Abstract: AIM: To investigate the role and possible mechanism of gastrodin combined with dexamethasone in myocardial cell injury induced by oxygen-glucose deprivation. METHODS: Oxygen-glucose deprivation (OGD) model was established. The cells were divided into 5 groups: normal control group, OGD group, DEX group, GAS group and DEX+GAS group. The activity of myocardial cells was detected by CCK-8 test in each group. The activity of LDH was detected by colorimetry in each group. The apoptosis of myocardial cells was detected by TUNEL method in each group. The ELISA assay was used to detect the inflammatory factors in culture medium of myocardial cells in each group. Western blot was used to detect the expression of Notch1, Bax, Bcl-2 and Beclin1 in myocardial cells in each group.RESULTS: The results showed that GAS combined with DEX could significantly increase the activity of myocardial cells and decrease the apoptosis, reduce production of TNF-α, IL-6, IL-1β and promote production of IL-10, decrease the release of LDH significantly of myocardial cells induced by OGD. The results of Western blot showed that GAS combined with DEX increased the expression of Notch1, Bcl-2 and autophagy-related gene Beclin1, but decreased the expression of Bax of myocardial cells induced by OGD. CONCLUSION: The combination of GAS and DEX may promote autophagy and increase cell activity, inhibit apoptosis and inflammatory reaction by activating Notch signaling pathway, thereby reducing OGD-induced myocardial cells damage.

Key words: gastrodin, dexamethasone, oxygen-glucose deprivation, autophagy, apoptosis, Notch signaling pathway