Propofol pretreatment alleviates mast cell degranulation by inhibiting SOC to protect the myocardium from ischemia–reperfusion injury

Propofol (PPF) has a protective effect on myocardial ischemia–reperfusion (I/R) injury (MIRI). The purpose of this study was to investigate whether the myocardial protective effect of propofol is related to the inhibition of mast cell degranulation and explore the possible mechanisms involved. Our in vivo results showed that compared with the sham group, cardiac function, infarct size, histopathological damage, apoptosis, and markers of myocardial necrosis were significantly increased in the ischemia–reperfusion group, and propofol pretreatment alleviated these effects. In the coculture system, propofol-treated mast cells reduced their tryptase activity, resulting in cardiomyocyte protective effects, such as decreased apoptosis of cardiomyocytes and decreased expression of myocardial necrosis markers. Finally, experimental results in vitro revealed that thapsigargin (TG) can increase mast cell degranulation, tryptase release, calcium ion concentration, and the expression of STIM1 and Orai1 induced by H/R, but propofol pretreatment can partially reverse the above effects. These results suggested that the cardioprotective effect of propofol is achieved in part by inhibiting calcium influx through store-operated Ca2+ channels (SOCs) and thus alleviating mast cell degranulation. [Display omitted] •As an important second messenger, Ca2+ participates in mast cell degranulation.•Mast cells are a kind of nonexcitatory cell, and their Ca2+ influx mainly depends on store operated Ca2+ channels (SOCs).•Propofol may inhibit mast cell degranulation by inhibiting SOC.•Propofol can play an anti-myocardial ischemia–reperfusion injury role through the aforementioned effects.