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ORIGINAL ARTICLE
Year : 2010  |  Volume : 6  |  Issue : 23  |  Page : 191-197

Preservation on calcium homeostasis is involved in mitochondrial protection of Limonium sinense against liver damage in mice


1 Jiangsu Provincial Key Laboratory of Coastal Wetland Bioresources and Environmental Protection, Yancheng Teachers' University, 50 Kaifang Road, Yancheng, 224002, China; School of Pharmacy, Jiangsu University, 301 Xuefu Road, Zhenjiang, 212013, China
2 School of Life Science, Nanjing University, 22 Hankou Road, Nanjing, 210009, China; Burnett School of Biomedical Sciences, University of Central Florida, Orlando, FL 32816, USA
3 Jiangsu Provincial Key Laboratory of Coastal Wetland Bioresources and Environmental Protection, Yancheng Teachers' University, 50 Kaifang Road, Yancheng, 224002, China
4 School of Pharmacy, Jiangsu University, 301 Xuefu Road, Zhenjiang, 212013, China

Correspondence Address:
Jing Gao
School of Pharmacy, Jiangsu University, 301 Xuefu Road, Zhenjiang, 212013, China

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Source of Support: Natural Science Fund of Jiangsu Province (No. BK2009172), the Natural Science Foundation of Education Department of Jiangsu Province (Key Project No. 07KJA18017), the Natural Science Research Foundation of Jiangsu Province Higher Education (No. 08KJB360011), the "333 Project" Funding for the Jiangsu Province, and the "Qinglan Project" Funding for the Young Core Teacher of Jiangsu Province, Conflict of Interest: None


DOI: 10.4103/0973-1296.66935

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Mechanisms underlying the mitochondrial protection of Limonium sinense extracts (LSE) was studied in lipopolysaccharide and D-galactosamine (LPS/D-GalN) intoxicated mice. It was found that increased activities of serum aspartate aminotransferase and alanine aminotransferase induced by LPS/D-GalN were significantly inhibited by pretreatment with LSE. The obvious disruption of membrane potential, intramitochondrial Ca 2+ overload and suppression in mitochondrial Ca 2+ -ATPase activity induced by LPS/D-GalN were significantly blocked by pretreatment with LSE. It was concluded that mechanisms underlying protection of LSE against liver mitochondria damage might be related to the preservation on mitochondrial Ca 2+ homeostasis through the preservation on mitochondrial Ca 2+ -ATPase activity.


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