Objective To analyse the efficacy of microvascular decompression for hemifacial spasm (HFS) caused by vertebral basilar artery compression. Methods A total of 141 patients with HFS treated by microvascular decompression in our hospital were collected in this study. The improvement of the symptoms after operation was compared between patients with HFS caused by vertebral basilar artery compression (28 cases) and patients with HFS caused by non-vertebral basilar artery compression (113 cases). Results There was no significant difference in the effective rate between the two groups of HFS (96.43%vs. 98.23%,P=0.49) with mean following-up 13.81 ± 1.57 months. And there was no significant difference in the delayed cure rate after surgery between two groups (37.04%vs. 20.72%,χ2=1.38, P>0.05). Conclusion Microvascular decompression is a safe and effective method for the treatment of HFS caused by compressed vertebral basilar artery.

Excess activation of cardiac fibroblasts inevitably induces cardiac fibrosis. Emodin has been used as a natural medicine against several chronic diseases. The objective of this study is to determine the effects of emodin on cardiac fibrosis and the underlying molecular mechanisms. Intragastric administration of emodin markedly decreased left ventricular wall thickness in a mouse model of pathological cardiac hypertrophy with excess fibrosis induced by transaortic constriction (TAC) and suppressed activation of cardiac fibroblasts induced by angiotensin II (AngII). Emodin upregulated expression of metastasis associated protein 3 (MTA3) and restored the MTA3 expression in the setting of cardiac fibrosis. Moreover, overexpression of MTA3 promoted cardiac fibrosis; in contrast, silence of MTA3 abrogated the inhibitory effect of emodin on fibroblast activation. Our findings unraveled the potential of emodin to alleviate cardiac fibrosis upregulating MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis.