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目的:研究坤舒康颗粒对大鼠慢性盆腔炎的治疗作用,探讨其可能的作用机制。方法:采用苯酚胶浆注射合并机械损伤的方法制备大鼠慢性盆腔炎模型,实验共分6组:假手术组,模型组,坤舒康颗粒5、10、20g/kg组,阳性药妇科千金片组。药物治疗20天后,计算各组大鼠子宫系数;检测血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、一氧化氮(NO)水平及血液流变学指标:全血及血浆粘度、红细胞压积;RT-PCR法检测子宫组织成纤维细胞生长因子-2(FGF-2)、胰岛素样生长因子-1(IGF-1)mRNA表达。结果:与模型组相比,5g/kg坤舒康颗粒可明显降低血清炎性因子TNF-α水平,红细胞压积,全血高、中切粘度;10g/kg坤舒康颗粒显著降低盆腔炎大鼠的子宫肿胀程度,TNF-α、IL-1β水平及各项血液流变学指标的异常;20g/kg坤舒康颗粒除了上述指标的明显改善外,还可显著降低血清NO含量;各剂量组均可明显降低子宫FGF-2、IGF-1 mRNA表达。结论:坤舒康颗粒可显著改善慢性盆腔炎大鼠的子宫肿胀与粘连,显著改善炎症反应及血液流变学异常,其作用机制与下调子宫FGF-2、IGF-1的表达密切相关。
Objective: To study the therapeutic effect of Kun Shukang Granules on chronic pelvic inflammatory disease in rats and its possible mechanism. Methods: Chronic pelvic inflammatory disease rat models were prepared by phenol glue injection combined with mechanical injury. The experiment was divided into 6 groups: sham operation group, model group, Kun Shukang Granules 5, 10, 20g / kg group, Chip set. Twenty days after the drug treatment, the uterine coefficient of each group was calculated. The levels of serum tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), nitric oxide (NO) and hemorheology : Whole blood and plasma viscosity, hematocrit; RT-PCR method was used to detect the expression of fibroblast growth factor-2 (FGF-2) and insulin-like growth factor-1 (IGF- Results: Compared with the model group, 5g / kg Kun Shukang Granules can significantly reduce serum levels of inflammatory cytokines TNF-α, hematocrit, whole blood high, medium viscosity; 10g / kg Kun Shukang Granules significantly reduce pelvic inflammatory disease The degree of uterine swelling, the levels of TNF-α and IL-1β, and the abnormalities of various hemorheological indexes in rats were significantly lower than those of the other groups. In addition to the significant improvement of the above indexes, 20g / kg Kun Shukang granules could significantly reduce the serum NO content. Dose group can significantly reduce uterine FGF-2, IGF-1 mRNA expression. CONCLUSION: Kunshukang granules can significantly improve uterine swelling and adhesion in rats with chronic pelvic inflammation and significantly improve inflammatory reaction and hemorheology abnormalities. Its mechanism is closely related to the down-regulation of the expression of FGF-2 and IGF-1.