Gallic acid attenuates chromium-induced thyroid dysfunction by modulating antioxidant status and inflammatory cytokines.
Hexavalent chromium-mediated oxidative stress causes severe organ damage. The present study was designed to investigate the possible thyroprotective effect and underlying mechanisms of gallic acid using rat model of potassium dichromate-induced thyroid dysfunction. Forty adult male albino rats were divided into 4 groups: control, gallic acid (20mg GA/kg b. wt), potassium dichromate (2mg PD/kg b. wt) and the fourth group was co-treated with PD and GA. PD-injection resulted in decreased serum free triiodothyonine (FT3), free thyroxine (FT4) with concomitant significant increase in thyroid stimulating hormone (TSH) levels. Superoxide dismutase (SOD), glutathione-S-transferase (GST) activities and their respective mRNA expression and reduced glutathione (GSH) content were significantly decreased. Thyroid nitrosative stress marker (NO level and iNOS mRNA and protein expression) and pro-inflammatory cytokines (serum TNF-α, IL-6 and thyroid TNF-α, IL-6 and COX-2 gene and protein expression levels) were disturbed. Histopathological changes revealed distended, collapsed and degenerated follicles with vacuolated cytoplasm. GA co-treatment attenuated pro-inflammatory cytokines, the thyroid expression of iNOS, TNF-α, IL-6 and COX-2, decreased the elevated lipid peroxidation biomarkers and NO level and up- regulated SOD and GST mRNA expression levels. In conclusion, GA has shown strong modulatory potential against PD-induced inflammation and oxidative stress in albino rats.
Genetic & Cell Biology, Zoology Department, Faculty of Science, Beni-Suef University, Egypt. Electronic address: menaa_5696@yahoo.com.
Hanaa M
HM
Mohamed
Physiology Division, Zoology Department, Faculty of Science, Beni-Suef University, Egypt.
Sanaa M
SM
Abd El-Twab
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000378:metabolism*; D017209:Apoptosis / Q000187:drug effects; D016207:Cytokines / Q000378:metabolism*; D052244:Endocrine Disruptors / Q000633:toxicity*; D005707:Gallic Acid / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects / Q000276:immunology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects / Q000276:immunology; D011192:Potassium Dichromate / Q000633:toxicity*; D051381:Rats; D013961:Thyroid Gland / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D016207:Cytokines; D052244:Endocrine Disruptors; D014284:Triiodothyronine; D005707:Gallic Acid; D013972:Thyrotropin; D013974:Thyroxine; D011192:Potassium Dichromate
Apoptosis; Chromium poisoning; Gallic acid; Inflammation; Oxidative stress