Bailing capsule alleviates autoimmune thyroiditis regulating peroxisome proliferator-activated receptor signaling pathway: a multi-omics analysis.

Wang Qixin, X U Liting, W U Jiangpeng, H E Xueling, Tang Huan, Cheng Guangqing, L U Tianming, Dai Chuanhao, Guo Qiuyan, Wang Jigang
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Abstract

Objective: To investigate the efficacy and potential mechanism of Bailing capsule (, BL) anti-autoimmune thyroiditis (AIT).

Methods: Based on the AIT rat model, the effect of BL in alleviating AIT was evaluated by detecting serum thyroid index free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH), thyroglobulin antibody (TGAb), thyroid peroxidase antibody (TPOAb), and inflammatory factors Interferon-gamma (IFN-γ), Interleukin-4, -10, and -12 (IL-4, IL-10, and IL-12) as well as thyroid tissue Hematoxylin-eosin (HE) staining and ultrastructure observation. The mechanism of BL was explored by combining transcriptome and proteome analysis, and further verified by Western blot (WB).

Results: BL effectively reduced serum FT3, FT4, TGAb, and TPOAb levels in AIT rats, restored TSH balance, inhibited the release of pro-inflammatory cytokines IFN-γ and IL-12, promoted the production of anti-inflammatory cytokines IL-4 and IL-10, and significantly reduced IFN-γ/IL-4 and IL-12/IL-10, improved thyroid follicular structure, and protected thyroid tissue from injury. Kyoto Encyclopedia of Genes and Genomes and protein interaction network analysis showed that BL affected the expression of fatty acid-binding protein 4, acyl-CoA synthetase long-chain family member 1, and acyl-CoA dehydrogenase long chain to regulate the peroxisome proliferator-activated receptor signaling pathway, thereby inhibiting the fatty acid metabolism and the inflammatory state of AIT rats.

Conclusions: BL could effectively reduce thyroid inflammation in AIT model rats. The possible BL mechanism was to regulate the peroxisome proliferator-activated receptor signaling pathway and inhibit fatty acid metabolism. This study suggested that BL has the potential to be used in clinical treatment of AIT.

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百龄胶囊调节过氧化物酶体增殖物激活受体信号通路缓解自身免疫性甲状腺炎:多组学分析。
目的:探讨百灵胶囊抗自身免疫性甲状腺炎(AIT)的疗效及其潜在机制。方法:以AIT大鼠模型为基础,通过检测血清甲状腺指数游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、促甲状腺激素(TSH)、甲状腺球蛋白抗体(TGAb)、甲状腺过氧化物酶抗体(TPOAb)、炎症因子干扰素-γ (IFN-γ)、白细胞介素-4、白细胞介素-10、白细胞介素-12 (IL-4、IL-10、IL-12)、甲状腺组织苏木精-伊红(HE)染色及超微结构观察,评价BL对AIT的缓解作用。结合转录组学和蛋白质组学分析探讨了BL的发病机制,并通过Western blot (WB)进一步验证。结果:BL能有效降低AIT大鼠血清FT3、FT4、TGAb、TPOAb水平,恢复TSH平衡,抑制促炎因子IFN-γ、IL-12的释放,促进抗炎因子IL-4、IL-10的产生,显著降低IFN-γ/IL-4、IL-12/IL-10,改善甲状腺滤泡结构,保护甲状腺组织免受损伤。京都基因基因组百科和蛋白质相互作用网络分析表明,BL通过影响脂肪酸结合蛋白4、酰基辅酶a合成酶长链家族成员1、酰基辅酶a脱氢酶长链的表达,调节过氧化物酶体增殖体激活受体信号通路,从而抑制AIT大鼠脂肪酸代谢和炎症状态。结论:BL能有效减轻AIT模型大鼠甲状腺炎症。BL的可能机制是调节过氧化物酶体增殖物激活受体信号通路,抑制脂肪酸代谢。本研究提示BL具有应用于临床治疗AIT的潜力。
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