Journal of Capital Medical University ›› 2019, Vol. 40 ›› Issue (5): 703-708.doi: 10.3969/j.issn.1006-7795.2019.05.008

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Effects of chrysophanol on Beclin1 and Bax protein expressions in mice with focal cerebral ischemia/reperfusion injury

Fang Yalan1,2, Huang Yuyou2, Zhao Yongmei2, Shi Wenjuan2, Li Jincheng2, Duan Yunxia2, Gao Li2, Luo Yumin2   

  1. 1. General Medical Treatment Ward, Pinggu District Hospital of Beijing, Beijing 101200, China;
    2. Xuanwu Hospital, Capital Medical University, Beijing Geriatric Medical Research Center, Beijing 100053, China
  • Received:2019-07-08 Online:2019-09-21 Published:2019-12-16
  • Supported by:
    This study was supported by National Natural Science Foundation of China (81620108011), National Key Clinical Specialty (Traditional Chinese Medicine, No.122).

Abstract: Objective To study the protective effect mechanism of chrysophanol (CHR) on focal cerebral ischemia/reperfusion mice by regulating the expressions of autophagy-related protein Beclin1 and apoptosis-related protein Bax. Methods A total of 18 male C57BL/B6 mice were randomly (random number) divided into three groups:Sham group (n=6), middle cerebral artery occlusion (MCAO)/perfusion (MCAO group, n=6), and CHR group (n=6). The right MCAO for 45 min was induced by thread embolism and the reperfusion lasted for 14 days. CHR in dose of 0.1 mg/kg was intraperitoneally injected in CHR group mice once a day. On 14 d after reperfusion, the brain tissue was obtained. The positive expressions of autophagy-related protein Beclin1 in the brain ischemic penumbra were observed with immunofluorescent staining. The level of apoptosis-related protein Bax in ischemic brain tissue sections was determined by Western blotting. Results 1) There was little Beclin1 positive cells in Sham group. Compared with Sham group, the number of Beclin1 positive cells in the penumbra of MCAO group obviously increased on 14 d after reperfusion (P<0.05). Compared with MCAO group, the number of positive cells of Beclin1 decreased significantly in the penumbra of CHR group on 14 d after reperfusion (P<0.05). 2) The Beclin1 positive cells were co-localized with NeuN, a general neuronal marker, in the brain ischemic penumbra. 3) Bax protein level was upregulated in the brains of MCAO mice on 14 d after reperfusion. CHR treatment decreased Bax protein level in the ischemic tissue compared with MCAO group (P<0.05). Conclusion CHR may reduce neuronal apoptosis and alleviate excessive activation of autophagy by inhibiting the production of Bax protein and reducing the production of Beclin1 protein, and thus exerts long-term neuroprotective effects on cerebral ischemia-reperfusion injury.

Key words: chrysophanol, cerebral ischemia/reperfusion, middle cerebral artery occlusion, autophagy, Beclin1, Bax

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