AIM: To investigate the effect of Bak Foong Pills (BFP) on the expression of β-amyloid (Aβ) in rats retina with optic nerve transection, and its roles and possible mechanisms in protecting optic nerve damage. METHODS: Seventy-two healthy, Sprague-Dawley, adult rats were randomly assigned to three groups: negative control group (control group), optic nerve transection group (model group) and BFP treatment group (BFP group, 100μg/mL) followed by establishing optic nerve transection model. The expression of Aβ was measured at 48 hours by Western-blotting. Moreover, the expressions of Bcl-2, Bax and Caspase-3 mRNA were evaluated at 48 hours by reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: There were significant differences among the control, model and BFP groups in the expression of Aβ (all P<0.01). Aβ expression was significantly higher in the model and BFP groups than that in the control group (P<0.01), with a more significant reduction in the BFP group than that in the model group (P<0.01). Moreover, there were also significant differences among the three groups in the expressions of Bcl-2/Bax (Bcl-2: anti-apoptotic; Bax: proapoptotic) and Caspase-3 mRNA (proapoptotic) (all P<0.01). Bcl-2/Bax ratio was significantly lower and Caspase-3 mRNA expression was significantly higher in the model and BFP groups than those in the control group (P<0.01), with a significant growing of Bcl-2/Bax and reduction of Caspase-3 in the BFP group than those in the model group (P<0.01). CONCLUSION: BFP can down-regulate Aβ expression in retina and may inhibit apoptosis and protect optic nerve by enhancing Bcl-2/Bax ratio and inhibiting Caspase-3 pathway.
AIM: To investigate the effect of Bak Foong Pills (BFP) on the expression of β-amyloid (Aβ) in rats retina with optic nerve transection, and its roles and possible mechanisms in protecting optic nerve damage. METHODS: Seventy-two healthy, Sprague-Dawley, adult rats were randomly assigned to three groups: negative control group (control group), optic nerve transection group (model group) and BFP treatment group (BFP group, 100μg/mL) followed by establishing optic nerve transection model. The expression of Aβ was measured at 48 hours by Western-blotting. Moreover, the expressions of Bcl-2, Bax and Caspase-3 mRNA were evaluated at 48 hours by reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: There were significant differences among the control, model and BFP groups in the expression of Aβ (all P<0.01). Aβ expression was significantly higher in the model and BFP groups than that in the control group (P<0.01), with a more significant reduction in the BFP group than that in the model group (P<0.01). Moreover, there were also significant differences among the three groups in the expressions of Bcl-2/Bax (Bcl-2: anti-apoptotic; Bax: proapoptotic) and Caspase-3 mRNA (proapoptotic) (all P<0.01). Bcl-2/Bax ratio was significantly lower and Caspase-3 mRNA expression was significantly higher in the model and BFP groups than those in the control group (P<0.01), with a significant growing of Bcl-2/Bax and reduction of Caspase-3 in the BFP group than those in the model group (P<0.01). CONCLUSION: BFP can down-regulate Aβ expression in retina and may inhibit apoptosis and protect optic nerve by enhancing Bcl-2/Bax ratio and inhibiting Caspase-3 pathway.
Entities:
Keywords:
Bak Foong Pills; Bcl-2/Bax; Caspase-3 mRNA; optic nerve damage; β-amyloid protein
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