Abstract
Houttuynia cordata Thunb. holds a longstanding reputation as a traditional folk remedy in East Asia, where it has been employed to treat a variety of inflammatory conditions, nephritis, hepatitis and cancer. Despite its extensive use, there exists a paucity of research examining its efficacy in managing thyroid disorders and diabetes. Moreover, the bioactive components responsible for modulating the molecular pathways remain elusive. Objectives: This research aimed to determine the key bioactive components in the ethanolic extract of H. cordata Thunb. (HCEE) responsible for its thyroid-modifying properties and examine its effects on rats with experimentally induced hypothyroidism and diabetes. Methods: Molecular docking was performed to investigate the possible mechanisms of thyroid regulation of HCEE constituents. Researchers induced hypothyroidism in rats by adding 6-propyl-2-thiouracil to their drinking water for a period of four weeks. To induce diabetes, the rats received an intraperitoneal injection of streptozotocin. The animals were then given daily oral doses of HCEE (500 mg/kg b.w.), levothyroxine (50 mg/kg b.w.), or glibenclamide (5 mg/kg b.w.) for 28 days. Following this treatment, standard methods were employed to measure biochemical parameters in the rats’ serum. Results: The results demonstrate that HCEE ameliorated hypothyroidism by increasing serum T3 (14.38%) and T4 (125.96%) levels and decreasing TSH (p < 0.01; −41.75%) levels. In diabetic rats with induced hypothyroidism, HCEE significantly (p < 0.001) increased T3 (149.51%) and T4 (73.54%) levels with reduced TSH (−64.39%) levels. In silico analysis demonstrated that the identified bioactive compounds from HCEE may enhance thyroid hormone function through interaction with the thyroid hormone receptor protein TRβ1 (PDB:3GWS), similar to the conventional pharmaceuticals levothyroxine and triiodothyronine (T3). Conclusions: HCEE exhibits potential as a natural alternative to synthetic medications in the prevention and treatment of thyroid dysfunctions.
Published Version
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