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Sepsis leads to thyroid impairment and dysfunction in rat model
Xingsheng Lin1, Songjing Shi2, Songchang Shi3
1The First Department of Intensive Care Medicine, Fujian Provincial South Branch Hospital, China; The Second Department of Intensive Care Medicine, Fujian Provincial Hospital, China.
Tissue & Cell
|August 14, 2016
Summary
Sepsis significantly reduces thyroid hormone levels and induces apoptosis in thyroid cells. This study reveals cellular and molecular changes in the thyroid during sepsis, offering insights into its pathological mechanisms.
Area of Science:
- Endocrinology
- Pathology
- Immunology
Background:
- Sepsis is a life-threatening systemic response to infection.
- Apoptosis, or programmed cell death, is a known feature of sepsis.
- The impact of sepsis on thyroid function and cellular integrity requires further elucidation.
Purpose of the Study:
- To investigate the effects of sepsis on thyroid hormone levels in an animal model.
- To examine the cellular and molecular changes within the thyroid gland during sepsis.
- To establish a sepsis model for studying thyroid pathology.
Main Methods:
- Cecal ligation and puncture (CLP) was used to induce sepsis in rats.
- Thyroid hormone levels (T3, T4, fT3, fT4) were measured.
- Caspase-3 expression and TUNEL assays were performed on thyroid tissue.
- Pathological ultrastructural changes in thyroid follicular epithelial cells were analyzed.
Main Results:
- Sepsis led to decreased levels of triiodothyronine (T3), thyroxine (T4), free T3 (fT3), and free T4 (fT4).
- Increased Caspase-3 expression and a higher ratio of TUNEL-positive cells were observed in the thyroid post-sepsis.
- Significant pathological ultrastructural alterations were noted in thyroid follicular epithelial cells.
Conclusions:
- Sepsis induces significant reductions in circulating thyroid hormones.
- Sepsis triggers apoptosis and cellular damage within the thyroid gland.
- This study provides a foundation for understanding sepsis-induced thyroid dysfunction.
