摘要
目的探讨红景天苷预处理对大鼠压疮模型组织损害程度和炎症反应的影响。方法 30只SD雄性大鼠随机分为对照组、模型组及红景天苷预处理组。红景天苷预处理组每日腹腔注射红景天苷12 mg/(kg·d),连续1周,最后一次给药后30 min建立压疮模型。再灌注后2 h取全血2 m L离心留血清,-20℃保存待测血清肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)水平以及髓过氧化物酶(MPO)和超氧化物歧化酶(SOD)的活力。结果模型组和红景天苷预处理组皮肤组织发生损伤,且模型组损伤程度重于红景天苷预处理组。红景天苷预处理组和模型组血清TNF-α和IL-6水平及MPO和SOD的活性与对照组比较差异有统计学意义(P均<0.05);红景天苷预处理组与模型组比较,血清TNF-α和IL-6水平及MPO活性更低(P均<0.05),SOD的活性更高(P<0.05)。结论红景天苷预处理可减轻大鼠压疮组织损害,其机制可能与抑制压疮引起的炎症反应有关。
Objective It is to study the effect of salidroside preconditioning on histopathological changes and inflammatory reaction in rat model of pressure ulcer. Methods Thirty SD male rats were randomly divided into sham operated group ( C group), model group (I/R group) and Saiidroside preconditioning group (S group). The animals were intraperitoneally administered with drugs for 7 days. Thirty minutes after the end administration, pressure ulcer models were made, Ten rats in each group were killed to obtain their serum 2h after successful modeling. The levels of TNF - α and IL - 6 and the activity of MPO and SOD in the serum were measured. Results Hematoxylin-eosin staining demonstrated tissue damage in I/R group and the S group were significantly severer than C group (P 〈 0. 05) ; whereas compared to I/R group, tissue damage in S group was significantly milder. The levels of TNF - α and IL - 6, and the activity of MPO and SOD in the serum in I/R group and the S group showed differences compared with those in C group ( all P 〈 0. 05). Compared to I/R group, the levels of TNF - α and IL-6, and the activity of MPO in the serum were significantly lower, and the activity of SOD in the serum were significantly higher in S group (P 〈 0. 05 ). Conclusion Salidroside could exert protective effect against ischemia - reperfusion injury in pressure ulcer rats, and its mechanism may be related to relieve the abnormity of inflammatory reactions.
出处
《现代中西医结合杂志》
CAS
2015年第22期2406-2408,共3页
Modern Journal of Integrated Traditional Chinese and Western Medicine
关键词
红景天苷
大鼠
压疮
缺血再灌注损伤
炎症反应
salidroside
rat
pressure ulcer
ischemia reperfusion injury
inflammatory reaction