Our data revealed that A23187 evidently promoted the concentration of intracellular Ca2+ and the incidence of l-Chicoric-acid acrosome reaction. When specific anti-VDAC2 antibody was added, intracellular Ca2+ increase induced by A23187 was inhibited. Our present study demonstrated that VDAC2 participated in the mediation of Ca2+ transmembrane transport, and the co-incubation of human spermatozoa with antiVDAC2 antibody inhibited A23187-induced Ca2+ flux. During acrosome reaction, the fusion and destruction of acrosomal membrane and plasma membrane might promote the binding and interaction of antibody with VDAC2. It then interfered with the permeability of VDAC channel to Ca2+ during the fusion of acrosomal membrane and plasma membrane. It is worth noting that the relationship between VDAC channel states and its permeability to Ca2+ remains controversial. A high quality research has reported that VDAC closure increases Ca2+ flux. Monocyte chemoattractant protein-1, a CC chemokine, promotes atherosclerosis by recruiting macrophages and monocytes to the vessel wall. MCP-1 was detected in atherosclerotic lesions and responsible for regulating the local expression of adhesion molecules, interleukin-1 -1, IL-6 and tissue factor. In recent years, MCP-1 has become an important therapeutic target for atherosclerosis and three treatment approaches have been developed in experimental studies. The first approach involved systemic blocking MCP-1 by injection of an N terminal-deletion mutant of the MCP-1 gene and Inoue S et al first showed that 7ND treatment attenuated progression of the atherosclerotic lesions in ApoE2/2 mice. Our group first reported that 7ND transfection reversed plaque progression and prevented vulnerable plaques from rupture in a rabbit model. However, it is difficult to translate this approach into clinical application because long-term injection of 7ND may cause hypersensitivity reaction and systemic immunosuppression. The second approach used CCR2 receptor blocker but a recent study found no beneficial effects with this therapy in a mouse model of atherosclerosis, possibly because the CCR2 receptor may have other functions beyond the control of monocyte EC emigration. The third approach entails local gene silencing of MCP-1 using RNA interference and if this technique proves effective and safe, it would be feasible to translate RNAi into clinical application by combining small interference RNA with interventional device to locally inhibit MCP-1 gene transcription.