Intervertebral disc tissue engineering is achieved by means of establishing complete intervertebral disc tissue in vitro and then implanting it to the primary degenerative intervertebral disc,thus conducting the treatment.Nowadays the research mainly focuses on the cultivation of intervertebral disc cell,the selection of the tissue engineering scaffold,the establishment and implantation of the intervertebral disc tissue engineering and so on.Recently there are three common ways to cultivate cell.The cell cultivation under the circumstance of zero-gravity and three-dimension not only accords the human being's natural three-dimensional structure,but also could reduce the mechanical shearing force of the medium and overcome the touching re-striction caused by the gravity sedimentation.It could make cell growth better and that is a new attempt to cultivate intervertebral disc cell.There are many species of scaffold of tissue engineering,and everyone has the advantage and disadvantage.Today none of these scaffold materials are accepted as the most suitable one so that it needs more and more study in these aspects.To establish complete intervertebral disc tissue and conduct implantation have already succeed in animal experiment.It is shown that implant-ing intervertebral disc cell which is cultivated by tissue engineering to degenerative intervertebral disc could partly reverse the degeneration.

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.