Abstract
Background:
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.
Materials and methods:
Twenty-four Sprague-Dawley adult albino rats were included in the work. They are divided into three groups (control, LC, and concomitant LC + GTE). The work was sustained for 8 weeks. Biochemical assays were achieved (thyroid hormone profile, IL-6). Histological, histochemical (PAS) and immunohistochemical (caspase-3, TNF-α, PCNA) evaluations were done. Oxidative/antioxidative markers (MDA / GSH, SOD) and western blot evaluation of the Bcl2 family were done.
Results:
LC induced hypothyroidism (decrease T3, T4/increase TSH). The follicles were distended, others were involuted. Some follicles were disorganized, others showed detached follicular cells. Apoptotic follicular cells were proved (Bax and caspase-3 increased, Bcl2 decreased, Bax/Bcl2 ratio increased). The collagen fibers' content and proinflammatory markers (TNF-α and IL-6) increased. The proliferative nuclear activity was supported by increase expression of PCNA. Oxidative stress was established (increase MDA/decrease GSH, SOD). With the use of GTE, the thyroid hormone levels increased, while the TSH level decreased. Apoptosis is improved as Bax decreased, Bcl2 increased, and Bax/Bcl2 ratio was normal. The collagen fibers' 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 (decrease MDA/increase GSH, SOD).
Conclusions:
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 achieved its structure and function. The protecting role of GTE is through antioxidant, antifibrotic, anti-inflammatory, and antiproliferative effects.
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