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作 者:郭静[1] 孟庆海[1] 殷秋忆 林超[1] 马志[1] 徐斌[1] 钱星[1] 包东桥[1] 张亚云[1] 张启春[1] 卞慧敏[1] 胡小鹰[1]
出 处:《中国中药杂志》2014年第11期2091-2096,共6页China Journal of Chinese Materia Medica
基 金:江苏省科技厅社会发展项目(BE2011846)
摘 要:目的:观察通塞脉片(TSM)对糖尿病足(DF)模型大鼠足部创伤的治疗作用,并探讨其可能的作用机制。方法:清洁级雄性SD大鼠,除10只作空白对照组外,其他大鼠成功复制糖尿病足溃疡模型,随机分为模型组,二甲双胍组,TSM高、中、低剂量组(12.44,6.22,3.11 g·kg-1)。分别于给药第1,4,8,13,18天对大鼠进行溃疡创面拍照观察伤口愈合情况,治疗18 d后对足溃疡组织进行病理组织学检查,羟胺法和TBA法检测血清中超氧化物歧化酶(SOD)和丙二醛(MDA)含量,放射免疫法检测血清白介素6(IL-6)和肿瘤坏死因子α(TNF-α)含量,免疫组织化学法观察大鼠创面组织中VEGF的表达和毛细血管数。结果:TSM可以改善糖尿病足大鼠的病理形态学改变,加速4,8,13,18 d各时相点伤口愈合,降低第18天(修复后期)大鼠血清中MDA,IL-6,TNF-α的含量,升高SOD含量,其中TSM高剂量组与模型组比较差异具有显著性(P<0.05,P<0.01);治疗后18 d(修复后期)TSM高、中剂量组VEGF的表达,TSM高剂量组毛细血管的数目明显低于模型组(P<0.05,P<0.01)。结论:TSM可以促进DF模型大鼠足部伤口愈合,降低血清中MDA,IL-6,TNF-α的含量,升高SOD含量,减少修复后期VEGF表达和毛细血管数量,其作用机制可能与抑制氧化应激损伤及炎性细胞浸润有关。Objective: To observe the effect of Tongsaimai (TSM) tablets in treating foot trauma of diabetic foot (DF) model rats, and discuss its potential mechanism. Method: Male SD rats were selected to duplicate the diabetic foot ulcer model and randomly divided into the blank control group, the model group, the metformin treatment group, and TSM 12.44, 6.22, 3.11 g·kg-1 groups (n=10). The healing of ulcer wounds were observed on day 1, 4, 8, 13 and 18. After 18 days, a histopathologic examination was conducted for ulcer tissues. The contents of superoxide dismutase (SOD) and malondialdehyde (MDA) were detected by hydroxylamine and TBA methods. The content of interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) were determined with the radioimmunoassay. The immunohistochemical method was used to observe the expression of vascular endothelial growth factor (VEGF) in ulcer tissues and the number of capillary vessels. Result: TSM could alleviate the pathological changes of diabetic foot rats, accelerate the ulcer healing on 4, 8, 13, 18 d, reduce MDA, IL-6, TNF-α, VEGF content in rat serum at 18 d (after the rehabilitation period), and enhance the SOD content. Specifically, the TSM 12.44 g·kg^-1 group showed significant differences compared with the model group (P〈0.05, P〈0.01). At 18 d after the treatment (the late rehabilitation period), the VEGF expression of TSM 12.44, 6.22 g·kg^-1 groups and the number of blood capillaries of the TSM 12.44 g·kg^-1 group were significantly lower than that of the model group (P〈0.05,P〈0.01). Conclusion: TSM could promote the foot wound healing of DF model rats, reduce MDA, IL-6 and TNF-α levels in serum, increase the SOD content and decrease the VEGF expression and the number of blood capillaries in the late rehabilitation period. Its action mechanism may be related to the inhibition of oxidative stress injury and the inflammatory cell infiltration.
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