Objective： To evaluate the clinical effect and safety of Safflower Yellow injection （SYI） in treating coronary heart disease angina pectoris （OHD-AP） with Xin-blood stagnation syndrome （XBSS）. Methods： Adopted...Objective： To evaluate the clinical effect and safety of Safflower Yellow injection （SYI） in treating coronary heart disease angina pectoris （OHD-AP） with Xin-blood stagnation syndrome （XBSS）. Methods： Adopted was the multi-centered, randomized, positive parallel controlled method, 448 patients with CHD-AP-XBSS were enrolled and divided into two groups, 336 in the tested group treated with SYI and 112 in the control group treated with Salvia injection by intravenous dripping once a day for 14 days, so as to observe the conditions of angina, electrocardiogram, and therapeutic effect on traditinal Chinese medicine （TCM） symptoms as well as the safety of the treatment. Results： The significantly effective rate and total effective rate in the tested group were 60.06% （194/323） and 91.02 % （294/323） respectively; those in improvement of TOM symptoms were 40. 18% （129/321） and 75.23% （243/323） respectively, which were better than those in the control group （P〈0.01）. Conclusion： SYI Injection is effective and safe in treating OHD-AP-XBSS.展开更多
Objective:To investigate the mechanism by which hydroxyl safflower yellow A,an active component of safflower (Carthamus tinctorius L.),promotes apoptosis in abnormal human umbilical vein endothelial cells (HUVECs).Met...Objective:To investigate the mechanism by which hydroxyl safflower yellow A,an active component of safflower (Carthamus tinctorius L.),promotes apoptosis in abnormal human umbilical vein endothelial cells (HUVECs).Methods:Supernatant of BGC-823 was used to stimulate HUVECs to establish a model of abnormal proliferation of HUVECs.After determining an ideal concentration of HSYA by MTT assay,apoptosis was detected with flow cytometry and TUNEL assay.Mechanism of apoptosis was assessed using quantitative real-time polymerase chain reaction,Western blot,and ELISA.Results:A range of concentrations of HSYA inhibited proliferation and promoted apoptosis of abnormal HUVECs.As the rate of apoptosis increased,mRNA expression of caspase-3 increased while expression of mutant p53 decreased.HSYA had no effect on Fas gene expression.Analogously,protein expression of Bax was increased while those of Bcl-2,Fas,and Fas-L were decreased.Conclusions:HSYA appears to induce apoptosis of HUVECs with the stimulation of the supematant of tumor cells.The mechanism of apoptosis by HSYA may involve activation of the mitochondrial apoptotic pathway and regulation of the expressions of Bcl-2,Bax,and p53.展开更多
Objective To explore the anti-tumor effect of safflower yellow(SY)against hepatocellular carcinoma(HCC)and the underlying potential mechanism.Methods An in vitro model was established by mixing Luc-Hepa1-6 cells and C...Objective To explore the anti-tumor effect of safflower yellow(SY)against hepatocellular carcinoma(HCC)and the underlying potential mechanism.Methods An in vitro model was established by mixing Luc-Hepa1-6 cells and CD3^(+)CD8^(+)T cells,followed by adding programmed cell death protein 1(PD-1)antibody(Anti-mPD-1)with or without SY.The apoptosis was detected by flow cytometry and the level of inflammatory cytokines was determined by enzyme-linked immunosorbent assay.The protein levels of programmed cell death 1 ligand 1(PD-L1),chemokine ligand(CCL5),C-X-C motif chemokine ligand 10(CXCL10)were measured by Western blot.An in situ animal model was established in mice followed by treatment with anti-mPD-1 with or without SY.Bioluminescence imaging was monitored with an AniView 100 imaging system.To establish the FAK-overexpressed Luc-Hepa1-6 cells,cells were transfected with adenovirus containing pcDNA3.1-FAK for 48 h.Results The fluorescence intensity,apoptotic rate,release of inflammatory cytokines,and CCL5/CXCL10 secretion were dramatically facilitated by anti-mPD-1(P<0.01),accompanied by an inactivation of PD-1/PD-L1 axis,which were extremely further enhanced by SY(P<0.05 or P<0.01).Increased fluorescence intensity,elevated percentage of CD3+CD8+T cells,facilitated release of inflammatory cytokines,inactivated PD-1/PD-L1 axis,and increased CCL5/CXCL10 secretion were observed in Anti-mPD-1 treated mice(P<0.01),which were markedly enhanced by SY(P<0.05 or P<0.01).Furthermore,the enhanced effects of SY on inhibiting tumor cell growth,facilitating apoptosis and inflammatory cytokine releasing,suppressing the PD-1/PD-L1 axis,and inducing the CCL5/CXCL10 secretion in Anti-mPD-1 treated mixture of Luc-Hepa1-6 cells and CD3+CD8+T cells were abolished by FAK overexpression(P<0.01).Conclusion SY inhibited the progression of HCC by mediating immunological tolerance through inhibiting FAK.展开更多
文摘Objective： To evaluate the clinical effect and safety of Safflower Yellow injection （SYI） in treating coronary heart disease angina pectoris （OHD-AP） with Xin-blood stagnation syndrome （XBSS）. Methods： Adopted was the multi-centered, randomized, positive parallel controlled method, 448 patients with CHD-AP-XBSS were enrolled and divided into two groups, 336 in the tested group treated with SYI and 112 in the control group treated with Salvia injection by intravenous dripping once a day for 14 days, so as to observe the conditions of angina, electrocardiogram, and therapeutic effect on traditinal Chinese medicine （TCM） symptoms as well as the safety of the treatment. Results： The significantly effective rate and total effective rate in the tested group were 60.06% （194/323） and 91.02 % （294/323） respectively; those in improvement of TOM symptoms were 40. 18% （129/321） and 75.23% （243/323） respectively, which were better than those in the control group （P〈0.01）. Conclusion： SYI Injection is effective and safe in treating OHD-AP-XBSS.
文摘Objective:To investigate the mechanism by which hydroxyl safflower yellow A,an active component of safflower (Carthamus tinctorius L.),promotes apoptosis in abnormal human umbilical vein endothelial cells (HUVECs).Methods:Supernatant of BGC-823 was used to stimulate HUVECs to establish a model of abnormal proliferation of HUVECs.After determining an ideal concentration of HSYA by MTT assay,apoptosis was detected with flow cytometry and TUNEL assay.Mechanism of apoptosis was assessed using quantitative real-time polymerase chain reaction,Western blot,and ELISA.Results:A range of concentrations of HSYA inhibited proliferation and promoted apoptosis of abnormal HUVECs.As the rate of apoptosis increased,mRNA expression of caspase-3 increased while expression of mutant p53 decreased.HSYA had no effect on Fas gene expression.Analogously,protein expression of Bax was increased while those of Bcl-2,Fas,and Fas-L were decreased.Conclusions:HSYA appears to induce apoptosis of HUVECs with the stimulation of the supematant of tumor cells.The mechanism of apoptosis by HSYA may involve activation of the mitochondrial apoptotic pathway and regulation of the expressions of Bcl-2,Bax,and p53.
基金Supported by 2021 Industry-University Cooperative Education Project of Ministry of Education(No.202101160003)。
文摘Objective To explore the anti-tumor effect of safflower yellow(SY)against hepatocellular carcinoma(HCC)and the underlying potential mechanism.Methods An in vitro model was established by mixing Luc-Hepa1-6 cells and CD3^(+)CD8^(+)T cells,followed by adding programmed cell death protein 1(PD-1)antibody(Anti-mPD-1)with or without SY.The apoptosis was detected by flow cytometry and the level of inflammatory cytokines was determined by enzyme-linked immunosorbent assay.The protein levels of programmed cell death 1 ligand 1(PD-L1),chemokine ligand(CCL5),C-X-C motif chemokine ligand 10(CXCL10)were measured by Western blot.An in situ animal model was established in mice followed by treatment with anti-mPD-1 with or without SY.Bioluminescence imaging was monitored with an AniView 100 imaging system.To establish the FAK-overexpressed Luc-Hepa1-6 cells,cells were transfected with adenovirus containing pcDNA3.1-FAK for 48 h.Results The fluorescence intensity,apoptotic rate,release of inflammatory cytokines,and CCL5/CXCL10 secretion were dramatically facilitated by anti-mPD-1(P<0.01),accompanied by an inactivation of PD-1/PD-L1 axis,which were extremely further enhanced by SY(P<0.05 or P<0.01).Increased fluorescence intensity,elevated percentage of CD3+CD8+T cells,facilitated release of inflammatory cytokines,inactivated PD-1/PD-L1 axis,and increased CCL5/CXCL10 secretion were observed in Anti-mPD-1 treated mice(P<0.01),which were markedly enhanced by SY(P<0.05 or P<0.01).Furthermore,the enhanced effects of SY on inhibiting tumor cell growth,facilitating apoptosis and inflammatory cytokine releasing,suppressing the PD-1/PD-L1 axis,and inducing the CCL5/CXCL10 secretion in Anti-mPD-1 treated mixture of Luc-Hepa1-6 cells and CD3+CD8+T cells were abolished by FAK overexpression(P<0.01).Conclusion SY inhibited the progression of HCC by mediating immunological tolerance through inhibiting FAK.
