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目的探讨自由基在糖尿病膀胱功能障碍病理生理学机制中的作用和意义。方法分组观测不同时间段T2DM大鼠与正常对照组大鼠膀胱逼尿肌肌条收缩实验,并将剩余膀胱组织制备匀浆,测定其中超氧化物歧化酶(SOD)的活力与丙二醛(MDA)的含量。结果不同时间段T2DM组引起逼尿肌收缩的最小牵张力高于对照组。T2DM组在0～16周的收缩频率较对照组增高,在20周后减低。T2DM组最大收缩力呈现降低趋势。正常对照组膀胱匀浆中SOD第8周达最高峰后,呈现出下降趋势,至24周时有所增高。T2DM组4周时SOD出现增高,在8周和24周组大鼠膀胱中SOD较对照组显著下降。MDA在两组动物中都表现为进行性下降趋势。在第4周,T2DM组大鼠膀胱中MDA含量较对照组显著性降低。第8周出现MDA增高。T2DM组SOD/MDA的值低于正常对照组。在第4周时,T2DM组比正常对照组显著增高,第8周时,出现显著性降低。逼尿肌肌条收缩频率与逼尿肌最大收缩力之间呈负相关,(r=-0.226,P<0.05);MDA与逼尿肌最大收缩力之间呈正相关(r=0.234,P<0.01)。结论糖尿病可导致膀胱逼尿肌功能受损。在发病初期机体清除氧自由基的能力提高,膀胱功能处于代偿状态;随着病情进展,机体氧自由基损伤严重,膀胱逼尿肌功能失代偿。自由基损伤也是糖尿病膀胱逼尿肌损伤的重要机制之一。
Objective To explore the role and significance of free radicals in the pathophysiology of diabetic bladder dysfunction. Methods The contraction of bladder detrusor muscle strips in T2DM rats and normal control rats at different time points was observed and the remaining bladder tissue was prepared for homogenization. The activities of superoxide dismutase (SOD) and malondialdehyde MDA) content. Results The minimum strain of detrusor contraction induced by T2DM group was higher than that of the control group at different time points. T2DM group in the 0-16 weeks of contraction frequency increased compared with the control group, decreased after 20 weeks. T2DM group showed a downward trend in maximum contractility. In the normal control group, the level of SOD in the bladder homogenate peaked at the 8th week, which showed a decreasing trend and increased to 24 weeks. SOD increased at 4 weeks in T2DM group and decreased significantly in bladder in 8 and 24 weeks group compared with control group. MDA showed a progressive decline in both groups of animals. In the fourth week, the content of MDA in the bladder of T2DM rats was significantly lower than that of the control group. The first 8 weeks increased MDA. The level of SOD / MDA in T2DM group was lower than that in normal control group. At the 4th week, the T2DM group was significantly higher than that of the normal control group, and significantly decreased at the 8th week. The contractile frequency of detrusor muscle strips was negatively correlated with the maximal contractility of detrusor muscle (r = -0.226, P <0.05). There was a positive correlation between MDA and detrusor contractility (r = 0.234, P < 0.01). Conclusion Diabetes can lead to impaired bladder detrusor function. In the early onset of the body’s ability to scavenge oxygen free radicals, bladder function in a compensatory state; with the progression of the disease, severe oxygen free radical damage, bladder detrusor dysfunction. Free radical damage is also one of the important mechanisms of detrusor damage in diabetic bladder.