Protective effect of epigallocatechin‐3‐gallate against neuroinflammation and anxiety‐like behavior in a rat model of myocardial infarction

OBJECTIVE: Individuals who experience myocardial infarction (MI) often experience anxiety. Green tea has potent antioxidative properties and, epigallocatechin‐3‐gallate (EGCG), which is a primary component of tea polyphenols, has advantageous effects on anxiety and depression. However, its mechanism of action regarding the inhibition of anxiety‐like symptoms after MI remains unclear. This study examined whether EGCG alleviated anxiety‐like behavior in MI rats and its possible mechanism. MATERIAL AND METHODS: Rats were administered a daily gavage of EGCG (50 mg/kg) 7 days before and 14 consecutive days after the MI procedure. The open‐field test and light/dark shuttle box were performed to evaluate anxiety‐like behavior. Serum and hippocampus interleukin (IL)‐6 levels were tested using ELISA. Caspase 3, caspase 8, caspase 9 and bcl‐2 messenger RNA levels in the hippocampus were determined using quantitative polymerase chain reaction, and STAT3 protein was detected by Western blot. RESULTS: Results of the open field test and light/dark shuttle box task demonstrated that the MI procedure induced anxiety‐like behavior in the animals, and this impairment was improved by EGCG. Daily EGCG administration significantly decreased the level of IL‐6 both in serum and hippocampus after MI. The administration of EGCG also significantly moderated the expression of caspases 3, 8, and 9 mRNA, which was related to apoptosis in the hippocampus. Furthermore, EGCG also downregulated the expression of STAT3, which was related to the activity of IL‐6. These results suggest that EGCG alleviated anxiety‐like behavior by inhibiting increases in neuroinflammation and apoptosis in the rat hippocampus. In addition, EGCG reversed alterations of IL‐6 and STAT3 in the brain to alleviate apoptosis in the hippocampus. CONCLUSIONS: Thus, EGCG reversed anxiety‐like behavior through an anti‐inflammation effect to alleviate apoptosis in neurons and may be a useful therapeutic material for anxiety‐like behavior after MI.