Effect of radix salivae miltiorrhizae on redox factor-1 protein and apoptosis of the cerebral cortex area in neonatal rats after hypoxia-ischemia brain damage
Lingling Zhu
Abstract
Lingling Zhu
Abstract
Objective To study the effect of radix salivae miltiorrhizae ( SM ) on Redox factor-1 (Ref-1) protein and apoptosis of the cerebral cortex area in neonatal rats after hypoxic-ischemic brain damage (HIBD). Methods The HIBD model was established with 7-day old SD neonatal rats. The expression of Ref-1 protein and apoptosis in the cerebral cortex area were determined by immunohistochemistry and terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) staining in sham operation group, HIBD group and SM group (treated by Compound Dan-shen) with intervals of 24h. Results Compared with the HIBD group, the expression of Ref-1 protein was increased (36. 1±6. 3 vs. 76. 3±5. 4, t = 2. 43 ,P 0. 05 ) and apoptosis cells were decreased significantly ( 68 ±2 vs. 12 ±5, t=7.02 ,P 0. 01 ) in SM group. Conclusions As free radical scavenge, SM can prevent neuron apoptosis after HIBD by enhancing expression of Ref-1 protein probably. It provides a new theoretic evidence for treating neonatal hypoxic-ischemic encephalopathy.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To study the effect of radix salivae miltiorrhizae ( SM ) on Redox factor-1 (Ref-1) protein and apoptosis of the cerebral cortex area in neonatal rats after hypoxic-ischemic brain damage (HIBD). Methods The HIBD model was established with 7-day old SD neonatal rats. The expression of Ref-1 protein and apoptosis in the cerebral cortex area were determined by immunohistochemistry and terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) staining in sham operation group, HIBD group and SM group (treated by Compound Dan-shen) with intervals of 24h. Results Compared with the HIBD group, the expression of Ref-1 protein was increased (36. 1±6. 3 vs. 76. 3±5. 4, t = 2. 43 ,P 0. 05 ) and apoptosis cells were decreased significantly ( 68 ±2 vs. 12 ±5, t=7.02 ,P 0. 01 ) in SM group. Conclusions As free radical scavenge, SM can prevent neuron apoptosis after HIBD by enhancing expression of Ref-1 protein probably. It provides a new theoretic evidence for treating neonatal hypoxic-ischemic encephalopathy.
Key concepts: TUNEL assay, Brain damage, Apoptosis, Medicine, Terminal deoxynucleotidyl transferase, Cerebral cortex, Ischemia, Immunohistochemistry