Scutellaria flavonoids inhibit abnormal changes of apoptotic factors in mitochondrial apoptotic path

来源 :第十六届全国神经精神药理学学术会议 | 被引量 : 0次 | 上传用户:ej17255
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  OBJECTIVE To study the apoptotic factors abnormalities of mitochondrial apoptotic pathway in cerebral corex of rats injected β-amyloid beta protein 25-35 (Aβ25-35) in combination with aluminum trichloride (AlCl3) and recombinant human transforming growth factor-β1 (rhTGF-β1) by the lateral cerebral ventricle, and to explore the effective mechanism of Scutellaria flavonoids (SSF) against AD by inhibiting the apoptotic factors abnormalities in mitochondrial apoptosis pathway.MEHTODS Male SD rats received intracerebroventricular injection of rhTGF-β1 1 μl (10 ng) on the day 1 of operation, and then intracerebroventricularly injected Aβ25-35 and AlCl3 from the day 2 of operation.Aβ25-35 4 μg·d-1 and 1% AlCl3 3 μL·d-1 were injected in every morning for consecutive 14 d and in every afternoon for consecutive 5 d, respectively.On the day 45 of operation, all rats were performed the Morris water maze training for successful memory impairment model screening.On the day 49 of operation, the successful model rats were randomly divided into 4 groups, model control and 3 doses of SSF group rats.The SSF group rats were daily administered SSF 35, 70 and 140 mg·kg-1 for 36 d.On the last administration 60 min, all the rats were decapitated.Western blotting method was used to detected the protein expressions of B cell lymphoma (Bcl-2), Bcl-2 associated X protein (Bax), B-cell lymphoma/leukemia-xL (Bcl-xL), Bcl-2 antagonist/killer (Bak) on the mitochondrial membrane of rats cerebral cortex.RESULTS The composite Aβ25-35 can dramatically cause the deleterious changes in Bcl-2, Bax, Bcl-xL and Bak on mitochondrial membrane of rats cerebral cortex.Compared with sham control, the protein expressions of BCI-2 and Bcl-xL markedly lowered (P<0.05, P<0.01), and protein expressions of Bax and Bak significantly increased (P<0.01, P<0.05), respectively in model control group.However, SSF 35, 70 and 140 mg·kg-1 treated rats for 36 d can differently reverse the above disorders induced by composite Aβ25-35.CONCLUSION The composite Aβ25-35 can result in abnormal of apoptotic factors in mitochondrial apoptosis pathway and SSF has improvement on above disturbances, which indicated that the amelioration of SSF on abnormal apoptotic factors in mitochondrial apoptosis pathway is one of effective mechanisms of SSF against AD.
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