Neuroprotective Effect of Ashwagandha Extract against the Neurochemical Changes Induced in Rat Model of Hypothyroidism

Abstract

The current aim is to evaluate the effect of ashwagandha root extract (AE) on the neurochemical changes induced in the cortex and hippocampus as a consequence of thyroid dysfunction induced by propylthiouracil (PTU). Male Wistar rats were divided into; control, AE treated rats, rat model of hypothyroidism and rat model of hypothyroidism treated with either AE or L-thyroxine (T4) for 1 month. Rat model of hypothyroidism showed a significant decrease in serum levels of tri-iodothyronine (T3) and T4 and a significant increase in cortical and hippocampal lipid peroxidation (MDA), nitric oxide (NO), superoxide dismutase (SOD) and catalase (CAT). However, reduced glutathione (GSH) decreased significantly. This was associated with a significant increase in hippocampal tumor necrosis factor-α (TNF-α) and cortical dopamine levels. Both L-thyroxine and AE restored T3 and T4 levels. In the hippocampus L-Thyroxine prevented the increase in MDA and restored GSH but failed to restore the increased NO and TNF-α. In the cortex L-thyroxine didn’t change the increased MDA and NO and the decreased GSH induced by PTU. L-thyroxine increased cortical and hippocampal SOD and CAT. AE prevented the increased hippocampal MDA, NO and TNF-α and the decreased GSH level induced by PTU. In the cortex AE failed to restore MDA and NO but prevented the decrease in GSH. The increase in cortical dopamine level induced by PTU was ameliorated by L-thyroxine and improved by AE. The present data indicate that AE could prevent thyroid dysfunction and reduce its complications on the nervous system including oxidative stress and neuroinflammation.

Keywords:

• Ashwagandha
• brain
• hypothyroidism
• inflammation
• monoamine
• oxidative stress

Declaration of interest

The authors declare no conflicts of interest. The authors alone are responsible for the content and writing of the article.

Additional information

Funding

The authors sincerely thank the authorities of the National Research Center, Giza, Egypt, for their financial supports and providing the facilities (Project Code: 11010331) to conduct and complete the present study.

Notes on contributors

Eman N. Hosny

Eman N. Hosny, PhD, is an Assistant Professor of Physiology in the Medical Physiology Department, Medical Division, National Research Centre, Giza, Egypt.

Mayada M. El-Gizawy

Mayada M. El-Gizawy, PhD, is an Assistant Professor of Physiology in the Medical Physiology Department, Medical Division, National Research Centre, Giza, Egypt.

Hussein G. Sawie

Hussein G. Sawie, PhD, is an Associate Professor of Physiology in the Medical Physiology Department, Medical Division, National Research Centre, Giza, Egypt.

Khaled G. Abdel-Wahhab

Khaled G. Abdel-Wahhab, PhD, is a Professor of Physiology in the Medical Physiology Department, Medical Division, National Research Centre, Giza, Egypt.

Yasser A. Khadrawy

Yasser A KhadrawyPhD, is a Professor of Neurophysiology and the Head of the Medical Physiology Department, Medical Division, National Research Centre, Egypt.