Konjac glucomannan defends against high-fat diet-induced atherosclerosis in rabbits by promoting the PI3K/Akt pathway

Figures

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  Fig. 1. Impacts of KGM and LY294002 on blood lipids in rabbits with high-fat diet-induced atherosclerosis. TC(A), TG(B), LDL-C(C), and HDL-C(D) were determined by the oxidase method using a Mindray automatic biochemical analyzer. The results are expressed as the mean ± standard deviation (n = 8). *P < 0.05 vs. the indicated groups. KGM = konjac glucomannan.

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  Fig. 2. Impacts of KGM and LY294002 on the inflammatory response in rabbits with high-fat diet-induced atherosclerosis rabbits. The concentrations of CRP(A), TNF-α(B), and IL-6(C) were determined by ELISA. The results are expressed as the mean ± standard deviation (n = 8). *P < 0.05 vs. the indicated groups. KGM = konjac glucomannan.

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  Fig. 3. Impacts of KGM and LY294002 on the positive expression of VCAM-1 in rabbits with high-fat diet-induced atherosclerosis. (A) Positive expression of VCAM-1 in the aortic wall was analyzed by immunohistochemistry. The brown-yellow granular products were observed as positive markers under the microscope, and the percentage of positive staining markers was calculated by automatic analysis with cell image analysis software. (SP method, DAB staining). (B) Characteristic blots of positive VCAM-1 of expression. The results are expressed as the mean ± standard deviation (n = 8). *P < 0.05 vs. the indicated groups. KGM = konjac glucomannan. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

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  Fig. 4. Impacts of KGM and LY294002 on endothelial function in rabbits with high-fat diet-induced atherosclerosis. (A) NO concentrations were determined by the nitrate reductase method. (B) ET concentrations were determined by ELISA. The results are expressed as the mean ± standard deviation (n = 8). *P < 0.05 vs. the indicated groups. KGM = konjac glucomannan.

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  Fig. 5. Impacts of KGM and LY294002 on pathological changes in the aorta in rabbits with high-fat diet-induced atherosclerosis. (A) Macroscopic pathology of the aorta (Sudan III staining), with AS patches are shown in orange-red. (B) Characteristic pathological images after H&E staining. The structure of the aorta in the CTR group was clear, and the intima was smooth. The intima of the aorta in the HFD group was thickened and contained a large number of foam cells. In the KGM group, the intima of the aorta was thickened and reduced, and a few foam cells were present. (C)Thicknesses of the tunica intima of the aorta were measured by a CIAS-100 cell image analyzer. (D)Tunica intima thickness/tunica media thickness ratio (TIT/TMT ratio) was calculated. The results are expressed as the mean ± standard deviation (n = 8). *P < 0.05 vs. the indicated groups. KGM = konjac glucomannan. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

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  Fig. 6. Impacts of KGM and LY294002 on oxidative stress in rabbits with high-fat diet-induced atherosclerosis. The levels of MPO(A), MDA(B), SOD(C), and GSH-px(D) were analyzed by ELISA. The results are expressed as the mean ± standard deviation (n = 8). *P < 0.05 vs. the indicated groups. KGM = konjac glucomannan.

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  Fig. 7. Impacts of KGM and LY294002 on PI3K/Akt in rabbits with high-fat diet-induced atherosclerosis. (A) Akt, P-Akt, PI3K, and P-PI3K expression in the aortic wall was analyzed by Western blot. β-actin was used as the internal control. (B) Calculated P-Akt/Akt ratios. (C) Calculated P-PI3K/PI3K ratios. The results are expressed as the mean ± standard deviation (n = 8). *P < 0.05 vs. the indicated groups. KGM = konjac glucomannan.