BACKGROUND: Valproate sodium is an anticonvulsant drug. Saussurea lappa (costus) is a medicinal plant rich with antioxidants. This research aimed to assess the protective effect of costus root extract against valproate sodium-induced thyrotoxicity.METHODS: Eighty adult male albino rats were equally divided into four groups; group I: untreated control, group II: rats were given 200 mg/kg BW valproate sodium orally and daily for 8 weeks, group III: rats were given 300 mg/kg BW costus root extract orally and daily for 8 weeks, and group IV: rats were given combination of valproate sodium and costus root extract. After 8 weeks, blood samples were collected to evaluate T3, T4 and thyroid-stimulating hormone (TSH) levels. Thyroid gland samples were handled for light and electron microscopic investigation. The heights of follicular cells, area % of collagen fibers and color intensity of thyroglobulin immunoreaction were statistically analyzed. RESULTS: After being given valproate sodium as an induction, hormonal assay showed significant decrease in serum T3 and T4 and significant increase of TSH. Follicular and cellular alterations were shown by light and electron microscopes. Morphometric study revealed increased follicular cell height and area % of collagen fibers and decreased color intensity of thyroglobulin. In contrast, costus root extract appeared to have a protective role against valproate sodium-induced thyroid injury. Most of the changes induced by valproate sodium were not observed after supplementation with the plant root extract.CONCLUSION: Valproate sodium has serious effects on the function and structure of thyroid gland, and this study shows that costus root extract could have a protective effect against these effects.KEYWORDS: valproate sodium, rat, thyrotoxicity, Saussurea lappa

Background: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is one of the most toxic artificial chemicals present in the environment. TCDD exposure is associ¬ated with stomach damage. Olive leaves extract (OLE) is a herbal agent, used in medication with a variety of beneficial therapeutic effects. Objective: To evaluate the protective effect of OLE against TCDD induced fundic mucosal damage in adult male albino rats. Materials and Methods: Seventy rats were divided into 3 groups: Group I (control group), group II (TCDD group): these rats received TCDD (100 μg/kg body weight/day) orally for 8 weeks, group III (TCDD and OLE group): rats of this group received TCDD and OLE (0.5 g/ body weight/day) orally for 8 weeks. Specimens from the gastric fundus were excised and stained with H&E and Periodic acid Schiff (PAS) for both routine histological and histochemical studies, and immunohistochemically for the detection of chromomgranin A. Morphometric and electron microscopic studies were also carried out. Results: TCDD induced mucosal injury, sloughing of surface mucosal cells, areas of gastric ulcer, glandular disarrangement, and decreased mucosal height, as well as a decrease in the PAS and chromogranin A positive reactions. Electron microscopic studies showed deteriorating changes in parietal cells, chief cells, mucous cells, and enteroendocrine cells. In contrast, most of the changes induced by TCDD were not observed in TCDD and OLE-treated group. Conclusion: TCDD has toxic effects on the histological and ultrastructure of fundic mucosa of rats, and OLE decreased these effects. OLE can be used to avoid TCDD-induced gastric complications.

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