摘要
目的:探讨表没食子儿茶素没食子酸酯(EGCG)对早期压疮的保护作用及初步机制。方法:雌性SD大鼠随机分为空白对照组、模型对照组和EGCG 10、20、40mg/kg剂量组,灌胃给予相应药物,连续7d后,用自制装置对大鼠进行早期压疮造模。造模完成后观察各组大鼠受压局部组织情况,并眼眶采血,组织取材,酶联免疫吸附法测定血清中IL-1β、LDH、CK的含量;HE染色观察各组大鼠组织病变,判断压疮病理变化严重程度;蛋白质印迹法测定大鼠受压组织中NLRP3、caspase-1、IL-1β蛋白的表达水平。结果:造模成功率为100%;实验组大鼠均存在皮肤层次欠清晰,皮下结缔组织和肌肉组织有炎性反应,病理变化严重程度随EGCG剂量的增加而减轻,大鼠血清中IL-1β、LDH、CK含量随EGCG剂量的增加明显降低。EGCG各剂量组大鼠受压组织中NLRP3、IL-1β、caspase-1蛋白表达显著降低,呈一定的剂量依赖性。结论:EGCG预处理可通过抑制炎症而减轻早期压疮缺血再灌注损伤,其作用机制可能主要与抑制NLRP3炎症小体的表达有关。
Objective: To investigate the protective effects of epigallocatechin gallate( EGCG) on ischemia-reperfusion injury( IRI) in early stage pressure ulcers and its possible mechanism. Methods: Female SD rats were randomly divided into the control group,the model group and EGCG groups at the doses of 10 mg/kg、20 mg/kg and 40 mg/kg,10 rats in each group. All animals were intraperitoneally injected with corresponding drugs for 7 days,then the pressure ulcer model was established by using a self-made simple modeling device. The compressed tissues of rats in each group were observed 4 hours after the modeling was completed,and the incidence and index of pressure ulcers were calculated. The blood was collected from the eyelids,then the rats were sacrificed and the tissues were taken. ELISA Kit was used to detect the serum levels of IL-1β,LDH and CK. Western-blot methods were used to determine the expression levels of NLRP3,caspase-1,and IL-1β in tissues. Results: The early stage pressure ulcer model was successfully established. Compared with the model group,the inflammatory responses in EGCG groups were significantly alleviated with the increase of the dose of EGCG. The skin level of the rats was not clear,and inflammatory reaction was observed in the subcutaneous connective tissue and muscle tissue. The pathological changes were improved with the increase of the concentration. The levels of IL-1β,LDH and CK in rats serum were significantly decreased with the increase of doses of EGCG.The expressions of Nlrp3,IL-1β and caspase-1 in the pressed tissues in EGCG groups was significantly decreased in a dose-dependent manner. Conclusion: EGCG pretreatment can reduce the ischemia-reperfusion injury in pressure ulcer by inhibiting inflammation. Its mechanism may be related to the inhibition of expression of Nlrp3 inflammatory bodies.
引文
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