OBJECTIVE: To investigate the effect and related mechanism of nobiletin in myocardial infarction based on regulation of nuclear factor-κB（NF-κB） signal by Rnd3. METHODS:（1） Totally 40 normal mice were selected and divided into four groups: sham surgery group

myocardial infarction（MI） surgery group

nobiletin gavage group and nobiletin gavage +MI surgery group

changes of cardiac function were detected by cardiac ultrasound

changes of expression of Rnd3 and Cleaved-caspase3 in heart tissues of the four groups of mice were detected by Western blotting.（2） Protein immunoprecipitation and chromatin immunoprecipitation assays of Rnd3 and NF-κB P65 were performed at the level of neonatal rat cardiomyocytes to detect the binding of Rnd3 and P65. Sh-Rnd3 and OE-Rnd3 lentiviruses were transfected in neonatal rat cardiomyocytes

and changes of NF-κB P65 were detected by Western blotting.（3） Forty mice with myocardial infarction were divided into the model group

model+nobiletin group

model+NF-κB agonist group and model+nobiletin+NF-κB agonist group

changes of cardiac function in four groups were detected by cardiac ultrasound

and changes of apoptotic cell expression in heart tissues of four groups were detected by Tunel staining; changes of expression of Cleaved-caspase3 in heart tissues of four groups were detected by Western blotting. RESULTS:（1） Results of cardiac ultrasound and Western blotting test showed that the cardiac ejection fraction and short-axis shortening fraction in MI surgery group were significantly lower than those in sham surgery group

the contents of Rnd3 and Cleaved-caspase3 in heart tissues in MI surgery group were significantly higher than those in sham surgery group; compared with the MI surgery group

the cardiac ejection fraction and short-axis shortening fraction were significantly higher in the nobiletin gavage+MI surgery group

the contents of Rnd3 and Cleaved-caspase3 in heat tissues were significantly lower in the nobiletin gavage+MI surgery group

with statistically significant differences（P<0.05）.（2） Results of protein immunoprecipitation and chromatin immunoprecipitation assays showed that Rnd3 combined with NF-κB P65 could regulate the apoptosis of neonatal rat cardiomyocytes. When Rnd3 expression was inhibited

the expression of NF-κB P65 increased; when Rnd3 was overexpressed

the expression of NF-κB P65 decreased.（3） Compared with the model group

the cardiac ejection fraction and short-axis shortening fraction increased

Cleaved-caspase3 expression and cell apoptosis decreased in the model+nobiletin group

the model+NF-κB agonist group and the model+nobiletin+NF-κB agonist group

with statistically significant differences（P<0.05）. CONCLUSIONS: Nobiletin can reduce myocardial apoptosis induced by acute myocardial infarction by inhibiting Rnd3 expression and activating NF-κB signaling pathway.