Abstract：Objective: To investigate the effect of Astragaloside on the cellular damage of thyroid tissue in hyperthyroidism model rats by intervening p38MAPK/NF-κBp65 signaling pathway. Methods: A total of 60 SPF grade Wistar rats were randomly divided into blank group, model group, methimazole group and Astragaloside low and high dose groups, with 12 rats in each group. The blank group was left untreated, and the other groups were treated with intervention after preparation of hyperthyroidism rat models. The basal metabolism of the rats in the five groups was compared before and after the intervention. The expression levels of NF-κBp65, p38MAPK protein and mRNA in thyroid tissues were detected by Western Blot and real-time fluorescence quantitative PCR. Results: After modeling, compared with the blank group, rats in the model group had increased food and water intake, decreased body mass, increased levels of T3, T4, TSH and IL-1β, IL-6, TNF-α, VEGF content (all P<0.05), increased histopathological damage, increased levels of apoptosis, and increased NF-κBp65, p38MAPK protein and mRNA expression in thyroid tissue were elevated (P<0.05). Compared with the model group, rats in the methimazole and astragaloside intervention groups showed decreased food and water intake, significantly increased body mass, decreased levels of T3, T4, TSH and IL-1β, IL-6, TNF-α and VEGF (all P<0.05), significantly improved histopathological damage, decreased levels of apoptosis, and increased levels of NF-κBp65, p38MAPK protein and mRNA in thyroid tissues (P<0.05), p38MAPK protein and mRNA expression in thyroid tissues were significantly reduced (P<0.05), in which the improvement in the high-dose group of astragaloside was significantly better than that in the low-dose group of astragaloside (P<0.01).Conclusion: Astragaloside can effectively improve the apoptosis and reduce the inflammatory factor expression in the thyroid tissue, which may be related to the regulation of the p38MAPK/NF- κB signaling pathway.
[1] Zhou Y L,Wang X X,Xin M Y,et al.Changes in bone mineral density,25hydroxyvitamin D3 and inflammatory factors in patients with hyperthyroidism[J].Experimental and Therapeutic Medicine,2021,21(6):1-5. [2] Bagaturiya G,Kurbanov R,Lebedev A,et al.Pro-inflammatory effects of experimental hyperthyroidism in colon of mice (immunohistocytochemical study)[J].Georgian Med News,2019,(292-293):81-87. [3] 利玲,胡秀,利莉.黄芪注射液在正常和甲亢模型大鼠体内药动学比较[J].中国现代应用药学,2021,38(14):1712-1716. [4] 张宁,李自辉,赵洪伟,等.玄参提取物对甲亢模型大鼠肝脏代谢组学的影响[J].北京中医药大学学报,2019,42(1):21-29. [5] Yu J W,Guo M F,Yang P W,et al.Astragaloside IV inhibits oxidative stress-mediated apoptosis of human SY5Y cells by activating Nrf-2/HO-1 signaling pathway[J].Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology,2022,38(11):979-985. [6] 周宇清,黄淑玲,张慧芬,等.玄栀颗粒对甲状腺功能亢进症大鼠的药效学及急性毒性实验的研究[J].广州中医药大学学报,2020,37(11):2188-2193. [7] 罗煜,吴嘉思,朱正文,等.盐酸巴马汀抑制NF-κB/p38 MAPK信号通路及NLRP3炎症小体抗炎机制研究[J].中药新药与临床药理,2020,31(7):762-768. [8] Unenkhuu B,Kim D B,Kim H S.MKP-3 suppresses LPS-induced inflammatory responses in HUVECs via inhibition of p38 MAPK/NF-κB pathway[J].Animal Cells and Systems,2021,25(4):235-244. [9] Li Z G,Qi X L,Zhang X,et al.TRDMT1 exhibited protective effects against LPS-induced inflammation in rats through TLR4-NF-κB /MAPK-TNF-αpathway[J].Animal Models and Experimental Medicine,2022,5(2):172-182. [10] 蒋晓玲,王阳,郭新玲,等.LncRNA ANRIL干扰miR-153并介导NF-κB P65的核转位诱导脑缺血再灌注小鼠脑组织损伤和细胞凋亡以及氧化应激[J].中国免疫学杂志,2021,37(2):139-144. [11] 赵慧,陈文文,朱丽萍,等.1,25(OH)_2D_3通过抑制TLR2/NF-κB信号通路保护实验性自身免疫性甲状腺炎大鼠甲状腺功能研究[J].中国比较医学杂志,2022,32(3):78-86.
2023, Vol. 29 
冀公网安备13080202000786号