Green tea extract modulates lithium-induced thyroid follicular cell damage in rats

Area of Science:

• Endocrinology
• Toxicology
• Pharmacology

Background:

• Long-term lithium carbonate (LC) use can negatively impact thyroid gland structure and function.
• The mechanisms underlying lithium-induced thyroid dysfunction require further elucidation.

Purpose of the Study:

• To investigate the modulatory effects of green tea extract (GTE) on thyroid gland alterations caused by prolonged lithium carbonate (LC) administration.
• To explore the underlying mechanisms of GTE's protective action against LC-induced thyroid damage.

Main Methods:

• Adult Sprague-Dawley rats were divided into control, LC-treated, and LC + GTE groups for 8 weeks.
• Evaluations included thyroid hormone profiles, inflammatory markers (IL-6, TNF-α), oxidative stress markers (MDA, GSH, SOD), apoptosis markers (caspase-3, Bcl2 family), and proliferation markers (PCNA).
• Histological and histochemical (PAS) analyses assessed structural changes.

Main Results:

• LC induced hypothyroidism, follicular damage, increased apoptosis, inflammation, collagen deposition, and oxidative stress.
• GTE treatment normalized thyroid hormone levels, reduced TSH, and improved histological and apoptotic markers.
• GTE counteracted LC-induced oxidative stress, inflammation, fibrosis, and cellular proliferation.

Conclusions:

• Prolonged LC use leads to hypothyroidism and structural thyroid damage via oxidative stress, inflammation, and apoptosis.
• GTE demonstrates significant protective effects against LC-induced thyroid toxicity.
• GTE's protective mechanisms involve antioxidant, anti-inflammatory, antifibrotic, and antiproliferative actions, restoring thyroid function and structure.