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目的:探讨赤雹果总有机酸(FTDBP)治疗原发性痛经作用机制。方法:将Wistar雌性大鼠48只随机分为正常对照组、模型组、元胡止痛片对照组、FTDBP高、中、低剂量组(剂量分别为0.13,0.26,0.52 g.kg-1)。以20 U.kg-1缩宫素腹腔注射建立大鼠痛经模型,采用酶联免疫分析法检测大鼠血清和子宫组织中前列腺素F2α(PGF2α)含量和子宫组织中内皮素(ET)含量;运用甲基百里香酚蓝比色法(MTB)检测大鼠子宫组织中钙离子(Ca2+)含量。结果:FTDBP高剂量组大鼠血清和子宫组织中前列腺素PGF2α含量均显著低于模型对照组(P<0.01),FTDBP中、低剂量组大鼠血清和子宫组织中PGF2α含量均显著低于模型对照组(P<0.05);子宫组织中Ca2+和ET含量显著低于模型对照组(P<0.01)。结论:FTDBP治疗原发性痛经的作用机制可能是通过抑制大鼠的PGF2α,Ga2+和ET的释放或合成。
Objective: To investigate the mechanism of action of FTDBP on primary dysmenorrhea. Methods: Forty-eight Wistar female rats were randomly divided into normal control group, model group, Yuanhu Zhitong Tablet control group, FTDBP high, medium and low dose groups (doses were 0.13,0.26,0.52 g.kg-1). The model of dysmenorrhea was established by intraperitoneal injection of oxytocin (20 U · kg-1). The content of prostaglandin F2α (PGF2α) and the content of endothelin (ET) in uterus were detected by enzyme linked immunosorbent assay (ELISA) The content of Ca2 + in rat uterine tissue was detected by methyl thymol blue colorimetry (MTB). Results: The levels of prostaglandin PGF2α in serum and uterus of FTDBP high dose group were significantly lower than those in model control group (P <0.01). The content of PGF2α in serum and uterus tissue of FTDBP medium and low dose groups were significantly lower than that of model (P <0.05). The levels of Ca2 + and ET in uterine tissue were significantly lower than those in the model control group (P <0.01). Conclusion: The mechanism of FTDBP in treating primary dysmenorrhea may be through inhibiting the release or synthesis of PGF2α, Ga2 + and ET in rats.