDA in the jejunum. Furthermore, intestinal protein expression of HMGB1/TLR4 pathway (TLR4, NF-κB, and HMGB1) was up-regulated by CM intervention. CM decreased the serum levels of TNF-α and IL-1β and increased IL-10 level.
CM extended the survival time and had a protective effect against radiation-induced jejunum injury by regulation of antioxidant capacity and HMGB1/TLR4/NF-κB/MyD88 inflammatory signaling pathway.
主要目的是研究骆驼奶(CM)对辐射诱导的肠道损伤的保护作用。
2个实验中的C57BL/6 J小鼠被分为对照组(Con)、照射组(IR)和CM +照射组(CM + IR)。通过灌胃给予CM 14天后,第一个实验中的小鼠接受6 Gy X射线全身照射,比较各组的存活率。第二个实验中的小鼠接受4 Gy照射,并在第7天处死。收集小肠以检查组织病理学变化,并测定抗氧化指标和HMGB1/TLR4炎症通路。空腹血液用于测量血清促炎因子。
与IR组相比,CM + IR组的存活时间延长,存活率提高。CM增加了空肠中SOD和GSH的水平,并降低了MDA水平。此外,CM干预上调了HMGB1/TLR4通路(TLR4、NF-κB和HMGB1)的肠道蛋白表达。CM降低了血清TNF-α和IL-1β水平,并提高了IL-10水平。
CM通过调节抗氧化能力和HMGB1/TLR4/NF-κB/MyD88炎症信号通路延长了存活时间,并对辐射诱导的空肠损伤具有保护作用。