2006Zhongguo xiaoer jijiu yixueRequires access

Effect of TGF-β_1 on the expression of Bcl-2 and Bax protein in neonatal rats with hypoxic-ischemic brain damage

XU Hua-me

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Abstract

Objective To explore the effect of exogenous TGF-β_1 on the expression of Bcl-2 and Bax protein in brain tissue following hypoxic-ischemic brain damage(HIBD) in newborn rat.Methods Unsexed 7-day-old Wistar rats were randomly divided into sham operation group,HIBD group,saline-treated control group and TGF-β_1-treated group.The TGF-β_1-treated group was divided into groups of high,middle and low dose.After the HIBD model was performed,different TGF-β_1 dosages(20?ng、10?ng、5?ng) were injected into the left lateral ventricle.The expression of Bcl-2 and Bax protein at 24?h after injection were measured by immunohistochemical method.Results the expression of Bcl-2 and Bax protein in HIBD group and saline-treated control group were significantly higher in comparison with that in sham operation group,the Bcl-2/Bax ratio was significantly lower.the expression of Bcl-2 protein and the Bcl-2/Bax ratio in TGF-β_1-treated group were significantly higher than HIBD group and saline-treated control group,the expression of Bax protein was significantly lower.Conclusion The neuronal protective mechanism of TGF-β_1 might be related to up-regulating the expression of Bcl-2 protein,down-regulating the expression of Bax protein and alter the Bcl-2/Bax ratio in brain tissue,consequently it could inhibit the apoptosis of neuron after HIBD.

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Objective To explore the effect of exogenous TGF-β_1 on the expression of Bcl-2 and Bax protein in brain tissue following hypoxic-ischemic brain damage(HIBD) in newborn rat.Methods Unsexed 7-day-old Wistar rats were randomly divided into sham operation group,HIBD group,saline-treated control group and TGF-β_1-treated group.The TGF-β_1-treated group was divided into groups of high,middle and low dose.After the HIBD model was performed,different TGF-β_1 dosages(20?ng、10?ng、5?ng) were injected into the left lateral ventricle.The expression of Bcl-2 and Bax protein at 24?h after injection were measured by immunohistochemical method.Results the expression of Bcl-2 and Bax protein in HIBD group and saline-treated control group were significantly higher in comparison with that in sham operation group,the Bcl-2/Bax ratio was significantly lower.the expression of Bcl-2 protein and the Bcl-2/Bax ratio in TGF-β_1-treated group were significantly higher than HIBD group and saline-treated control group,the expression of Bax protein was significantly lower.Conclusion The neuronal protective mechanism of TGF-β_1 might be related to up-regulating the expression of Bcl-2 protein,down-regulating the expression of Bax protein and alter the Bcl-2/Bax ratio in brain tissue,consequently it could inhibit the apoptosis of neuron after HIBD.

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Available abstract

Objective To explore the effect of exogenous TGF-β_1 on the expression of Bcl-2 and Bax protein in brain tissue following hypoxic-ischemic brain damage(HIBD) in newborn rat.Methods Unsexed 7-day-old Wistar rats were randomly divided into sham operation group,HIBD group,saline-treated control group and TGF-β_1-treated group.The TGF-β_1-treated group was divided into groups of high,middle and low dose.After the HIBD model was performed,different TGF-β_1 dosages(20?ng、10?ng、5?ng) were injected into the left lateral ventricle.The expression of Bcl-2 and Bax protein at 24?h after injection were measured by immunohistochemical method.Results the expression of Bcl-2 and Bax protein in HIBD group and saline-treated control group were significantly higher in comparison with that in sham operation group,the Bcl-2/Bax ratio was significantly lower.the expression of Bcl-2 protein and the Bcl-2/Bax ratio in TGF-β_1-treated group were significantly higher than HIBD group and saline-treated control group,the expression of Bax protein was significantly lower.Conclusion The neuronal protective mechanism of TGF-β_1 might be related to up-regulating the expression of Bcl-2 protein,down-regulating the expression of Bax protein and alter the Bcl-2/Bax ratio in brain tissue,consequently it could inhibit the apoptosis of neuron after HIBD.

Key concepts: BAX Protein, Brain damage, Apoptosis, Saline, Medicine, Immunohistochemistry, Bcl-2-associated X protein, Protein expression

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Effect of TGF-β_1 on the expression of Bcl-2 and Bax protein in neonatal rats with hypoxic-ischemic brain damage — Research Paper | ScholarLens