Objective To explore the mechanism by which QingguangannIFormula(QGAI)inhibits the apoptosis of retinal ganglion cells(RCCs)in glaucoma through the regulation of B-cell lymphoma 2(Bcl-2)/Bcl-2-associated X protein(Bax...Objective To explore the mechanism by which QingguangannIFormula(QGAI)inhibits the apoptosis of retinal ganglion cells(RCCs)in glaucoma through the regulation of B-cell lymphoma 2(Bcl-2)/Bcl-2-associated X protein(Bax)/Cysteine-aspartic protease 3(Caspase-3)by Brain-specific homeobox/POU domain protein 3B(Brn-3b).Methods After one week of acclimatization sixty healthy male SPF SD rats were randomly divided into control group,model group,lowdose,medium-dose,and high-dose QGA II group,and Yimaikang group,10 in each group.Except for the control group,elevated intraocular pressure was induced in the other groups by cauterizing the episcleral veins.The control and model groups were treated with saline,while the Yimaikang(9.67 g·kg^(-1).d^(-1))and QGA II(3.375,6.75,13.5 g·kg^(-1).d^(-1))groups received their respective treatments via gavage for 4 weeks.Intraocular pressure was measured preoperatively and at 30 minutes,1,7,14,and 28 days postoperatively.After euthanizing the rats,retinal tissues were isolated for histological examination and analysis of RGC apoptosis and the expression of Brn-3b,Caspase-3,Bcl-2,and Bax proteins and mRNA.Results Intraocular pressure was significantly elevated in all model groups compared to baseline(P<0.05)and remained high at 4 weeks.Compared to the model group,the QGA II and Yimaikang groups exhibited significantly reduced RGC apoptosis(P<0.01).Among them,the high-dose QGA II group showed the lowest RGC apoptosis rates(P<0.05).Compared to the model group,expressions of Caspase-3 and Bax proteins and mRNA increased in the Yimaikang and high-dose QGA II groups(P<0.01),while expressions of Brn-3b and Bcl-2 proteins and mRNA significantly decreased(P<0.01).Conclusion QGA I inhibits RGC apoptosis by regulating Brn-3b,Bax/Bcl-2/Caspase-3,withefficacyycomparableto Yimaikang.展开更多
文摘Objective To explore the mechanism by which QingguangannIFormula(QGAI)inhibits the apoptosis of retinal ganglion cells(RCCs)in glaucoma through the regulation of B-cell lymphoma 2(Bcl-2)/Bcl-2-associated X protein(Bax)/Cysteine-aspartic protease 3(Caspase-3)by Brain-specific homeobox/POU domain protein 3B(Brn-3b).Methods After one week of acclimatization sixty healthy male SPF SD rats were randomly divided into control group,model group,lowdose,medium-dose,and high-dose QGA II group,and Yimaikang group,10 in each group.Except for the control group,elevated intraocular pressure was induced in the other groups by cauterizing the episcleral veins.The control and model groups were treated with saline,while the Yimaikang(9.67 g·kg^(-1).d^(-1))and QGA II(3.375,6.75,13.5 g·kg^(-1).d^(-1))groups received their respective treatments via gavage for 4 weeks.Intraocular pressure was measured preoperatively and at 30 minutes,1,7,14,and 28 days postoperatively.After euthanizing the rats,retinal tissues were isolated for histological examination and analysis of RGC apoptosis and the expression of Brn-3b,Caspase-3,Bcl-2,and Bax proteins and mRNA.Results Intraocular pressure was significantly elevated in all model groups compared to baseline(P<0.05)and remained high at 4 weeks.Compared to the model group,the QGA II and Yimaikang groups exhibited significantly reduced RGC apoptosis(P<0.01).Among them,the high-dose QGA II group showed the lowest RGC apoptosis rates(P<0.05).Compared to the model group,expressions of Caspase-3 and Bax proteins and mRNA increased in the Yimaikang and high-dose QGA II groups(P<0.01),while expressions of Brn-3b and Bcl-2 proteins and mRNA significantly decreased(P<0.01).Conclusion QGA I inhibits RGC apoptosis by regulating Brn-3b,Bax/Bcl-2/Caspase-3,withefficacyycomparableto Yimaikang.
