Li Li1, Hui-yu Tao, Jie-bin Chen. 1. Department of Pediatrics, The First Affiliated Hospital of Nanhua University, Hengyang.
Abstract
OBJECTIVE: To study the possible mechanism of anti-myocardial cell apoptosis of astragaloside induced by adriamycin (ADR). METHODS: Fifty SD rats were randomized into five groups: the normal control group,the model group, the astragaloside low dose (A-L) group, the astragaloside medium dose (A-M) group and the astragaloside high dose (A-H) group, 10 in each group. The normal control group was given normal saline by intraperitoneal injection, while the other four groups were given ADR by intraperitoneal injection once every other day for six times with the total dosage of 15 mg/kg. At the same time, different dosage of astragaloside was administrated by gavage to the three treated groups, and sodium carboxymethycellulose (SCMC) was given to the normal control and the model group. Myocardial cell apoptosis was examined by in situ end-labeled DNA (TUNEL), protein and mRNA expressions of bax, bcl-2 were detected respectively with immunohistochemistry assay and RT-PCR. RESULTS: Compared with those in the normal control, apoptosis index was significantly higher, the protein and mRNA expressions of bcl-2 were lower and those of bax were higher, in the model group, resulted in lower ratio of bcl-2/bax (P < 0.05 or P < 0.01). However, in the A-H group, apoptosis index decreased significantly, the expressions of bcl-2 were higher, those of bax were lower, and ratio of the bcl-2/bax increased (all P < 0.05). CONCLUSION: High dose of astragaloside could suppress the myocardial cell apoptosis induced by ADR with the possible mechanism related to regulating the expressions of bcl-2 and bax.
OBJECTIVE: To study the possible mechanism of anti-myocardial cell apoptosis of astragaloside induced by adriamycin (ADR). METHODS: Fifty SD rats were randomized into five groups: the normal control group,the model group, the astragaloside low dose (A-L) group, the astragaloside medium dose (A-M) group and the astragaloside high dose (A-H) group, 10 in each group. The normal control group was given normal saline by intraperitoneal injection, while the other four groups were given ADR by intraperitoneal injection once every other day for six times with the total dosage of 15 mg/kg. At the same time, different dosage of astragaloside was administrated by gavage to the three treated groups, and sodium carboxymethycellulose (SCMC) was given to the normal control and the model group. Myocardial cell apoptosis was examined by in situ end-labeled DNA (TUNEL), protein and mRNA expressions of bax, bcl-2 were detected respectively with immunohistochemistry assay and RT-PCR. RESULTS: Compared with those in the normal control, apoptosis index was significantly higher, the protein and mRNA expressions of bcl-2 were lower and those of bax were higher, in the model group, resulted in lower ratio of bcl-2/bax (P < 0.05 or P < 0.01). However, in the A-H group, apoptosis index decreased significantly, the expressions of bcl-2 were higher, those of bax were lower, and ratio of the bcl-2/bax increased (all P < 0.05). CONCLUSION: High dose of astragaloside could suppress the myocardial cell apoptosis induced by ADR with the possible mechanism related to regulating the expressions of bcl-2 and bax.