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目的:从分子水平探讨肝病患者不同血瘀证及其形成的病理机制。方法:采用前瞻性研究的方法进行肝病瘀血舌患者血液血栓素B2(TXB2)、6-酮-前列腺素F1α(6-keto-PGF1α)的测定。结果:肝病各组的TXB2显著增高(P<0.01),6-keto-PGF1α显著降低(P<0.05,P<0.01)。TXB2/6-keto-PGF1α显著增高(P<0.01);不同肝病血瘀证组与正常组的TXB2、6-keto-PGF1α、TXB2/6-keto-PGF1α的比较有显著性差异(P<0.01),湿热瘀滞、肝瘀痰阻、气滞血瘀的TXB2、6-keto-PGF1α、TXB2/6-keto-PGF1α与气虚血瘀组比较有显著差异(P<0.01)。结论:肝病及不同血瘀证组的TXB2与TXB2/6-keto-PGF1α显著增高,6-keto-PGF1α显著降低,说明血浆TXA2-PGI2平衡失调与血瘀证发生发展密切相关,通过测定TXB2、6-keto-PGF1α的含量可以反映肝病瘀血舌象及其不同血瘀证的发生机制。
Objective: To explore the pathological mechanism of different blood stasis syndromes and their formation in liver disease patients at the molecular level. Methods: A prospective study was conducted to determine the levels of blood thromboxane B2 (TXB2) and 6-keto-PGF1α in patients with liver stasis and blood stasis. Results: The levels of TXB2 in liver disease group were significantly increased (P <0.01), and 6-keto-PGF1α was significantly decreased (P <0.05, P <0.01). TXB2 / 6-keto-PGF1α significantly increased (P <0.01). There was significant difference in TXB2, 6-keto-PGF1α and TXB2 / 6-keto-PGF1α between different syndromes ), TXB2, 6-keto-PGF1α, TXB2 / 6-keto-PGF1α in stagnation of blood stasis, liver stasis and phlegm obstruction, qi stagnation and blood stasis were significantly different from those in qi deficiency and blood stasis group (P <0.01). Conclusion: The levels of TXB2 and TXB2 / 6-keto-PGF1α in liver cirrhosis and different blood stasis syndrome groups were significantly higher than those in control group, and 6-keto-PGF1α was significantly decreased. This indicates that the imbalance of plasma TXA2-PGI2 is closely related to the occurrence and development of blood stasis syndrome. 6-keto-PGF1α content can reflect the tongue of liver disease and its different blood stasis syndrome mechanism.