NaoXinTong Inhibits the Advanced Atherosclerosis and Enhances the Plaque Stability in Apolipoprotein E Deficient Mice.
Buchang NaoXinTong (NXT), a Chinese medicine, has been widely used to treat patients with coronary heart disease in China. However, the underlying mechanisms need more elucidations. In this study, we investigated if NXT can inhibit the progression of the established lesions while stabilizing plaques. Apolipoprotein E deficient (apoE(-/-)) mice in 3 groups received following treatment: group 1 was fed a high-fat diet (HFD) for 18 weeks; group 2 was prefed HFD for 12 weeks followed by HFD containing NXT for additional 6 weeks; group 3 was prefed HFD for 8 weeks followed by HFD containing NXT for additional 10 weeks. After treatment, serum and aorta samples were collected and determined lipid profiles, lesions, collagen content, mineralization, and macrophage accumulation in aortic root, respectively. NXT had slight effect on serum lipid profiles but significantly reduced progression of the advanced lesions. In aortic wall, NXT increased smooth muscle cell/collagen content in lesion cap while reducing buried fibrous caps, mineralization, and macrophage accumulation within lesions, which suggests that NXT can stabilize plaques. In addition, NXT increased expression of smooth muscle 22α mRNA while inhibiting expression of matrix metalloproteinase-2 and tumor necrosis factor α mRNA in aortas. Our study demonstrates that NXT can reduce advanced atherosclerosis and enhance the plaque stability in apoE(-/-) mice.
*College of Life Sciences, Nankai University, Tianjin, China; †Buchang Pharmaceutical Co, Ltd, Xi'an, China; ‡College of Medical Engineering, Hefei University of Technology, Hefei, China; §Collaborative Innovation Center for Biotherapy, School of Medicine, Nankai University, Tianjin, China.
Xiaoxiao
X
Yang
Lei
L
Sun
Yan
Y
Li
Chuanrui
C
Ma
Jie
J
Yang
Wenwen
W
Zhang
Buchang
B
Zhao
Lifu
L
Jia
Yajun
Y
Duan
Jihong
J
Han
Xiaoju
X
Li
Yuanli
Y
Chen
D000199:Actins / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D001018:Aortic Diseases / Q000097:blood / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D050197:Atherosclerosis / Q000097:blood / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D015415:Biomarkers / Q000097:blood; D002317:Cardiovascular Agents / Q000494:pharmacology*; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D005355:Fibrosis; D005786:Gene Expression Regulation; D020022:Genetic Predisposition to Disease; D008055:Lipids / Q000097:blood; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000235:genetics / Q000378:metabolism; D018345:Mice, Knockout; D010641:Phenotype; D008517:Phytotherapy; D010946:Plants, Medicinal; D058226:Plaque, Atherosclerotic; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012422:Rupture, Spontaneous; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D000199:Actins; D001057:Apolipoproteins E; D015415:Biomarkers; D002317:Cardiovascular Agents; D004365:Drugs, Chinese Herbal; D008055:Lipids; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C544013:alpha-smooth muscle actin, mouse; C571443:naoxintong; D020778:Matrix Metalloproteinase 2; C522362:Mmp2 protein, mouse