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.
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