富氢盐水抑制大鼠压疮深部骨骼肌NLRP3炎性小体活化

Hydrogen-rich saline inhibits NLRP3 inflammasome activation in skeletal muscle of pressure ulcer model rats

目的观察富氢盐水对大鼠压疮深部骨骼肌氧化应激及炎性反应的干预效果,探讨NLRP3炎性小体在其中的生物效应。方法 30只SD大鼠随机分为对照组(C)、压疮+生理盐水组(PU+S)和压疮+富氢盐水组(PU+HS)。PU+S和PU+HS组大鼠双下肢制备压疮模型。模型建立成功后,PU+HS组大鼠每日腹腔注射富氢盐水(10 ml/kg体重)1次,连续5 d。末次注射后24 h处死大鼠,检测骨骼肌MDA、IL-1β含量、Caspase-1活性、NLRP3和ASC蛋白表达。结果 PU+HS组与PU+S组比较,MDA、IL-1β含量和Caspase-1活性均显著降低(分别为14.92±3.11 vs 27.40±4.42,1.13±0.25 vs 1.42±0.35和0.69±0.18 vs 1.05±0.19,P<0.05),NLRP3和ASC蛋白表达均显著降低(分别为122.29±19.96 vs 178.49±18.62,105.33±16.67 vs 129.49±18.77,P<0.01)。结论富氢盐水可能通过抑制氧化应激下调NLRP3炎性反应小体活化水平,进而抑制压疮诱导深部骨骼肌的炎性反应。

Objective To explore the effect of hydrogen-rich saline on the oxidative stress and inflammation in skeletal muscle of pressure ulcer model rats,and to investigate the biological effect of NLRP3 inflammasome. Methods Thirty male Sprague Dawley rats were randomly divided into three groups： control group（ C）,pressure ulcer ＋ saline group（ PU ＋ S）,and pressure ulcer ＋ hydrogen-rich saline group（ PU ＋ HS）. The PU ＋ S and PU ＋ HS rats were loaded with 22. 47 k Pa pressure and kept 2 hours for simulation of ischemia,and simulate reperfusion 30 minutes later. Every rat was performed this treatment 5 cycle everyday,for 3 days. After pressure ulcer model established,PU ＋ HS rats subjected to intraperitoneal injection of hydrogen-rich saline（ 10 ml/kg） for 5 days.Then MDA level,IL-1β content,Caspase-1 activity,NLRP3 and ASC protein expression were measured. Results As compared with PU ＋ S group,in PU ＋ HS group,MDA level,IL-1β content and Caspase-1 activity were significantly decreased（ 14. 92 ± 3. 11 vs27. 40 ± 4. 42,1. 13 ± 0. 25 vs 1. 42 ± 0. 35 and 0. 69 ± 0. 18 vs 1. 05 ± 0. 19,respectively,P〈0. 05 - 0. 01）. Furthermore,NLRP3 and ASC protein expression were significantly suppressed（ 122. 29 ± 19. 96 vs 178. 49 ± 18. 62 and 105. 33 ± 16. 67 vs 129. 49 ±18. 77,respectively,P〈0. 01）. Conclusion Hydrogen-rich saline could prevent NLRP3 inflammasome activation through suppressing oxidative stress,which in turn inhibit pressure ulcer induced inflammation in skeletal muscle.