N‑acetylcysteine prevents hypothyroidism‑induced impairment of learning and memory in adolescent male rats via affecting oxidative status, inflammatory response and BDNF in hippocampal tissues.

Abstract

The present study was assumed that N‑acetylcysteine (AC) might improve cognitive function in adolescent rats with hypothyroidism through various mechanisms. Sixty adolescent rats were randomly divided into the following groups: Vehicle (received normal saline intraperitoneally (IP)); Propylthiouracil (PTU)‑induced hypothyroidism (0.05%, dissolved in drinking water); Hypothyroid rats were IP treated with different doses of AC (50, 100, and 150 mg/kg/day) for a period of six weeks; Normal rats treated with the highest doses of AC (150 mg/kg/day). Behavioral and biochemical analyses were studied for all groups. In the Morris water maze test, AC significantly reduced both the time to find the hidden platform and the distance travelled as compared to non‑treated hypothyroid rats. In the passive avoidance test, the latency of entering the dark chamber was significantly increased by AC, whereas decreased the time spent in the darkroom of the chamber compared to the hypothyroid rats. In biochemical results, AC reduced both malondialdehyde content and nitrite while increased the thiol content, catalase and superoxide dismutase enzymes activity in both the cortex and the hippocampus, and a notable improvement in brain‑derived neurotrophic factor (BDNF) levels in hippocampal tissues of the hypothyroid rats, while decreasing the level of interleukin‑6 in rat hippocampal region. Therefore, based on the results, the beneficial effects of AC on cognitive impairment in adolescent hypothyroid rats are probably related to its anti‑oxidant properties and notable improvement in BDNF levels.