| Cell apoptosis (programmed cell death) is a initiative process of cell death directed by gene regulation. Diseases would break out once the process of cell apoptosis is uncontrolled. The relationship between apoptosis and diseases is one of the hot spots currently.It is well known that Bcl-2 family plays an important role in the process of apoptosis regulation. Once the mechanisms manifest, many diseases would break out. Bcl-2 is regarded as one of the final common pathway, whose autoploid, Bax, plays a reverse role in the process. The ratio of Bcl-2 and Bax determine if apoptosis can take place. If the expression of Bax is more than that of Bcl-2, the Bax–Bax homodimer take predominance and the process would be induced, otherwise, both would be inhibited. Bcl-2 and Bax express generally in many tissue.It is known as myocardial fibrosis that the extracellular matrix over expressed in the normal cardial interstitial. In many heart diseases, myocardial apoptosis take important role, such as virus infection, hypertension, myocardiopathy, and exc.Catecholamines including adrenal, demethlated adrenaline and isoproterenol hydrochloride (Isp), lead to multiple focal myocardiolysis and the fibrosis. The animal model of myocardial hypertrophy and myocardial fibrosis can be copied by Isp hypodermical injection. In this study, we duplicated myocardial ischemia necrosis model through isoprenaline subcutaneous injection once at five points. Bcl-2 and Bax was detected by immunohistochemistry and RT-PCR at 12 h, 1 w and 3 w. The results are below:1. The results of immunohistochemistryThere is little positive signal of Bax in the normal heart, and after Isp injection, the amount of Bax expression increased significantly compared to normal control group (P<0.05) at 12 h and 1 w. The peak appeared at 1w after Isp injection, but decreased in 3 w group.Inversely, Bcl-2 positive signal expressed greatly in normal heart, but it decreased significantly after Isp injection compared to normal control group (P<0.05).The ratio of Bcl-2/bax decreased significantly compared to normal control group (P<0.05) after Isp injection at 12 h, 1 w and 3 w, with minimum at 1w.2. Little expression of Bax mRNA took place in the normal heart, but it increased significantly fter Isp injectioncompared to normal control group (P<0.05) at 12 h, 1 w, and 3 w after Isp injection, with the peak at 1w.Inversely, Bcl-2 expressed largely in normal heart tissue, but it decreased significantly after Isp injection compared to normal control group in 24 h, 1 w group (P<0.05).The ratio of Bcl-2/bax decreased significantly compared to normal control group (P<0.05) after Isp injection 12 h, 1 w and 3 w, with minimum in 1w after Isp injection.The main conclusion of this research:1. Isp induces myocardial apoptosis in which way myocardial cell death is induced generally.2. Isp induces great expression of Bax both in mRNA and protein level, inhibiting Bcl-2's expression. The abnormal decrease of Bcl-2/Bax leads to myocardial apoptosis.3. The expression of Bax increases after the injection of Isp, while that of Bcl-2 decreased. Both processes induced myocardial apoptosis.4. Myocardial apoptosis is the foundation of myocardial fibrsis.
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