Efficacy of Liangxue Guyuan decoction on radiation-induced intestinal injury in rats via the toll-like receptor 4/myeloid differentiation primary response 88/ nuclear factor-kappa B pathway

被引:2
作者
Wang Yuguo [1 ]
Dou Yongqi [2 ]
Feng Jian [2 ]
Xu Chengyong [2 ]
Wang Qian [2 ]
机构
[1] Chinese Peoples Liberat Army, Chinese Peoples Liberat Army Gen Hosp, Med Sch, Beijing 100853, Peoples R China
[2] Chinese Peoples Liberat Army Gen Hosp, Dept Tradit Chinese Med, Beijing 100853, Peoples R China
关键词
radiation; intestinal injuries; toll-like receptor 4; myeloid differentiation factor 88; NF-kappa B; Liangxue Guyuan decoction; MESENCHYMAL STEM-CELLS; ANTIOXIDANT; MANAGEMENT; MICE;
D O I
10.19852/j.cnki.jtcm.2021.02.005
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
OBJECTIVE: To evaluate the efficacy of Liangxue Guyuan decoction (LGD) on radiation-induced intestinal injury in rats, and the possible underlying mechanism of action. METHODS: A total of 255 male Sprague-Dawley rats were used. 15 rats were assigned to the control group and the remaining 240 rats were exposed to a Co-60 source at a dose of 11 Gy. Irradiated rats were randomly divided into model, dexamethasone (DXM), low-dose LGD (LGDl), and high-dose LGD (LGDh) groups and treated for 11 d. The survival rate, weight of body, intestinal pathology and the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), and nuclear factor-kappa B (NF-kappa B) were recorded. RESULTS: Radiation reduced the survival rate and weight of rats, destroyed the intestinal structure, induced an inflammatory reaction, and increased both protein and mRNA expression of TLR4, MyD88, and NF-kappa B in ileum. However, LGDh increased the survival rate, inhibited weight loss, alleviated inflammation and improve the expression of TLR4 pathway. CONCLUSIONS: LGD increased the survival rate and inhibit weight loss of irradiated rats, and reduced inflammation and intestinal injury. The underlying mechanism may involve regulation of the TLR4/MyD88/NF-kappa B pathway. (C) 2021 JTCM. All rights reserved.
引用
收藏
页码:254 / 261
页数:8
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