Journal of ethnopharmacology · 2011
Protective effect of Shenfu injection on thromboangiitis obliterans model rats.
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Hong Fenfang, He Changsheng, Liu Xiaojun, Tu Guilin, Guo Faxian, Yang Shulong
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Thromboangiitis obliterans (TAO) or Buerger's disease is a non atherosclerotic, segmentar inflammatory vasculitis that is incurable at present. Shenfu injection (SFI), a traditional Chinese formulation, have been confirmed to produce protective influences on several organs and limb during ischemia and reperfusion (IR) injury in rats. However, the effects of SFI on TAO remain unclear.
MATERIALS AND METHODS: Adult male Sprague Dawley rats were randomly divided into sham operated group, TAO model group, SFI 2.5mg/kg (low dose), 5mg/kg (medium dose) and 10mg/kg (high dose) groups (n=8). Rats were intravenously administered SFI 2.5, 5 and 10mg/kg or saline once per day for 15 days. TAO model was prepared by injecting sodium laurate into the femoral artery of rats. Then we examined the changes of pathological signs, pathologic grading of thrombus, the indexes of hematology, the contents of thromboxane B2 (TXB2), 6-keto-prostaglandin F(lα) (6-K-PGF(1α)) in plasma following SFI or saline treatment.
RESULTS: More pathological signs of lesions, higher grades of pathological thrombosis, increased blood platelet counts, the increase in the TXB2 and TXB2/6-K-PGF(1α) ratio, as well as the decrease of 6-K-PGF(1α) in TAO model group were shown in present experiments; SFI treatment significantly improved the pathological signs of lesions induced by sodium laurate injection, reduced the numbers of thrombus formation, blood platelet counts, the TXB2 and TXB2/6-K-PGF(1α) ratio but increased the 6-K-PGF(1α) compared with TAO model group. However, there were no significant alterations in the counts of red blood cell, leucocyte and neutrophil among these groups.
CONCLUSIONS: Our preliminary findings first indicated that SFI can produce significant therapeutic effects on experimental Buerger's disease model rats in a dose independent manner. The underlying mechanisms may be due to its modifying hematology, inhibiting platelet aggregation and enhancing anti-thrombotic function of vessel endothelia.
MATERIALS AND METHODS: Adult male Sprague Dawley rats were randomly divided into sham operated group, TAO model group, SFI 2.5mg/kg (low dose), 5mg/kg (medium dose) and 10mg/kg (high dose) groups (n=8). Rats were intravenously administered SFI 2.5, 5 and 10mg/kg or saline once per day for 15 days. TAO model was prepared by injecting sodium laurate into the femoral artery of rats. Then we examined the changes of pathological signs, pathologic grading of thrombus, the indexes of hematology, the contents of thromboxane B2 (TXB2), 6-keto-prostaglandin F(lα) (6-K-PGF(1α)) in plasma following SFI or saline treatment.
RESULTS: More pathological signs of lesions, higher grades of pathological thrombosis, increased blood platelet counts, the increase in the TXB2 and TXB2/6-K-PGF(1α) ratio, as well as the decrease of 6-K-PGF(1α) in TAO model group were shown in present experiments; SFI treatment significantly improved the pathological signs of lesions induced by sodium laurate injection, reduced the numbers of thrombus formation, blood platelet counts, the TXB2 and TXB2/6-K-PGF(1α) ratio but increased the 6-K-PGF(1α) compared with TAO model group. However, there were no significant alterations in the counts of red blood cell, leucocyte and neutrophil among these groups.
CONCLUSIONS: Our preliminary findings first indicated that SFI can produce significant therapeutic effects on experimental Buerger's disease model rats in a dose independent manner. The underlying mechanisms may be due to its modifying hematology, inhibiting platelet aggregation and enhancing anti-thrombotic function of vessel endothelia.