ObjectiveTo observe the effects of hydroxysafflor yellow A (HSYA) on microvessel density (MVD) of mice transplanted Lewis lung cancer and mRNA expression of vascular endothelial growth factor (VEGF) so as to explore the tumor-inhibiting mechanism of HSYA. MethodsSixty tumor-bearing C57/BL mice were randomly divided into five groups, with 12 mice in each group, namely a control group, a cyclophosphamide (CTX) group (25mg/kg), a large dose HSYA group (112mg/L), a medium dose HSYA group (56mg/L), and a small dose HSYA group (28mg/L). These different drugs were administered by intraperitoneal injection. The mice were sacrificed 22 days after the treatment. Tumor tissues were sampled and examined by immunohistochemical method and quantitative real-time PCR to detect the expression of MVD and VEGF mRNA. ResultsThe MVD of the medium and small dose HSYA groups and CTX group were 30.01±3.12, 22.56±2.11 and 16.21±2.40, respectively, which were significantly lower than 41.10±2.93 of the control group and 37.66±3.04 of the large dose HSYA group (χ2=2.82, P=0.010;χ2=3.16, P=0.007;χ2=4.58, P=0.000) and (χ2=1.98, χ2=0.038;χ2=2.45, P=0.016;χ2=3.82, P=0.001). The difference in VEGF amplified fluorescence expression threshold between the HSYA groups and the control group was not significant. However, after amplification, the expression of VEGF mRNA in the small dose HSYA group was only 0.43±0.16, which was obviously lower than 0.82±0.06 in the control group (F=0.77, P=0.038). ConclusionHSYA can significantly reduce MVD in mice transplanted Lewis lung cancer and down-regulate expression of VEGF mRNA to achieve tumor-inhibiting effect.
ObjectiveTo study the effects of hydroxysafflow yellow A (HSYA) in inhibiting inflammatory signal transduction in lungs of acute lung injury mice induced by lipopolysaccharide (LPS). MethodsEighty-four male Kunming mice were randomly divided into 7 groups, ie. a sham group, a LPS group, a LPS+3 mg/kg dexamethason (DXM) group, a LPS+6 mg/kg HSYA group, a LPS+15 mg/kg HSYA group, a LPS+37.5 mg/kg HSYA group, and a saline+37.5 mg/kg HSYA group (n=12 in each group). The mice were intraperitoneally pretreated with normal saline or DXM or HSYA 0.5 hour prior to intravenous adminstration of LPS. TNF-α, IL-1β and IL-6 levels in mice serum were measured by ELISA and the mRNA and protein levels of TLR4 in mice lungs were assessed by RT-qPCR and Western blot, respectively. ResultsAfter being treated with HSYA in doses of 6 mg/kg, 15 mg/kg, and 37.5 mg/kg, the increased expression levels of TLR4 mRNA and protein induced by LPS were significantly inhibited, as well as the increased expression levels of TNF-α, IL-1β and IL-6. The inhibitoty effect enhanced with the doses of HSYA. DXM could inhibit more significantly the increased expression levels of all the indexes. ConclusionHSYA can inhibit inflammatory signal transduction in acute lung injury mice induced by LPS in a dose-dependent manner, but is less effective than DXM.