Protective effects of rosiglitazone on retinal ganglion cells injury induced by high glucose
Yu Xiao
Abstract
Yu Xiao
Abstract
Objective To study the protective effects of rosiglitazone on retinal ganglion cells (RGC) injury induced by high glucose.Methods Rats RGC-5 line cells were cultured in vitro,and incubated with 50 mol·L-1 glucose to induce the injury.The growth inhibitive rate was measured by CCK-8 analysis.The apoptotic rate was tested by flow cytometry.Content of glutamic acid in the medium was detected by a full-automatic biochemical analyzer.The content of malonaldehyde (MDA) and activity of superoxide dismutase (SOD) in cells were measured.Results High glucose (50 mmol·L-1) inhibited significantly the growth of RGC-5 cells in a time-dependent manner,the growth inhibitive rate were (22.37±3.49)%,(42.18±6.34)% and (57.33±5.39)% at 24 hours,48 hours and 72 hours after treatment,respectively(all P0.05).Compared with high glucose group,the growth inhibitive rate of RGC-5 cells decreased in a dose-dependent manner in high glucose combined with rosiglitazone (0.1×10-6 mol·L-1,10-6 mol·L-1 and 10×10-6 mol·L-1) group for 48 hours,which were (42.18±6.34)%,(35.66±4.73)%,(27.35±4.15)% and (25.17±3.42)%,respectively(all P0.05).Compared with control group,the apoptotic rate of RGC-5 cells in high glucose group increased significantly in a time-dependent manner (all P0.05).Compared with high glucose group,apoptotic rate of high glucose combined with rosiglitazone (0.1×10-6 mol·L-1,10-6 mol·L-1 and 10×10-6 mol·L-1) group for 48 hours decreased in a dose-dependent manner,which were (31.55±5.34)%,(23.75±3.72)%,(18.75±2.17)% and (17.53±3.05)%,respectively (all P0.05).Compared with control group,the release of Glu in RGC-5 cells significantly increased in high glucose group,which were (85.64±12.75)μg·L-1 and (246.84±33.48)μg·L-1,respectively(P0.05).Compared with high glucose group,the release of Glu in RGC-5 cells of high glucose combined with rosiglitazone (0.1×10-6 mol·L-1,10-6 mol·L-1 and 10×10-6 mol·L-1) group for 48 hours decreased in dose-dependent manner,which were (246.84±33.48)μg·L-1,(175.34±23.69)μg·L-1,(117.25±18.76)μg·L-1 and (109.34±15.54)μg·L-1,respectively (all P0.05).Compared with control group,SOD activity in high glucose group were significantly depressed,which were (3.06±0.38)kU·g-1 and (0.56±0.07)kU·g-1,respectively(P0.05) and the level of MDA greatly increased,which were (5.67±0.76)μmol·g-1 and (37.64±4.37)μmol·g-1,respectively (P0.05).Compared with high glucose group,SOD activity in high glucose + rosiglitazone(0.1×10-6 mol·L-1,10-6 mol·L-1 and 10×10-6 mol·L-1) group for 48 hours were significantly enhanced (all P0.05),and the level of MDA (0.1×10-6 mol·L-1,10-6 mol·L-1 and 10×10-6 mol·L-1) group for 48 hours significantly decreased (all P0.05).Conclusion Rosiglitazone can inhibit the high glucose-induced RGC injury in rat RGC-5 line cells,and the mechanism is related with the inhibition of glutamic acid release and oxidative stress induced by rosiglitazone.
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Objective To study the protective effects of rosiglitazone on retinal ganglion cells (RGC) injury induced by high glucose.Methods Rats RGC-5 line cells were cultured in vitro,and incubated with 50 mol·L-1 glucose to induce the injury.The growth inhibitive rate was measured by CCK-8 analysis.The apoptotic rate was tested by flow cytometry.Content of glutamic acid in the medium was detected by a full-automatic biochemical analyzer.The content of malonaldehyde (MDA) and activity of superoxide dismutase (SOD) in cells were measured.Results High glucose (50 mmol·L-1) inhibited significantly the growth of RGC-5 cells in a time-dependent manner,the growth inhibitive rate were (22.37±3.49)%,(42.18±6.34)% and (57.33±5.39)% at 24 hours,48 hours and 72 hours after treatment,respectively(all P0.05).Compared with high glucose group,the growth inhibitive rate of RGC-5 cells decreased in a dose-dependent manner in high glucose combined with rosiglitazone (0.1×10-6 mol·L-1,10-6 mol·L-1 and 10×10-6 mol·L-1) group for 48 hours,which were (42.18±6.34)%,(35.66±4.73)%,(27.35±4.15)% and (25.17±3.42)%,respectively(all P0.05).Compared with control group,the apoptotic rate of RGC-5 cells in high glucose group increased significantly in a time-dependent manner (all P0.05).Compared with high glucose group,apoptotic rate of high glucose combined with rosiglitazone (0.1×10-6 mol·L-1,10-6 mol·L-1 and 10×10-6 mol·L-1) group for 48 hours decreased in a dose-dependent manner,which were (31.55±5.34)%,(23.75±3.72)%,(18.75±2.17)% and (17.53±3.05)%,respectively (all P0.05).Compared with control group,the release of Glu in RGC-5 cells significantly increased in high glucose group,which were (85.64±12.75)μg·L-1 and (246.84±33.48)μg·L-1,respectively(P0.05).Compared with high glucose group,the release of Glu in RGC-5 cells of high glucose combined with rosiglitazone (0.1×10-6 mol·L-1,10-6 mol·L-1 and 10×10-6 mol·L-1) group for 48 hours decreased in dose-dependent manner,which were (246.84±33.48)μg·L-1,(175.34±23.69)μg·L-1,(117.25±18.76)μg·L-1 and (109.34±15.54)μg·L-1,respectively (all P0.05).Compared with control group,SOD activity in high glucose group were significantly depressed,which were (3.06±0.38)kU·g-1 and (0.56±0.07)kU·g-1,respectively(P0.05) and the level of MDA greatly increased,which were (5.67±0.76)μmol·g-1 and (37.64±4.37)μmol·g-1,respectively (P0.05).Compared with high glucose group,SOD activity in high glucose + rosiglitazone(0.1×10-6 mol·L-1,10-6 mol·L-1 and 10×10-6 mol·L-1) group for 48 hours were significantly enhanced (all P0.05),and the level of MDA (0.1×10-6 mol·L-1,10-6 mol·L-1 and 10×10-6 mol·L-1) group for 48 hours significantly decreased (all P0.05).Conclusion Rosiglitazone can inhibit the high glucose-induced RGC injury in rat RGC-5 line cells,and the mechanism is related with the inhibition of glutamic acid release and oxidative stress induced by rosiglitazone.
Key concepts: Rosiglitazone, L-Glucose, Endocrinology, Internal medicine, Retinal, Apoptosis, Chemistry, In vitro