2006•Zhonghua mazuixue zazhiRequires access

The effects of hydroxybutyrate on the expression of Bcl-2 and Bax in cerebral cortex induced by hypoxic-ischemic brain injury in neonatal rats

Zhengliang Ma

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Abstract

Objective To investigate the effects of sodium hydroxybutyrate (γ-OH) on the expression of Bcl-2 and Bax in cerebral cortex induced by hypoxic-ischemic brain injury (HIBI) .Methods γ-day-old SD rats weighing 12.0-16.0 g were randomized into 5 groups: sham operation group; HIBI group and 3 γ-OH groups which received intraperitoneal γ-OH 50, 100 or 200 mg·kg-1 3 times a day for a maximum of 7 days immediately after HIBI. HIBI was produced by left common carotid artery ligation followed by 2 h hypoxic air (8% O2) inhalation. The animals were killed at 1h, 3h, 1d, 3d and 7 d (n =6 each) after HIBI and their brains were removed for detection of Bcl-2 and Bax expression in the left cerebral cortex using immuno-histochemical staining. Results The expression of Bcl-2 and Bax in cerebral cortex was significantly increased at 1 h and 3 h after HIBI and peaked at 1 d and returned to the normal level at 7 d in HIBI and 3 γ-OH groups as compared to the sham operation group. The Bcl-2 expression was significantly higher while Bax expression significantly lower at 1 d and 3 d after HIBI in group γ-OH 1 and 2 than in group HIBI. There was no significant difference in Bcl-2 and Bax expression between group HIBI and γ-OH 3. Conclusion Sodium hydroxybutyrate upregulates Bcl-2 expression and downregulates Bax expression in cerebral cortex induced by HIBI.

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Objective To investigate the effects of sodium hydroxybutyrate (γ-OH) on the expression of Bcl-2 and Bax in cerebral cortex induced by hypoxic-ischemic brain injury (HIBI) .Methods γ-day-old SD rats weighing 12.0-16.0 g were randomized into 5 groups: sham operation group; HIBI group and 3 γ-OH groups which received intraperitoneal γ-OH 50, 100 or 200 mg·kg-1 3 times a day for a maximum of 7 days immediately after HIBI. HIBI was produced by left common carotid artery ligation followed by 2 h hypoxic air (8% O2) inhalation. The animals were killed at 1h, 3h, 1d, 3d and 7 d (n =6 each) after HIBI and their brains were removed for detection of Bcl-2 and Bax expression in the left cerebral cortex using immuno-histochemical staining. Results The expression of Bcl-2 and Bax in cerebral cortex was significantly increased at 1 h and 3 h after HIBI and peaked at 1 d and returned to the normal level at 7 d in HIBI and 3 γ-OH groups as compared to the sham operation group. The Bcl-2 expression was significantly higher while Bax expression significantly lower at 1 d and 3 d after HIBI in group γ-OH 1 and 2 than in group HIBI. There was no significant difference in Bcl-2 and Bax expression between group HIBI and γ-OH 3. Conclusion Sodium hydroxybutyrate upregulates Bcl-2 expression and downregulates Bax expression in cerebral cortex induced by HIBI.

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Available abstract

Objective To investigate the effects of sodium hydroxybutyrate (γ-OH) on the expression of Bcl-2 and Bax in cerebral cortex induced by hypoxic-ischemic brain injury (HIBI) .Methods γ-day-old SD rats weighing 12.0-16.0 g were randomized into 5 groups: sham operation group; HIBI group and 3 γ-OH groups which received intraperitoneal γ-OH 50, 100 or 200 mg·kg-1 3 times a day for a maximum of 7 days immediately after HIBI. HIBI was produced by left common carotid artery ligation followed by 2 h hypoxic air (8% O2) inhalation. The animals were killed at 1h, 3h, 1d, 3d and 7 d (n =6 each) after HIBI and their brains were removed for detection of Bcl-2 and Bax expression in the left cerebral cortex using immuno-histochemical staining. Results The expression of Bcl-2 and Bax in cerebral cortex was significantly increased at 1 h and 3 h after HIBI and peaked at 1 d and returned to the normal level at 7 d in HIBI and 3 γ-OH groups as compared to the sham operation group. The Bcl-2 expression was significantly higher while Bax expression significantly lower at 1 d and 3 d after HIBI in group γ-OH 1 and 2 than in group HIBI. There was no significant difference in Bcl-2 and Bax expression between group HIBI and γ-OH 3. Conclusion Sodium hydroxybutyrate upregulates Bcl-2 expression and downregulates Bax expression in cerebral cortex induced by HIBI.

Key concepts: Cerebral cortex, Cortex (anatomy), Intraperitoneal injection, Immunohistochemistry, Internal medicine, Endocrinology, Chemistry, Biology

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