Department of Anatomy, Fakeeh College for Medical Sciences, Jeddah, Saudi Arabia.
Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Egypt.
Folia Morphol (Warsz). 2022;81(3):594-605. doi: 10.5603/FM.a2021.0052. Epub 2021 May 21.
The aim of the current work was to clarify the modulation role of green tea extract (GTE) over structural and functional affection of the thyroid gland after long term use of lithium carbonate (LC). The suggested underlying mechanisms participating in thyroid affection were researched.
Twenty-four Sprague-Dawley adult albino rats were included in the work. They were divided into three groups (control, LC, and concomitant LC + GTE). The work was sustained for 8 weeks. Biochemical assays were performed (thyroid hormone profile, interleukin 6 [Il-6]). Histological, histochemical (Periodic Acid Schiff [PAS]) and immunohistochemical (caspase-3, tumour necrosis factor alpha [TNF-α], proliferating cell nuclear antigen [PCNA]) evaluations were done. Oxidative/antioxidative markers (malondialdehyde [MDA]/gluthathione [GSH], superoxide dismutase [SOD]) and Western blot evaluation of the Bcl2 family were done.
Lithium carbonate induced hypothyroidism (decreased T3, T4/increased thyroid-stimulating hormone [TSH]). The follicles were distended, others were involuted. Some follicles were disorganised, others showed detached follicular cells. Apoptotic follicular cells were shown (BAX and caspase-3 increased, Bcl2 decreased, BAX/Bcl2 ratio increased). The collagen fibres' content and proinflammatory markers (TNF-α and IL-6) increased. The proliferative nuclear activity was supported by increased expression of PCNA. Oxidative stress was established (increased MDA/decreased GSH, SOD). With the use of GTE, the thyroid hormone levels increased, while the TSH level decreased. Apoptosis was improved as BAX decreased, Bcl2 increased, and BAX/Bcl2 ratio was normal. The collagen fibres' content and proinflammatory markers (TNF-α and IL-6) decreased. The expression of PCNA and caspase-3 were comparable to the control group. The oxidative markers were improved (decreased MDA/increased GSH, SOD).
In conclusion, prolonged use of LC results in hypothyroidism, which is accompanied by structural thyroid damage. LC induced thyroid damage through oxidative stress that prompted sterile inflammation and apoptosis. With the use of GTE, the thyroid gland regained its structure and function. The protecting role of GTE is through antioxidant, antifibrotic, anti-inflammatory, and antiproliferative effects.
本研究旨在探讨绿茶提取物（GTE）对长期碳酸锂（LC）使用后甲状腺结构和功能的调节作用，并研究可能参与甲状腺损伤的潜在机制。
将 24 只成年 Sprague-Dawley 白化大鼠纳入研究，分为三组（对照组、LC 组和 LC+GTE 组），持续 8 周。进行生化检测（甲状腺激素谱、白细胞介素 6 [IL-6]）。进行组织学、组织化学（过碘酸雪夫染色 [PAS]）和免疫组织化学（半胱天冬酶-3、肿瘤坏死因子-α [TNF-α]、增殖细胞核抗原 [PCNA]）评估。检测氧化/抗氧化标志物（丙二醛 [MDA]/谷胱甘肽 [GSH]、超氧化物歧化酶 [SOD]）和 Bcl2 家族的 Western blot 评估。
碳酸锂导致甲状腺功能减退（T3、T4 降低，促甲状腺激素 [TSH]升高）。滤泡扩张，其他滤泡萎缩。一些滤泡排列紊乱，其他滤泡显示滤泡细胞脱落。可见凋亡的滤泡细胞（BAX 和半胱天冬酶-3 增加，Bcl2 减少，BAX/Bcl2 比值增加）。胶原纤维含量和促炎标志物（TNF-α和 IL-6）增加。增殖细胞核活性通过 PCNA 表达增加得到支持。氧化应激（MDA 增加，GSH 减少，SOD 减少）。使用 GTE 后，甲状腺激素水平升高，而 TSH 水平降低。BAX 减少，Bcl2 增加，BAX/Bcl2 比值正常，凋亡得到改善。胶原纤维含量和促炎标志物（TNF-α和 IL-6）减少。PCNA 和半胱天冬酶-3 的表达与对照组相似。氧化标志物改善（MDA 减少，GSH 增加，SOD 增加）。
长期使用 LC 可导致甲状腺功能减退，伴有甲状腺结构损伤。LC 通过诱导氧化应激引起无菌性炎症和细胞凋亡导致甲状腺损伤，而 GTE 可恢复甲状腺的结构和功能。GTE 的保护作用是通过抗氧化、抗纤维化、抗炎和抗增殖作用实现的。
