姜黄素与桥本甲状腺炎

Hashimoto's thyroiditis (HT) is an inflammatory autoimmune disease and patients with HT may benefit from interventions that incorporate anti‐inflammatory components. This study aimed to assess the combined effects of an anti‐inflammatory diet and curcumin supplementation on thyroid hormones and lipid profile in patients with HT.

ABSTRACT Hashimoto's thyroiditis (HT) is a chronic autoimmune condition characterized by persistent thyroid inflammation. Patients with HT may benefit from anti‐inflammatory strategies. This study was designed to examine the combined impact of an anti‐inflammatory diet and curcumin supplementation on inflammatory markers in individuals with HT. In this randomized controlled clinical trial, 57 individuals diagnosed with Hashimoto's thyroiditis (HT) in Tehran, Iran, were recruited and randomly allocated to two intervention arms. One group received an anti‐inflammatory diet in conjunction with 1500 mg of curcumin daily, while the other group followed the same diet but was administered a placebo. Inflammatory biomarkers including high‐sensitivity C‐reactive protein (hs‐CRP), interleukin‐6 (IL‐6), and nuclear factor kappa B (NF‐κB) were measured at the start of the study and again following a 12‐week supplementation period to assess the additive effect of curcumin. Curcumin supplementation resulted in a reduction in IL‐6 (−5.28 ± 9.75, p = 0.009). Additionally, it decreased hs‐CRP levels in patients with HT, with a mean reduction of −1.17 ± 5.70 mg/L, whereas the placebo group exhibited an increase of +1.53 ± 3.33 mg/L (p = 0.305). Also, curcumin supplementation significantly reduced NF‐κB levels in patients with HT (−0.09 ± 0.22 vs. 0.03 ± 0.15, p = 0.019), while the placebo group showed a slight increase (0.65 ± 0.16 to 0.68 ± 0.13). Curcumin, by reducing inflammation, can be effective as an adjunctive treatment alongside an anti‐inflammatory diet in individuals with HT. Additional studies are warranted. Name of the Registry: National Nutrition and Food Technology Research Institute. Trial Registration Number: NCT0597586. Date of Registration: 2023‐08‐04. URL of Trial Registry Record: https://www.clinicaltrials.gov/study/NCT05975866?term = NCT05975866&rank = 1.

The many facets of Hashimoto's Thyroiditis (HT), a common autoimmune disease marked by chronic thyroid gland inflammation that results in hypothyroidism, are explained in this chapter. It emphasizes how genetic predisposition, environmental variables, and immunological dysregulation interact intricately in the pathogenesis of HT. The chapter highlights the emerging significance of the thyroid-gut axis, emphasizing how gut dysbiosis, increased intestinal permeability, and microbiotaderived metabolites influence thyroid function and autoimmunity. It explores the roles of inflammatory cytokines, oxidative stress, and autoantibodies in exacerbating thyroid dysfunction and systemic symptoms. Furthermore, the chapter explores the therapeutic potential of secondary plant metabolites, particularly flavonoids, polyphenols, and terpenoids, which exhibit anti-inflammatory, antioxidant, and immunomodulatory properties. These metabolites are discussed in the context of their mechanisms of action, including inhibition of pro-inflammatory enzymes, downregulation of NF-I-B signaling, and modulation of immune cell activities. The chapter also addresses the impact of dietary factors, such as gluten, dairy, and goitrogens, on thyroid health. It provides practical dietary recommendations, emphasizing the inclusion of selenium, zinc, omega-3 fatty acids, and a variety of plant-based foods rich in beneficial metabolites. This comprehensive review integrates current understanding of HT's pathophysiology with emerging insights into the therapeutic potential of plant metabolites, offering a foundation for future research and personalized nutritional strategies in managing this complex autoimmune disorder.

Hashimoto’s thyroiditis (HT) is not only the most frequent autoimmune thyroid disease (AITD), but it also has a significant impact on patients’ health-related quality of life (HRQoL), and it has been variably associated with differentiated thyroid carcinoma. Even though its pathogenesis is still incompletely understood, oxidative stress is believed to play an important role. Hypothyroidism related to later stages of HT can be treated with levothyroxine substitution therapy; various approaches such as selenium supplementation and iodine-restricted diets have been proposed as disease-modifying treatments for earlier stages, and even thyroidectomy has been suggested for refractory cases of painful HT. Nevertheless, many patients still report suboptimal HRQoL, highlighting an unmet medical need in this area. The concepts and approaches of traditional Chinese medicine (TCM) in treating HT are not broadly known in the West. Here, we provide an overview of TCM for HT, including combinations of TCM with selenium. We encompass evidence from clinical trials and other studies related to complex TCM prescriptions, single herbs used in TCM, and phytochemicals; wherever possible, we delineate the probable underlying molecular mechanisms. The findings show that the main active components of TCM for HT have commonly known or presumed antioxidant and anti-inflammatory activities, which may account for their potential utility in HT. Further exploring the practices of TCM for HT and combining them with evidence- and mechanism-based approaches according to Western standards may help to identify new strategies to alter the clinical course of the disease and/or to treat patients’ symptoms better and improve their HRQoL.

Follicular thyroid cancer (FTC) is a highly aggressive type of endocrine malignancy. It is necessary to investigate the mechanisms of tumorigenesis and therapeutic pathways in patients with FTC. Haem oxygenase-1 (HO-1) can regulate oxidative stress and the occurrence of tumors and diseases. In this study, we discovered that HO-1 was abnormally overexpressed in FTC compared with adjacent tissues. However, the HO-1 overexpression was demonstrated to decrease cell viability and to potentially activate the ferroptosis signalling pathway. Ferroptosis is a newly identified form of oxidative cell death and is currently being targeted as a new cancer treatment. Tumorigenesis is significantly inhibited by curcumin. The present study shows that curcumin inhibits the growth of FTC by increasing the HO-1 expression, further activating the ferroptosis pathway. This study demonstrates that the HO-1-ferroptosis signalling pathway might play an important role in FTC tumorigenesis, and that curcumin inhibits the growth of FTC cells by affecting this pathway.

Curcumin, a polyphenolic compound, is a well-known anticancer agent, although its poor bioavailability remains a big concern. Recent studies suggest that autophagy-targeted therapy may be a useful adjunct treatment for patients with thyroid cancer. Curcumin acts as an autophagy inducer on many cancer cells. However, little is known about the exact role of curcumin on thyroid cancer cells. In the present study, curcumin significantly inhibited the growth of thyroid cancer cells. Autophagy was markedly induced by curcumin treatment as evidenced by an increase in LC3-II conversion, beclin-1 accumulation, p62 degradation as well as the increased formation of acidic vesicular organelles (AVOs). 3-MA, an autophagy inhibitor, partially rescued thyroid cancer cells from curcumin-induced cell death. Additionally, curcumin was found to exert selective cytotoxicity on thyroid cancer cells but not normal epithelial cells and acted as an autophagy inducer through activation of MAPK while inhibition of mTOR pathways. Hyperactivation of the AKT/mTOR axis was observed in the majority of PTC samples we tested, and thyroid cancer cell lines along with cancer tissue specimens sustained a low basal autophagic activity. Taken together, our results provide new evidence that inducing autophagic cell death may serve as a potential anti-cancer strategy to handle thyroid cancer.

… of vitamin E and curcumin alleviates hyperthyroidism-… role of vitamin E and curcumin on antioxidant gene (AOG) … E (200mg/kg body weight) and curcumin (30mg/kg body weight) were …

AIMS: In the present study, the effects of vitamin E and curcumin on hepatic dysfunction, … normal by vitamin E and curcumin treatment. Regulation of hypothyroidism induced decrease in …

ABSTRACT Purpose TAO is an organ specific autoimmune disease associated with thyroid, and inflammation of the orbit and periorbital tissues, which is different from systemic autoimmune diseases such as SLE. However, Grave’s disease is a kind of systemic autoimmune syndrome which might involve the thyroid, the eye ball and the anterior tibial tissue. Considering the inexplicable understanding of TAO pathogenesis, the disease worsens for the patients. Therefore, this manuscript provides insights into the recent advancements of clinical features, epidemiology, pathogenesis with gene-interactions, diagnosis, including available and novel treatment options for TAO, based on available data including RCTs, meta-analyses, and systematic reviews. Methods Articles with clinical features, epidemiology, pathogenesis, diagnosis, and treatment of the disease were thoroughly studied. To perform the gene expression and pathway analysis, articles were searched on PubMed, MEDLINE Cochrane Library and ClinicalTrial.gov from 1982 to 2020. To predict novel TAO-specific therapeutic molecule, structure-based drug design (SBDD) was performed. Results We observed gene expression and pathway analysis and SBDD approaches might bring new insights in the field of TAO pathogenesis, diagnosis, and treatment. A genome-wide map of human genetic interactions revealed involvement of crucial cell-signalling pathways, such as TNF-mediated signalling pathway, type-I interferon signalling pathway, toll-like receptor signalling pathway, transforming growth factor-beta receptor signalling pathway etc. Recently, FDA-approved teprotumumab a breakthrough, first drug for the treatment of active thyroid eye disease, which reduces proptosis and the need for orbital decompression surgery. Furthermore, our SBDD results revealed that cost-effective Curcumin, Withaferin A, Resveratrol, Scopolamine, Quercetin, and Berberine may have significant binding affinity for hyaluronan protein and may be exploited for therapeutic purposes in TAO. Conclusions Considering the increasing risk and nature of disease, novel drug therapies and markers for prognosis need to be investigated. Moreover, evidence-based non-invasive/minimal surgical therapies should be developed for the better management of the disease. Abbreviations: ADIPOQ: Adiponectin; CAS: Clinical Activity Score; CCL5: C-C Motif Chemokine Ligand 5; CT: Computed Tomography; DON: Dysthyroid Optic Neuropathy; EUGOGO: European Group of Graves’ Orbitopathy; FDA: U.S. Food and Drug Administration; FOS: Fos Proto-Oncogene, AP-1 Transcription Factor Subunit; HLA: Human Leukocyte Antigen; HLA-DRA: Major Histocompatibility Complex, Class II, DR Alpha; ICAM1: Intercellular Adhesion Molecule 1; IFNG: Interferon Gamma; IGF-1: Insulin-like Growth Factor 1; IGF-1R: Insulin-like Growth Factor-1 Receptor; IL12B: Interleukin 12B; IL23R: Interleukin 23 Receptor; IL6: Interleukin 6; IOP: Intraocular Pressure; IRF1: Interferon Regulatory Factor 1; IRF5: Interferon Regulatory Factor 5; IRF7: Interferon Regulatory Factor 7; IRF9: Interferon Regulatory Factor 9; JUN: Jun Proto-Oncogene, AP-1 Transcription Factor Subunit; JUNB: JunB Proto-Oncogene, AP-1 Transcription Factor Subunit; MHC: Major Histocompatibility Complex; MRI: Magnetic Resonance Imaging; NFKB1: Nuclear Factor Kappa B Subunit 1; NFKBIA: Nuclear Factor Kappa B Inhibitor Alpha; OADSCs: Orbital Adipose Derived Stromal Cells; PDGFB: Platelet Derived Growth Factor Subunit B; PPARG: Peroxisome Proliferator Activated Receptor Gamma; RANTES: Regulated on Activation Normal T cell Expressed and Secreted; RARA: Retinoic Acid Receptor Alpha; RCTs (Randomized Controlled Trials; SLE: Systemic lupus erythematosus; SOCS3: Suppressor of Cytokine Signaling 3; STAT1: Signal Transducer and Activator of Transcription 1; TAO: Thyroid-Associated Ophthalmopathy; TED: Thyroid eye disease; TGFB1: Transforming Growth Factor Beta 1; TGFB2: Transforming Growth Factor Beta 2; TGF-β: Transforming Growth Factor-beta; TLR7: Toll like Receptor 7; TLR9: Toll like Receptor 9; TNFRSF18: Tumor Necrosis Factor Receptor Superfamily Member 18; TNFSF11: Tumor Necrosis Factor Receptor Superfamily Member 11; TNF-α: Tumor Necrosis Factor-alpha; TSHR: Thyroid Stimulating Hormone Receptor; TSIs: Thyroid Stimulating Immunoglobulin; WNT5A: Wingless-Type MMTV Integration Site Family, Member 5A.

Hashimoto’s thyroiditis (HT), also known as chronic lymphocytic thyroiditis is one of the most frequent types of inflammation of the thyroid gland. The prevalence of the overt HT is about 2% but it is believed that Hashimoto thyroiditis is more frequent than expected. Hashimoto’s thyroiditis is characterized by dysfunction of the immune system, which leads to impaired tolerance of own tissues and increased production of autoantibodies against the thyroid cells. Thyroid peroxidase antibodies (anti-TPO), thyroglobulin antibodies (anti-Tg) and/or TSH receptors antibodies are the principal markers of the disease. The essential element of the treatment of HT is the supplementation of L-thyroxine. In Hashimoto’s disease, like in many other autoimmune diseases, researchers attempted to support pharmacological treatment by adequate nutrition. The aim of this paper was to review the existing literature on the levels of antioxidants (vitamin A, C, E, selenium, zinc) and vitamin D in patients with HT, as well as the influence of the nutritional supplementation of the above mentioned elements on the metabolism of the thyroid gland hormones and the level of anti-thyroid peroxidase (anti-TPO) antibodies.