Conocarpus erectus extracts restore thyroid architecture and downregulate pro-apoptotic markers in propylthiouracil-treated rats

Abstract

Background

Programmed cell death, or apoptosis, influences the onset and progression of autoimmune thyroid conditions like hypothyroidism. In Hashimoto’s thyroiditis, disrupted immune regulation and abnormal cytokine profiles accelerate thyroid tissue loss through apoptotic pathways. With its antioxidant-rich composition, Conocarpus erectus has been explored for its ability to mitigate oxidative damage and inhibit apoptosis in thyroid cells.

Methods

Leaves of C. erectus were air-dried, ground, and defatted with hexane. A Soxhlet extractor produced a crude methanolic extract, which was concentrated and partitioned into chloroform and ethyl acetate fractions. Sixty female Wistar albino rats were randomized into six groups: a control, a propylthiouracil (PTU)-treated hypothyroid group, and two PTU groups receiving either the ethyl acetate or chloroform fraction (500 and 1000 mg/kg/day). After treatment, thyroids underwent histopathological examination and molecular analysis by ELISA, Western blot, and RT-qPCR to assess apoptotic and inflammatory markers.

Results

Phytochemical screening identified flavonoids, saponins, tannins, coumarins, and phenolics, while HPLC profiling confirmed the presence of bioactive compounds such as quercetin, kaempferol, and gallic acid. Histological analysis in extract-treated hypothyroid rats revealed improved follicular regeneration and neovascularization. Western blotting showed increased Bcl-2 and decreased cleaved caspase-3 and caspase-8 levels in the ethyl acetate group. RT-qPCR demonstrated significant downregulation of proinflammatory and apoptotic genes TNF, NLRP3, TRAIL, and NF-κB.

Conclusions

These results indicate that C. erectus extracts protect against PTU-induced oxidative and apoptotic damage in thyroid tissue. Antioxidant-rich phytochemicals appear to modulate apoptotic pathways and support structural repair, suggesting potential as complementary agents in thyroid disorder therapy.