摘要
目的:探讨补肾温阳化瘀方治疗内异症的可能作用机制。方法:选用SPF级雌性大鼠复制腹膜型内异症大鼠模型,将造模成功的大鼠分为4组:补肾温阳化瘀方高剂量组(16只)、低剂量组(16只)、丹那唑组(16只)、模型组(17只),并设对照组(12只)。运用免疫组化(S-P)法,检测内异症模型大鼠治疗前、后异位内膜组织中缺氧诱导因子-1α(HIF-1α)、葡萄糖转运因子-1(GLUT-1)的表达,并比较治疗前后异位灶体积变化。结果:补肾温阳化瘀方高、低剂量组及丹那唑组治疗后子宫内膜异位灶体积较治疗前明显缩小(P<0.05),且以补肾温阳化瘀方高剂量组最显著(P<0.01);HIF-1α,GLUT-1在模型组异位内膜的表达与对照组在位内膜相比显著升高(P<0.01);补肾温阳化瘀方高、低剂量组及丹那唑组均能够显著抑制HIF-1α,GLUT-1的高表达(P<0.01),与对照组表达无明显差异,且以中药高剂量组作用效果最显著,低剂量组次之;丹那唑组与补肾温阳化瘀方高剂量组比较抑制效果有差异(P<0.05)。结论:补肾温阳化瘀方可能通过抑制HIF-1α与GLUT-1的表达达到治疗内异症的目的。
Objective:To explore the mechanism of Bushen Wenyang Huayu(BSWYHY) on endometriosis(EMs).Method: The peritoneal type endometriosis in SPF-grade female rats was established.They were then divided into 4 groups: BSWY high dose group(16),BSWYHY low dose group(16),danazol group(16),model group(17),and control group(12).Immunohistochemistry was performed to examine the expression of HIF-1α and GLUT-1 in the ectopic endometrial tissues of the EMs model rats before and after treatment,and the volume change in endometriotic lesions before and after treatment was compared.Result:After treatment with high dose and low dose of BSWY and danazol,volumes of ectopic lesions were reduced obviously(P 〈 0.05),and the volume of the high dose group demonstrated the most notable reduction(P 〈 0.01).The expression of HIF-1α and GLUT-1 in ectopic EMs of the model group is significantly higher than that in eutopic endometrium in the control group(P 〈 0.01).The BSWYHY high and low dose group and the danazol group were able to inhibit the high expression of HIF-1α and GLUT-1 substantially(P 〈 0.01),with the high dose group as the best,followed by the low dose anddanazol group(P 〈 0.05).Conclusion: BSWY can be an effective measure for reducing the high expression of HIF-1α and GLUT-1 for the treatment of EMs.
出处
《中国实验方剂学杂志》
CAS
北大核心
2010年第15期132-135,共4页
Chinese Journal of Experimental Traditional Medical Formulae
关键词
子宫内膜异位症
补肾温阳化瘀
中药
缺氧诱导因子-1Α
葡萄糖转运因子-1
endometriosis; Bushen Wenyang Huayu; traditional Chinese medicine; hypoxia-inducible factor-1α:glucose transporter factor-1;