Tenuifolin ameliorates chronic restraint stress-induced cognitive impairment in C57BL/6J mice

The general consensus is that stress affects the central nervous system and can lead to cognitive problems. The root of Polygala tenuifolia (P. tenuifolia) is a well-known traditional Chinese medicine used for improving brain function. Tenuifolin (TEN) is the major constituent of P. tenuifolia and has a promising neuroprotective property. The purpose of this study was to investigate the alleviating effect of TEN on cognitive impairment induced by chronic restraint stress (CRS) and its mechanism. Our results showed that CRS exposure resulted in impaired cognitive performance in CS7BL/6J mice, as indicated by decreased responses in Y-maze, novel objects recognition, and step-through passive avoidance tests. TEN treated daily orally (10 and 20 mg/kg) for 30 days reversed these behavior changes. Meanwhile, TEN could significantly regulate interleukin (IL)-6 and IL-10 levels in the hippocampus. TEN inhibited the toll-like receptor 4/nuclear factor-kappa B-mediated inflammation, as well as adrenocorticotropic hormone and corticosterone levels in serum. Most importantly, we found that TEN also upregulated the expressions of brain-derived neurotrophic factor, tropomyosin kinase B, glucocorticoid receptor, glutamate receptor 1, and synapse-associated proteins. Collectively, these data suggest that TEN has a potential improvement effect on memory loss caused by CRS.

Automated summary

It is widely accepted that stress affects the central nervous system and can lead to cognitive problems. This study found that Tenuifolin (TEN), the major constituent of Polygala tenuifolia, has potential neuroprotective properties and improves cognitive impairment induced by chronic restraint stress (CRS). TEN regulates interleukin (IL)-6 and IL-10 levels, inhibits toll-like receptor 4/nuclear factor-kappa B-mediated inflammation, and decreases levels of adrenocorticotropic hormone and corticosterone in serum. Furthermore, TEN upregulates the expressions of brain-derived neurotrophic factor, tropomyosin kinase B, glucocorticoid receptor, glutamate receptor 1, and synapse-associated proteins.