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1. Ligustrazine improves atherosclerosis in rat via attenuation of oxidative stress | |||
Liu Chang,Jiang Fengrong,Chen Siyu,Zhang Wenbo,Qian Jinchun | |||
Biology 27 December 2010 | |||
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Abstract:Context: Ligustrazine (Lig) is a compound isolated from the rhizome of Ligusticum walliichi (Ligusticum Chuanxiong Hort) and has been reported to be effective for the treatment of a variety of vascular diseases.Objective: The anti-atherosclerotic activities of Lig are evaluated in vivo for the first time in the present study. Materials and methods: We gave rats a single injection of vitamin D3 and then fed them with an atherogenic diet for 6 weeks to induce atherosclerosis. Lig was simultaneously given to rats by gavage in the therapy groups. The effects of Lig on blood parameters, aorta and liver histology, and gene expression were investigated. In addition, the solely effects of Lig on food intake, body weight gain, and taste preference were also evaluated.Results: We found that Lig decreased the total cholesterol, triglyceride, and low density lipoprotein levels while it increased high density lipoprotein level in the plasma. The circulating endothelial cells were also decreased in Lig-treated rats, indicating the attenuation of endothelial injury. In contrast, Lig restored the total antioxidant capacity and SOD1 activity while decreasing the MDA generation. Furthermore, Lig improved liver dysfunction by decreasing ALT and AST levels. Histological examinations revealed that Lig suppressed atherosclerotic plaque progression in the thoracic aorta and lipid accumulation in the liver. At the transcriptional level, Lig inhibited the induction of antioxidant genes both in aorta and in liver. Lig also suppressed the mRNA expression of the genes involved in the hepatic fatty acid oxidation. Finally, Lig had a minimum effect on food intake, body weight gain, and taste preference.Discussion and conclusion: Our results suggest that Lig suppresses the development of atherosclerosis and hepatic lipid accumulation via the alleviation of oxidative stress and the improvement of dyslipidemia. | |||
TO cite this article:Liu Chang,Jiang Fengrong,Chen Siyu, et al. Ligustrazine improves atherosclerosis in rat via attenuation of oxidative stress[J]. |
2. PGC-1 coactivators in the control of energy metabolism | |||
Liu Chang,Lin Jiandie | |||
Biology 27 December 2010 | |||
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Abstract: Chronic disruption of energy balance, where energy intake exceeds expenditure, is a major risk factor for the development of metabolic syndrome. The latter is characterized by a constellation of symptoms including obesity, dyslipidemia, insulin resistance, hypertension, and non-alcoholic fatty liver disease (NAFLD). Altered expression of genes involved in glucose and lipid metabolism as well as mitochondrial oxidative phosphorylation (OXPHOS) has been implicated in the pathogenesis of these disorders. The peroxisome proliferator-activated receptor (PPAR)-γ coactivator-1 (PGC-1) family of transcriptional coactivators is emerging as a hub linking nutritional and hormonal signals and energy metabolism. PGC-1α and PGC-1βare highly responsive to a variety of environmental cues and coordinates metabolic gene transcription through interaction with transcription factors and chromatin-remodeling proteins. PGC-1α has been implicated in the pathogenic conditions such as obesity, type 2 diabetes, neurodegeneration, and cardiomyopathy, whereas PGC-1βplays an important role in plasma lipoprotein homeostasis and serves as a hepatic target for niacin, a potent hypotriglyceridemic drug. Here, we review recent advances in the identification of physiological and pathophysiological contexts involving PGC-1 coactivators, and also discuss their implications for therapeutic development. | |||
TO cite this article:Liu Chang,Lin Jiandie. PGC-1 coactivators in the control of energy metabolism[J]. |
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