Molecular mechanism of inhibition of the abnormal proliferation of human umbilical vein endothelial cells by hydroxysafflor-yellow A

Figures & data

Figure 1. Molecular structure of hydroxysafflor-yellow A.

Table 1. Primer sequences for real-time quantitative PCR.

Gene name	Forward primer (5′ to 3′)	Reverse primer (5′–3′)	Annealing temperature (°C)	Length of product (bp)
VEGF	CGA GAC CCT GGT GGA CAT CT	ACA AAT GCT TTC TCC GCT CTG	58	296
KDR	CGG TAG CAC AGC CCA GAT TC	GGT CAC AAG CCT CTT CCA GGA	60	244
bFGF	GGT GTG CCT GTG GAG GAA CT	GGC TCA TGA GAG AAG ACG GAA TC	60	293
GAPDH	AGA AGG CTG GGG CTC ATT TG	AGG GGC CAT CCA CAG TCT TC	58	258
c-myc	TGT CCG TCC AAG CAG AGG AG	CCC AAA GTC CAA TTT GAG GCA	60	270
N-ras	GGT GCT AGT GGG AAA CAA GTG T	CCC TGA GTC CCA TCA CTG	56	207
NF-κB1	CCC TGA GAC AAA TGG GCT ACA	GGT CCT TCC TGC CCA TAA TCA	60	265

Figure 2. The figure of HUVEC cells. HUVEC were stimulated with factor VIII, and the related antigen-antibody complexes had red-brown precipitate in the cytoplasm (× 40 magnification).

Figure 3. mRNA and protein expression of HUVEC VEGF and KDR in each group. Note: compared with the control group, **p <0.01; compared with the TCCS group, #p <0.05, ##p <0.01.

Figure 4. Expression level of bFGF in HUVEC cell culture supernatant treated with HSYA. Note: compared with the control group, *p < 0.05, **p < 0.01.

Figure 5. Expression level of related molecules in the ERK pathway of HUVECs. Of the three protein band patterns on each gel, the control group (left), tumour cell culture supernatant-induced group (middle) and the HSYA-treated group (right) are shown.

Figure 6. The mRNA expression of c-myc, N-ras and NF-κB₁ in the tumour cell culture supernatant-induced HUVEC. Note: compared with the control group, *p < 0.05, **p < 0.01; compared with the TCCS group, #p < 0.05, ##p < 0.01.

Figure 7. Content in cell lysates of c-myc and N-ras in the tumour cell culture supernatant-induced HUVEC. Note: compared with the control group, *p < 0.05; compared with the TCCS group, #p < 0.05.