Ginkgolide B attenuates myocardial infarction-induced depression-like behaviors via repressing IL-1β in central nervous system.

Depression is common in patients with myocardial infarction (MI), attributing to worse outcomes. Inflammatory response in the central nervous system (CNS) is considered to be a potential mechanism underlying MI induced depression. Our former research demonstrated Ginkgo biloba extract played an important role in the repression of hippocampus inflammation in heart failure mice with depressive behaviors. This study was designed to investigate the effect of Ginkgolide B (GB) on MI-induced depression-like behaviors in post MI mice. After MI surgery induced by coronary ligation, MI mice behaved depressingly, detected by open field test (OFT) and the sucrose preference test (SPT), which was reserved by GB treatment. Meanwhile, the reduction of 5-HT and increase of interleukin 1 beta (IL-1β) in median raphe nucleus and cortex indicated potential mechanisms underlying MI-induced depression-like behaviors, which were significantly reserved by GB treatment. Moreover, the consistent variation of IL-1β and phospho-STAT3 expression in brain tissues, indicated a role of STAT3 pathway in IL-1β production and anti-inflammatory effect of GB. In conclusion, GB has great benefits in effective treatment for depression post MI through reducing the levels of proinflammatory cytokines via STAT3 pathway, implicating potential effects in improving depression status in patients with MI.