Inhibitory action of tripchlorolide on activation of gliacyte and p38MAPK induced by Aβ_(25- 35)injected into hippocampus of rats
Wang Yuan-we
Abstract
Wang Yuan-we
Abstract
Aim To investigate the protective effect of tripchlorolide( T4) on neuronal injury induced by injecting Aβ25- 35into dorsal hippocampus in rats and its possible mechanism. Methods The model was established by using stereotaxic technique to inject 10 μg aggregated Aβ25- 35into dorsal hippocampus in rats.Rats were treated with different doses of T4. The expression of ox-42,GFAP and p-p38MAPK were observed by immunohistochemistry or Western blot,the levels of TNF-α and IL-1β were measured by ELISA,and neuronal injury of hippocampus was evaluated by TUNEL and Nissl staining. Results After injection of Aβ25- 35, the expression of ox-42, GFAP and pp38MAPK increased and achieved the peak on 7th day,and the levels of TNF-α,IL-1β significantly increased too. Meanwhile,the apoptosis of hippocampal neurons was gradually increased and peaked on 7th day. After treatment with T4,the expression of gliacyte,p-p38MAPK,the levels of TNF-α and IL-1β,and the apoptosis of hippocampal neurons were significantly decreased. The dose of 20 μg·kg- 1was more effective. Conclusion The possible protective mechanism of T4may be associated with decreasing the levels of cytokines by inhibiting the activation of gliacyte and p38MAPK induced by injecting Aβ25- 35into hippocampus.
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Aim To investigate the protective effect of tripchlorolide( T4) on neuronal injury induced by injecting Aβ25- 35into dorsal hippocampus in rats and its possible mechanism. Methods The model was established by using stereotaxic technique to inject 10 μg aggregated Aβ25- 35into dorsal hippocampus in rats.Rats were treated with different doses of T4. The expression of ox-42,GFAP and p-p38MAPK were observed by immunohistochemistry or Western blot,the levels of TNF-α and IL-1β were measured by ELISA,and neuronal injury of hippocampus was evaluated by TUNEL and Nissl staining. Results After injection of Aβ25- 35, the expression of ox-42, GFAP and pp38MAPK increased and achieved the peak on 7th day,and the levels of TNF-α,IL-1β significantly increased too. Meanwhile,the apoptosis of hippocampal neurons was gradually increased and peaked on 7th day. After treatment with T4,the expression of gliacyte,p-p38MAPK,the levels of TNF-α and IL-1β,and the apoptosis of hippocampal neurons were significantly decreased. The dose of 20 μg·kg- 1was more effective. Conclusion The possible protective mechanism of T4may be associated with decreasing the levels of cytokines by inhibiting the activation of gliacyte and p38MAPK induced by injecting Aβ25- 35into hippocampus.
Key concepts: Hippocampus, Nissl body, TUNEL assay, Hippocampal formation, Apoptosis, Western blot, Internal medicine, Endocrinology