Inhibitory effect of basic fibroblast growth factor on apoptosis induced by β-amyloid in cultured hippocampal neurons of neonatal rats
Hong An
Abstract
Hong An
Abstract
Aim: To clarify the effect of bFGF on the apoptosis in the primary cultured hippocampal neurons of neonatal rats and its potential application in the treatment of Alzheimer's disease. Methods: Hoechst staining, Annexin-V, DNA agarose gel electophoresis, Western blot were used to detect the expression of apoptosis-related gene bcl-2, bax. Results: Morphological and biochemical characteristics of apoptosis, such as internuclear DNA fragment, production of apoptotic bodies, were observed in hippocampal neurons treated with Aβ_(25-35). However, in hippocampal neurons treated with bFGF+Aβ_(25-35), the above changes were significantly reversed. The expression of Bcl-2 was up-regulated while that of Bax was down-regulated. Conclusion:bFGF can inhibit the neurotoxity of A β_(25-35) to neurons by regulating the expression of the apoptosis-related gene Bcl-2 and Bax.
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.
Aim: To clarify the effect of bFGF on the apoptosis in the primary cultured hippocampal neurons of neonatal rats and its potential application in the treatment of Alzheimer's disease. Methods: Hoechst staining, Annexin-V, DNA agarose gel electophoresis, Western blot were used to detect the expression of apoptosis-related gene bcl-2, bax. Results: Morphological and biochemical characteristics of apoptosis, such as internuclear DNA fragment, production of apoptotic bodies, were observed in hippocampal neurons treated with Aβ_(25-35). However, in hippocampal neurons treated with bFGF+Aβ_(25-35), the above changes were significantly reversed. The expression of Bcl-2 was up-regulated while that of Bax was down-regulated. Conclusion:bFGF can inhibit the neurotoxity of A β_(25-35) to neurons by regulating the expression of the apoptosis-related gene Bcl-2 and Bax.
Key concepts: Hippocampal formation, Apoptosis, Basic fibroblast growth factor, Annexin, Molecular biology, Western blot, Biology, Cell biology