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SMND‐309, a Novel Derivate of Salvianolic Acid B, Attenuates Apoptosis and Ameliorates Mitochondrial Energy Metabolism in Rat Cortical Neurons
Author(s) -
Tian Jingwei,
Li Guisheng,
Zhang Shumin,
Gao Yubai,
Jiang Wanglin,
Fu Fenghua,
Liu Zhifeng
Publication year - 2009
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2008.00349.x
Subject(s) - lactate dehydrogenase , mitochondrion , chemistry , apoptosis , antioxidant , intracellular , malondialdehyde , adenosine triphosphate , pharmacology , biochemistry , mitochondrial respiratory chain , enzyme , medicine
SMND‐309, a novel compound (2E)‐2‐{6‐[(E)‐2‐carboxyvinyl]‐2,3‐dihydroxyphenyl}‐3‐(3,4‐dihydroxyphenyl) acrylic acid, is a new derivate of salvianolic acid B. The present study elucidates the effects of SMND‐309 on the cultured rat cortical neuron damage induced by oxygen‐glucose deprivation. The results show that SMND‐309 treatment obviously attenuates apoptosis and ameliorates mitochondrial energy metabolism in rat cortical neurons by increasing cell survival rate, mitochondrial antioxidant enzyme activities, mitochondrial respiratory enzymes activities, mitochondrial respiratory control ratio and the adenosine triphosphate content, and by decreasing mitochondrial malondialdehyde content, lactate dehydrogenase release, intracellular Ca 2+ level and caspase‐3 activity in a concentration‐dependent manner. Moreover, SMND‐309 exhibits significantly higher potency as compared to salvianolic acid B. These findings indicate that SMND‐309 has a protective potential against cerebral ischaemic injury and its protective effects may be due to the suppression of intracellular Ca 2+ elevation and caspase‐3 activity, and improvement of mitochondrial energy metabolism and antioxidant property.