Magnolia Extract (BL153) Protection of Heart from Lipid Accumulation Caused Cardiac Oxidative Damage, Inflammation, and Cell Death in High-Fat Diet Fed Mice

被引:18
|
作者
Sun, Weixia [1 ,2 ,3 ]
Zhang, Zhiguo [1 ,2 ,3 ]
Chen, Qiang [3 ,4 ]
Yin, Xia [1 ,2 ]
Fu, Yaowen [1 ,2 ]
Zheng, Yang [1 ,2 ]
Cai, Lu [3 ,5 ]
Kim, Ki-Soo [6 ]
Kim, Ki Ho [7 ]
Tan, Yi [3 ,5 ]
Kim, Young Heui [7 ]
机构
[1] Jilin Univ, Hosp 1, Dept Nephrol, Changchun 130021, Peoples R China
[2] Jilin Univ, Hosp 1, Dept Cardiol, Changchun 130021, Peoples R China
[3] Univ Louisville, Dept Pediat, Kosair Childrens Hosp, Res Inst, Louisville, KY 40202 USA
[4] Jilin Univ, Prevent Med Sch, Changchun 130021, Peoples R China
[5] Wenzhou Med Univ, Chinese Amer Res Inst Diabet Complicat, Wenzhou 325035, Peoples R China
[6] Bioland Biotec Co Ltd, Shanghai 201201, Peoples R China
[7] Bioland R&D Ctr, Cheonan 330863, Chungnam, South Korea
基金
中国国家自然科学基金;
关键词
ENDOPLASMIC-RETICULUM STRESS; NECROSIS-FACTOR-ALPHA; CARDIOMYOCYTE APOPTOSIS; UP-REGULATION; MITOCHONDRIAL; DYSFUNCTION; ACTIVATION; EXPRESSION; PATHWAYS; DISEASE;
D O I
10.1155/2014/205849
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Magnolia as an herbal material obtained from Magnolia officinalis has been found to play an important role in anti-inflammation, antioxidative stress, and antiapoptosis. This study was designed to investigate the effect of Magnolia extract (BL153) on obesity-associated lipid accumulation, inflammation, oxidative stress, and apoptosis in the heart. C57BL/6 mice were fed a low- (10 kcal% fat) or high-fat (60 kcal% fat) diet for 24 weeks to induce obesity. These mice fed with high-fat diet (HFD) were given a gavage of vehicle, 2.5, 5, or 10 mg/kg body weight BL153 daily. The three doses of BL153 treatment slightly ameliorated insulin resistance without decrease of body weight gain induced by HFD feeding. BL153 at 10 mg/kg slightly attenuated a mild cardiac hypertrophy and dysfunction induced by HFD feeding. Both 5 mg/kg and 10 mg/kg of BL153 treatment significantly inhibited cardiac lipid accumulation measured by Oil Red O staining and improved cardiac inflammation and oxidative stress by downregulating ICAM-1, TNF-alpha, PAI-1, 3-NT, and 4-HNE. TUNEL staining showed that BL153 treatment also ameliorated apoptosis induced by mitochondrial caspase-3 independent cell death pathway. This study demonstrates that BL153 attenuates HFD-associated cardiac damage through prevention of HFD-induced cardiac lipid accumulation, inflammation, oxidative stress, and apoptosis.
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页数:13
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