[ ABSTRACT ] AIM: To investigate the toxicity and reproductive effect of vascular endothelial growth factor ( VEGF)/basic fibroblast growth factor ( bFGF) complex peptide vaccine ( VBP3) on the female-mice.METHODS:The VBP3 was purified with Ni-NTA affinity chromatography.The female BALB/c mice were immunized with the purified VBP3.The antibody titer in the serum was detected by ELISA.The data of the body weight and the organ weight of the par-ent mice were gathered and analyzed, and the pathological changes of the organs were observed with HE staining to investi-gate the toxicity of VBP3.To investigate the toxicity of VBP3 in the F1 mice, the parent immunized female mice were ma-ted with the parent non-immunized male mice.After the F1 mice were born, the survival rate was calculated, the change of the body weight and the organ weight of the F1 mice were also determined.The pathological changes of the organs in F1 mice were also observed with HE staining.RESULTS: In the parent mice, high titers of the antibodies were detected against VEGF and bFGF, and no difference of the body weight, the organ weight and the pathological change between the immunized mice and control mice was found.In the F1 mice, a low titer of anti-bFGF antibody was detected compared with blank group.The survival rate in control group was higher than that in immunized group.In the 2 groups of the F1 mice, no obvious difference of the weight of the spleen, kidney, lung and heart was observed, and there was some difference in the weight of liver between the 2 groups.The results of the HE staining in the F1 mice showed some difference in the liver between the 2 groups.CONCLUSION:VEGF/bFGF complex peptide vaccine has no obvious organ toxicity in the parent female mice, but has some side effects on the reproductive and the healthy processes of F1 mice.

AIM:To analyze the expression profiles of long non-coding RNAs(lncRNAs)in the aortas of ath-erosclerotic mice,and explore the role and mechanism of lncRNA AI662270 in regulating macrophage inflammation and lipid phagocytosis.METHODS:Twenty 8-week-old male apolipoprotein E gene knockout(ApoE-/-)mice were randomly divided into experimental and control groups,with 10 mice in each group.The experimental group was fed a high-fat diet for 12 weeks to induce atherosclerosis,while the control group received a normal diet.Body weight and blood lipid levels were measured,and atherosclerotic lesions were detected using Oil Red O staining.High-throughput RNA sequencing(RNA-seq)was used to analyze the lncRNA expression profiles in mouse aortas,and differentially expressed lncRNAs were validated by RT-qPCR.Antisense oligonucleotides(ASO)were used to knock down the expression of lncRNA AI662270 in mouse macrophage RAW264.7 cells.Six treatment groups were established:blank(no treatment)group,ox-idized low-density lipoprotein(oxLDL)group(80 mg/L oxLDL),negative control ASO(ASO-NC)group(transfected with ASO-NC),oxLDL+ASO-NC group(transfected with ASO-NC and treated with 80 mg/L oxLDL),ASO-AI662270 group(transfected with ASO-AI662270),and oxLDL+ASO-AI662270 group(transfected with ASO-AI662270 and treated with 80 mg/L oxLDL).Tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)levels were measured using Enzyme-linked immunosorbent assay(ELISA).NF-κB p65,pNF-κB p65,IκBα and pIκBα levels were detected by Western blot,and NF-κB p65 in the cell nucleus was examined using fluorescent probes.RESULTS:The atherosclerosis mouse model showed significant differences in body weight,serum lipids,and aortic plaque area compared to the control group(P<0.01).A total of 29 differentially expressed lncRNAs were identified involved in metabolic pathways,autophagosome for-mation,and cell adhesion molecule expression(P<0.05).LncRNA AI662270 was significantly upregulated in lesions and oxLDL-stimulated macrophages(P<0.05).Knockdown of AI662270 significantly reduced TNF-α and IL-6 expression in oxLDL-induced RAW264.7 cells(P<0.01),suppressed lipid phagocytosis,and inhibited pNF-κB p65 and pIκBα ex-pression(P<0.05).Additionally,the knockdown of AI662270 reduced the nuclear content of NF-κB p65.CONCLU-SION:The lncRNA expression profiles in the aortas of atherosclerotic mice were significantly altered.LncRNA AI662270 is crucial in modulating inflammation and lipid phagocytosis in mouse macrophages through the NF-κB signaling pathway.