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目的:观察肌肽对糖皮质激素诱导的白内障形成和Na+-K+ATP酶失活的保护作用。方法:220只透明的大鼠晶状体随机分为5组:对照组(DMEM)、地塞米松诱导的白内障组(DMEM+地塞米松10μmol/L)、低浓度肌肽治疗组(DMEM+地塞米松10μmol/L+肌肽2mmol/L)、高浓度肌肽治疗组(DMEM+地塞米松10μmol/L+肌肽5mmol/L)和肌肽组(DMEM+肌肽5mmol/L)。体外培养7d,动态观察晶状体的混浊情况。在培养的1,3,5,7d分别从各组取10只晶状体,使用分光光度计测定晶状体中的Na+-K+ATP酶活性。结果:随着培养时间的延长,晶状体混浊程度逐渐加重。第7d,对照组和肌肽组晶状体呈雾状混浊,地塞米松组晶状体出现重度核混浊,而肌肽治疗组晶状体皮质和核之间出现可见分界。地塞米松组在培养的第3,5,7d,Na+-K+ATP酶活性分别比1d下降约22.34%(P=0.002),47.98%(P<0.001),75.37%(P<0.001)。肌肽组在培养的7d时间内酶的活性始终与对照组接近,提示肌肽本身对晶状体Na+-K+ATP酶的活性无影响。在低浓度肌肽治疗组,培养3,5,7dNa+-K+ATP酶活性分别比地塞米松组增加了同期对照组酶活性的10.8%(P<0.05)、44.6%(P<0.01)和57.4%(P<0.01)。在高浓度肌肽组,培养3,5,7dNa+-K+ATP酶活性分别比地塞米松组增加了同期对照组酶活性的11.3%(P<0.05)、45.7%(P<0.01)和57.6%(P<0.01)。在培养7d,两个肌肽治疗组Na+-K+ATP酶活性仅比1d的酶活性下降6.7%和6.5%。地塞米松组和肌肽治疗组Na+-K+ATP酶活性的差异具有显著的统计学意义(P<0.01)。结论:肌肽有效的抑制了糖皮质激素诱导的晶状体混浊,并且显著的抑制了糖皮质激素诱导Na+-K+ATP酶失活。
Objective: To observe the protective effects of carnosine on glucocorticoid-induced cataract formation and Na + -K + ATPase inactivation. Methods: A total of 220 transparent rat lens were randomly divided into five groups: control group (DMEM), dexamethasone induced cataract (DMEM + dexamethasone 10μmol / L), low concentration carnosine treatment group (DMEM + dexamethasone 10μmol / L + carnosine 2mmol / L), high concentration of carnosine treatment group (DMEM + dexamethasone 10μmol / L + carnosine 5mmol / L) and carnosine group (DMEM + carnosine 5mmol / L). Culture in vitro 7d, dynamic observation of lens opacity. At 1, 3, 5, and 7 days after culture, 10 lenses were taken from each group, and the Na + -K + ATPase activity in the lens was measured by spectrophotometer. Results: With the extension of culture time, the degree of lens opacity gradually increased. On the 7th day, the lens of the control group and carpeptide group appeared haze cloudy, the lens of dexamethasone group had severe nuclear opacity, and the visible boundary between the lens cortex and the nucleus of the carnosine treatment group. The activities of Na + -K + ATPase in dexamethasone group decreased by 22.34% (P = 0.002), 47.98% (P <0.001) and 75.37% (P <0.001), respectively. Carnosine group in the culture of 7d time enzyme activity and the control group always close, suggesting that carnosine itself has no effect on the lens Na + -K ATPase activity. In the low concentration carnosine treatment group, the activity of 3,5,7 dNa + -K + ATPase increased by 10.8% (P <0.05), 44.6% (P <0.01) and 57.4 % (P <0.01). In the high-concentration carnosine group, the activities of 3,5,7 dNa + -K + ATPase increased 11.3% (P <0.05), 45.7% (P <0.01) and 57.6% (P < (P <0.01). At 7 days of culture, the activities of Na + -K + ATPase in the two carnosine treated groups decreased by 6.7% and 6.5%, respectively, compared with that of 1d. The difference of Na + -K + ATPase activity in dexamethasone group and carnosine group was statistically significant (P <0.01). Conclusion: Carnosine effectively inhibits glucocorticoid-induced lens opacity and significantly inhibits glucocorticoid-induced inactivation of Na + -K + ATPase.