Liquiritin improves depressive behavior in rats with post-stroke depression by reducing apoptosis of amygdala cells / 国际脑血管病杂志

ABSTRACT

Objective:To investigate the effect of liquiritin on the apoptosis of amygdala cell and the expression of apoptosis-related factors Bax and Bcl-2 protein in rats with post-stroke depression (PSD).Methods:Sixty rats were randomly divided into normal control group, stroke group, PSD group, citalopram group, liquiritin group, and normal saline control group ( n=10 in each group). The middle cerebral artery was occluded with a suture method to induce focal cerebral ischemia, and the PSD model was established by chronic and unpredictable mild stress stimulation and orphanism. At the same time every week after the model was made, the weight of rats in each group was measured and the depression behavior was evaluated, including sucrose water test and open field test. At 6 weeks after the model was made, TUNEL staining was used to detect the apoptosis of amygdala cell, immunofluorescence staining was used to detect the expression of Bax and Bcl-2 in the amygdala, and Western blot analysis was used to detect the protein expression of Bax and Bcl-2 in the amygdala. Results:Compared with the liquiritin group, citalopram group and normal control group, the body weight and sucrose solution preference of rats in the stroke group, PSD group and normal saline control group were decreased, and the horizontal and vertical movements in open field test were decreased; the differences were statistically significant (all P<0.01). TUNEL staining results showed that compared with the liquiritin group, citalopram group and normal control group, the number of apoptotic cells was significantly increased in the stroke group, PSD group, and normal saline control group; the difference was statistically significant (all P<0.01). The results of immunofluorescence staining showed that compared with the liquiritin group, citalopram group and normal control group, the number of bcl-2 immunoreactive cells in amygdala of the stroke group, PSD group and normal saline control group was significantly decreased, while the number of Bax immunoreactive cells was significantly increased; the difference was statistically significant (all P<0.01). Western blot analysis showed that compared with the liquiritin group and citalopram group, the expression of bcl 2 protein in amygdala of the stroke group, PSD group and normal saline control group was significantly decreased, while the expression of Bax protein was significantly increased; the difference was statistically significant (all P<0.01). Conclusion:Liquiritin can alleviate the symptoms of PSD, and its mechanism may be related to inhibiting the apoptosis of amygdala cells and regulating the expression of apoptosis-related factors.