Adipose-Derived Stem Cell Transplantation Inhibits Vascular Inflammatory Responses and Endothelial Dysfunction in Rats with Atherosclerosis

Figures

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  Fig. 1. Successful construction of rat atherosclerosis (AS) model (n=8 in each group). (A) Hematoxylin-Eosin (HE) staining of aortic cross-sections. Arrows indicate atheromatous plaque. Magnification: ×200. (B) Oil Red O staining of aortic sections. Magnification: ×400. (C) Ratio of I/(I+M) (I=thickness of aortic intima, M=thickness of aortic media). (D) The levels of total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were measured by automatic biochemical analyzer. Data are presented as mean±standard deviation, with repetition of three times. Bar=100 µm. *p<0.05, †p<0.01, ‡p<0.001, vs. Normal group.

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  Fig. 2. Identification of adipose-derived stem cells (ADSCs). (A) Morphological characteristics of ADSCs at three passages. Magnification: ×200. Bar=100 µm. (B) Expressions of ADSC surface antigens (CD34, CD44, CD45, and CD90) were detected by flow cytometry.

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  Fig. 3. Adipose-derived stem cells (ADSC) transplantation alleviated the pathological symptoms of aortic atherosclerosis (AS) (n=8 in each group). (A) Expression of PKH26-labeled ADSCs in aortic tissues of rats. Bar=100 µm. (B) Hematoxylin-Eosin (HE) staining of aortic sections. Magnification: ×200. (C) Ratio of I/(I+M) (I=thickness of aortic intima, M=thickness of aortic media). Data are presented as mean±standard deviation, with repetition of three times. ‡p<0.001, vs. Normal group and Normal+ADSCs group; ∥p<0.01, vs. AS group.

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  Fig. 4. Adipose-derived stem cell (ADSC) transplantation decreased the levels of lood lipids and inflammatory cytokines in atherosclerosis (AS) rats (n=8 in each group). (A) The levels of total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were measured by automatic biochemical analyzer. (B–D) Expression of interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), and c-reactive protein (CRP) was detected by Enzyme linked immunosorbent assay. Data are presented as mean±standard deviation, with repetition of three times. †p<0.01, ‡p<0.001, vs. Normal group and Normal+ADSCs group; §p<0.05, ∥p<0.01, ¶p<0.001, vs. AS group.

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  Fig. 5. Adipose-derived stem cell (ADSC) transplantation inhibited endothelial dysfunction in atherosclerosis (AS) rats (n=8 in each group). (A–D) The levels of vascular endothelial growth factor (VEGF), endothelin-1 (ET-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) were detected by Enzyme linked immunosorbent assay. (E) The mRNA expressions of VEGF, ET-1, VCAM-1, and ICAM-1 were measured by quantitative real-time polymerase chain reaction (qRT-PCR). (F) Protein expressions of VEGF, ET-1, VCAM-1, and ICAM-1 were measured by western blot. Data are presented as mean±standard deviation, with repetition of three times. †p<0.01, ‡p<0.001, vs. Normal group and Normal+ADSCs group; §p<0.05, ∥p<0.01, ¶p<0.001, vs. AS group. GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

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  Fig. 6. Adipose-derived stem cell (ADSC) transplantation inhibited NF-κB signaling pathway in atherosclerosis (AS) rats (n=8 in each group). (A) Expression of NF-κB p65 was measured by immunofluorescence staining. Scale bar=20 µm. (B) Expression of NF-κB p65 was detected by quantitative real-time polymerase chain reaction (qRT-PCR). (C) Expressions of NF-κB p65, p-NF-κB p65, and IκBα were measured by western blot. Data are presented as mean±standard deviation, with repetition of three times. †p<0.01, ‡p<0.001, vs. Normal group and Normal+ADSCs group; §p<0.05, ∥p<0.01, vs. AS group. DAPI, 4′, 6-diamidino-2-phenylindole; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.